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Neonatology Notes

Medicine Notes > Paediatrics Notes

This is an extract of our Neonatology document, which we sell as part of our Paediatrics Notes collection written by the top tier of University Of Nottingham students.

The following is a more accessble plain text extract of the PDF sample above, taken from our Paediatrics Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Neonatology The Normal Newborn Physiology

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In the fetus:

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Lungs are filled with fluid

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Oxygen is supplied by the placenta

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There is a high pulmonary vascular resistance

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LA pressure is low due to limited return from the lungs

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RA>LA, due to RA receiving venous return including blood from the placenta maintains foramen ovale (right to left shunt)

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SEE pg 142 of Illustrated for Fetal Circulation diagram

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The first breath occurs (on average) 6 seconds after delivery with regular breathing after about 30 seconds

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Pulmonary expansion at birth is associated with a rise in oxygen tension, and with falling pulmonary vascular resistance the pulmonary blood flow increases sixfold

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Increased LA filling and reduced pressure in the RA due to exclusion of the placenta closes the foramen ovale

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After an elective CS - mother has not gone through labour and the infant's chest has not been squeezed, it may take several hours for pulmonary fluid to be reabsorbed leading to rapid, labored breathing transient tachypnea of the newborn.

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Failure to breath at birth - causes include

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Asphyxia

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Birth trauma

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Maternal analgesia or anaesthetic agents

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Retained lung fluid, preterm infant or congenital malformation

Asphyxia may be:

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Continous asphyxia - abruption or cord prolapse

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Intermitten asphyxia - prolonged and frequent contractions. Etc.

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A fetus deprived of oxygen in utero will try to breath - when this fails primary apnoea, HR is maintained

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Primary apnoea may be followed by irregular gasping and a second period of apnoea secondary or terminal apnoea - HR and BP fall

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Requires CPAP

Apgar Score Heart Rate Respiratory Rate Muscle Tone Reflex Irritability Colour

0 Absent Absent Flaccid None Pale/blue

1 <100 bpm Gasping / irregular Some flexion Grimace Body pink, extremities blue

2 >100 bpm Regular, strong cry Well flexed, active Cry, cough Pink

Routine Examination of the Newborn

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Birthweight, gestational age and birthweight noted

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General observation

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Head circumference normal at term is 3337cm

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Fontanelle and sutures are palpated anterior normally is 4 x 4cm

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Tense fontanelle when the baby isn't crying may indicate raised ICP

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May also be a sign of meningitis

Face is observed

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Characteristic facies in certain syndromes

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If plethoric or pale - check hematocrit to identify polycythaemia or anaemia

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Jaundice within 24 hours required further evaluation

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Eyes are checked for a red reflex

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Absent may be due to cataracts, retinoblastoma and corneal opacity

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Palate needs to be inspected

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Breathing and chest movement

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Auscultate the heart

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Normal rate is 110160 bpm in term babies

Palpate the abdomen

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Liver extends 12cm below the costal margin

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Spleen tip may be palpable as may the left kidney

Femoral pulses are palpated

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RR normally 4060 per minute

Reduced in coarction confirm by measuring the blood pressure in the arms and legs

Inspect genitalia and anus

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Clitoris and labia

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Descent of testes in males

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Muscle tone assess by observing limb movements

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Whole of the back and spine inspected

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Hips are checked for DDH

o Vitamin K Therapy

Barlow manoeuvre and Ortolani manoeuvre

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Vitamin K deficiency can result in haemorrhagic disease of the newborn

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Can occur early during the first week of life or between 1 and 8 weeks

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Haemorrhage can be mild bruising, haematemesis, malaena or prolonged bleeding from the umbilical stump

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Some suffer from intracranial haemorrhage - resulting in disability or death

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Breast milk is a poor source of vitamin K Vs. formula feed

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Disease can be prevented by IM vitamin K immediately after birth

Guthrie Screening

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Heel prick is taken on day 59

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In the UK all infants are screened for:

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PKU (phenylalanine)

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Hypothyroidism

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Haemoglobinopathies (sickle cell and thalassaemia)

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CF - measure serum immunoreactive trypsin (raised if there is pancreatic duct obstruction) - if raised DNA analysis

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MCAD (medium chain acylCoA dehydrogenase) deficiency

Know the Important Time Frames for the Newborn

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Bowels - usually within 6 hours up to 24 hours

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Bladder - up to 24 hours

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Weight - newborns lose around 710% of weight but should regain it by 2 weeks

HypoxicIschaemic Encephalopathy

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Perinatal asphyxia gas exchange (placental or pulmonary) is compromised

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Respiratory depression hypoxia, hypercarbia and respiratory acidosis

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Circulatory depression low CO, reduced tissue perfusion, ischaemia, metabolic acidosis, capillary leak and oedema

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Leads to Hypoxic Ischaemic Encephalopathy (HIE) with multi organ dysfunction

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Encephalopathy abnormal neurology and seizures

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Respiratory failure persistent pulmonary hypertension of the newborn (PPHN)

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Myocardial dysfunction hypotension

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Metabolic hypoglycaemia, hypocalcaemia, hyponatraemia

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Other organ dysfunction renal failure, D

Occurs in 0.51 per 1000 infants develop HIE and 0.3 per 1000 have significant disability

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Causes include:

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Failure of placental gas exchange - excessive contractions, abruption, ruptured uterus

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Interruption of umbilical blood flow - cord compression (shoulder dystocia, cord prolapse)

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Inadequate maternal placental perfusion - maternal hypo or hypertension

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Compromised fetus - anaemia, IUGR

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Failure of cardiorespiratory adaptation at birth

Clinical manifestations occur 48 hours after asphyxia

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Mild irritable, responds excessively to stimulation, staring eyes, hyperventilation and impaired feeding

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Moderate marked abnormal tone and movement, cannot feed, may have seizures

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Severe

no normal spontaneous movements or response to pain, fluctuating hypo and

hypertonia, seizures are prolonged and refractory to treatment, multi organ failure

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Management

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Respiratory support

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Amplitudeintegrated electroencephalogram (aEEG)

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Treat seizures

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Fluid restriction due to renal impairment

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Treat hypotension by volume and inotrope support

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Monitor and treat hypoglycaemia and electrolyte imbalance

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Mild hypothermia may be beneficial if started within 6 hours

Prognosis

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If MILD complete recovery may be expected

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If MODERATE with full neuro recovery and feeding by 2 weeks - looking goodo

Persistent beyond this time - not looking great

SEVERE - mortality of 3040%, 80% have disabilityEsp. Cerebral palsy

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Esp. if MRI at 414 days shows bilateral abnormality in the basal ganglia, thalamus and lack of myelin in the posterior limb of the internal capsule

The Preterm Infant Respiratory Distress Syndrome

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Deficiency of surfactant which lowers surface tension

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Leads to widespread alveolar collapse and inadequate gas exchange

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Glucocorticoids given to the mother stimulate surfactat production

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Development of surfactant therapy which can be instilled directly into the lung by an endotracheal tube

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At delivery or within 4 hours babies develop clincal signs:

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Tachypnoea >60 breaths per min

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Laboured breathing - chest wall recession, and nasal flaring

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Expiratory grunting in an attempt to generate positive airway pressure during expiration

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Cyanosis if sever

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Characteristic chest XR ground glass appearance with air bronchograms

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Treatment with raised ambient oxygen is required

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Supplement with CPAP via nasal cannulae

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OR artificial ventilation via a tracheal tube

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Ventilatory requirements matched to the infants oxygenation, chest wall movement and blood gases

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Surfactant therapy as above

Pneumothorax

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In RDS - air from the overdistended alveoli may track into the intersititium resulting in pulmonary interstitial emphysema

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In up to 10% of infants ventilated for RDS air leaks into the pleural cavity causing pneumothoraz

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Oxygen requirement will increase

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Breath sounds and chest movement on the affected side are reduced

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Demonstrated by transillumination

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Tension pneumothorax is relieved by inserting a chest drain

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Prevent ventilate at low pressures (which provide adequate chest movement and blood gases)

Apnoea, Bradycardia and Desaturation

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Episodes are common in very low birthweight infants until they reach 32 weeks gestational age

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Bradycardia may occur when an infant stops breathing for 2030 seconds or when breathing continues against a closed glottis

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Underlying cause should be excluded (hypoxia, anaemia, infection, electrolyte disturbance, hypoglycaemia, seizures, HF or aspiration due to reflux)

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Commonly due to immaturity of the central respiratory control

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Breathing starts after tactile stimulation

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Treatment with caffeine or CPAP may be necessary

Bronchopulmonary Dysplasia

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Also known as chronic lung disease

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Defined as infants who still require oxygen at a postmenstrual age of 36 weeks (OR oxygen dependence at 28 days)

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Lung damage comes from trauma from artificial ventilation, oxygen toxicity and infection (possible Ureaplasma urealyticum)

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Features include: dyspnoea, supplemental oxygen dependence, bronchospasm, feeding difficulty and growth failure

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CXR areas of widespread opacification, sometimes with cystic changes

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Most infants are weaned onto CPAP followed by ambient oxygen

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Keep sats above 95% to reduce pulmonary HTN risk

Corticosteroid therapy may allow earlier weaning

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Concern over increased risk of abnormal neuro development and cerebral palsy

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Short courses to severely ill babies

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Few infants with severe disease may die of intercurrent infection or pulmonary hypertension

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Subsequent pertussis or RSV may cause respiratory failure

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Consider palivizumab Vs. RSV

Temperature Control

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Temperature causes increased energy consumption and may result in hypoxia and hypoglycaemia, failure to gain weight and increased mortality

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Preterm infants are vulnerable due to

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Large surface area (heat loss) to mass (heat production)

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Skin is thin and heat permeable

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Little subcutaneous fat

Prevention of heat loss in newborn infants

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Convection ambient air incubator, clothes (cover head), avoid draughts

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Radiation cover baby, double walls of incubators

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Evaporation dry and wrap at birth, place in plastic bag, humidify incubator

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Conduction heated mattress

Necrotising Enterocolitis

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Affects preterm infants in 1st week

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Bacterial invasion of ischaemic bowel wall

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Decreased risk in those who are breast fed

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Predisposing Factors

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Prematurity

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IUGR

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Hypoxia

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Polycythaemia

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Exchange transfusion

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Cow's milk

Clinically - Early

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Non specific illness

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Infants stop feeding

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Bilious vomiting

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Blood, mucus or tissue in stool

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Abdomen becomes distended

Clinically Late

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Bowel perforation

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Shock may develop

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DIC, multiorgan failure

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Pneumatosis intestinalis (cysts soap bubble sign)

Investigations

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FBC, U&E, Creatinine, Coagulation Screen, Albumin

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ABG

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Blood culture, Stool Culture

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Characteristic XR shows distended loops of bowel, thickening of bowel wall with intramural gas

Can progress to bowel perforation (transillumination of bowel and football sign on XR [gas outlining falciform ligament])

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Rx stop oral feeding, give broad spec antibiotics, parenteral nutrition

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Mortality of 20%

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