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PAEDS - NEONATAL Flashcards

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1
Q

PAEDIATRIC LIFE SUPPORT
What is the first step of neonatal resuscitation?
How does it differ if the baby is <28w?

A
  • Warm + dry baby ASAP by vigorous drying (may stimulate breathing)
  • Heat lamp
  • Babies <28w in plastic bag while still wet + manage under heat lamp
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2
Q

PAEDIATRIC LIFE SUPPORT
What should be calculated whilst neonatal resuscitation occurs?
What is the next stage?

A
  • APGAR at 1, 5 + 10m
  • Stimulate breathing with vigorous drying
  • Place baby’s head in neutral position to keep airway open (towel under shoulder can help)
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3
Q

PAEDIATRIC LIFE SUPPORT
If breathing stimulation fails what is the next stage of neonatal resuscitation?

A

Inflation breaths if gasping or not breathing –

  • 2 cycles of 5 inflation breaths
  • No response + HR low = 30s of ventilation breaths
  • No response, HR <60bpm = chest compressions (3:1 with ventilation breaths)
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4
Q

PAEDIATRIC LIFE SUPPORT
You come across an unconscious child.
What are the first steps you would perform?

A
  • Danger = ensure safety
  • Unresponsive = shout for help
  • Open airway = head tilt + chin lift or jaw thrust
  • Look, listen + feel for breathing (noisy gasps do not count)
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5
Q

PAEDIATRIC LIFE SUPPORT
It appears that this child is not breathing.
What is your next step and explain how this would differ depending on the child’s age?

A
  • 5 rescue breaths
  • Infants = neutral position, cover mouth + nose with whole mouth
  • > 1y = head tilt chin lift, pinch soft part of nose + seal mouths
  • Ensure chest rise/fall for effectiveness (if not ?obstruction or try jaw thrust)
  • Note any gag or cough response to actions as sign of life
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6
Q

PAEDIATRIC LIFE SUPPORT
You have performed your 5 rescue breaths but there was no coughing or response to your efforts
What should be done next?

A

Check circulation –

  • Infant = brachial or femoral
  • Child = femoral or carotid
  • If pulse felt = continue rescue breathing until child takes over
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7
Q

PAEDIATRIC LIFE SUPPORT
You do not feel a pulse.
What should you do now?

A
  • Chest compressions 15:2 rescue breaths
  • Depress sternum by one-third depth of chest
  • Rate of 100-120bpm
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8
Q

PAEDIATRIC LIFE SUPPORT
How will your CPR technique depend on the child?

A
  • Infant = tips of two fingertips or encircle with thumbs
  • > 1y = heel of 1 hand on lower sternum
  • Larger = 2 hands interlocked as for adults
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9
Q

PAEDIATRIC LIFE SUPPORT
You are at a restaurant and notice a situation at the table next to you and offer support. A child appears to be choking.
What would indicate an effective cough and how would you manage this?

A
  • Loud, responsive, able to breathe, verbal
  • Encourage cough + continue to observe for deterioration or until obstruction relieved
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10
Q

PAEDIATRIC LIFE SUPPORT
What would indicate an ineffective cough and how would you manage this?

A
  • Unable to vocalise/breathe, cyanosis, silent/quiet cough
  • Conscious = 5 back blows, 5 thrusts
  • Unconscious = open airway, 5 breaths, CPR
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11
Q

PAEDIATRIC LIFE SUPPORT
How do the choking techniques differ for age?

A
  • Chest thrusts for infant, abdominal if >1y
  • Infants head down prone for back blows, supine for thrusts
  • Back blows more effective if child’s head down
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12
Q

PREMATURITY
What are some respiratory complications of prematurity?

A
  • Apnoea,
  • RDS,
  • bronchopulmonary dysplasia,
  • infections
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13
Q

PREMATURITY
What are some GI complications of prematurity?

A
  • Necrotising enterocolitis,
  • neonatal jaundice,
  • feeding issues
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14
Q

PREMATURITY
What are some neuro complications of prematurity?

A
  • Cerebral palsy,
  • hearing/visual impairment,
  • intraventricular haemorrhage
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15
Q

PREMATURITY
What are some metabolic complications of prematurity?

A
  • Hypoglycaemia,
  • hypocalcaemia,
  • electrolyte imbalance,
  • fluid imbalance
  • hypothermia
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16
Q

PREMATURITY
What causes feeding problems in prematures babies?
How quickly should you build up feeds and why?

A
  • Unable to suck + swallow until 33–34w so will need NG
    • Build feeds up slowly to reduce risk of NEC
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17
Q

PREMATURITY
What causes hypoglycaemia?

A

Lack of glycogen stores

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18
Q

PREMATURITY
What causes hypocalcaemia?

A

Kidneys + parathyroid not fully developed

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19
Q

PREMATURITY
What causes electrolyte, fluid imbalance + hypothermia?

A

Excess losses through skin

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20
Q

RDS
What is the pathophysiology respiratory distress syndrome (RDS)?

A
  • Inadequate surfactant > high surface tension within alveoli
  • Leads to atelectasis (lung collapse) as more difficult for alveoli + lungs to expand so there’s inadequate gas exchange > hypoxia, hypercapnia + respiratory distress
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21
Q

RDS
What are some risk factors of RDS?

A
  • Prematurity #1
  • Maternal DM
  • 2nd premature twin
  • C-section
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22
Q

RDS
What is the clinical presentation of RDS?

A
  • Tachypnoea >60bpm
  • Increasing oxygen need
  • Laboured breathing = sternal + subcostal indrawing, nasal flaring, grunting
  • Cyanosis if severe
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23
Q

RDS
What is the investigation for RDS?

A

CXR –

  • Reticular “ground-glass” changes
  • Heart borders indistinct
  • Air bronchograms
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24
Q

RDS
What are the short and long term complications of RDS?

A
  • Short = pneumothorax, infection, apnoea, necrotising enterocolitis
  • Long = bronchopulmonary dysplasia, retinopathy of prematurity
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25
RDS What emergency treatment is required before the delivery of any preterm infant?
- Antenatal dexamethasone - Increases surfactant production
26
RDS What is the management of RDS?
- Assisted ventilation by CPAP keeping lungs inflated or intubation if severe - Endotracheal surfactant via endotracheal tube - Supplementary oxygen for SpO2 91–95% - Breathing support gradually stepped down as baby develops
27
NEC. ENTEROCOLITIS What is necrotising enterocolitis?
- Disorder affecting premature neonates where part of bowel becomes necrotic - Associated with bacterial invasion of ischaemic bowel wall
28
NEC. ENTEROCOLITIS What are some risk factors for necrotising enterocolitis?
- Very LBW + premature - Formula feeds (breast milk protective) - RDS + assisted ventilation - Sepsis - PDA + other CHD
29
NEC. ENTEROCOLITIS What is the clinical presentation of necrotising enterocolitis?
- Bilious vomiting - Intolerance to feeds - Distended, tender abdo with absent bowel sounds - Bloody stools
30
NEC. ENTEROCOLITIS What are some investigations for necrotising enterocolitis?
- Blood culture (sepsis) - CRP - Capillary blood gas = metabolic acidosis - AXR is diagnostic
31
NEC. ENTEROCOLITIS What would an AXR show in necrotising enterocolitis?
- Dilated loops of bowel - Bowel wall oedema (thickened bowel walls) - Pneumatosis intestinalis (intramural gas) - Pneumoperitoneum (free gas in peritoneum = perf) - Football sign = air outlining falciform ligament - Rigler's sign = air both inside/outside bowel wall - Gas in portal veins
32
NEC. ENTEROCOLITIS What are some complications of necrotising enterocolitis?
- Dead bowel > perforation + peritonitis > sepsis + shock - Stricture formation - Short bowel syndrome (malabsorption) if extensive resection required
33
NEC. ENTEROCOLITIS What is the management of necrotising enterocolitis?
- A–E if shocked, ?artificial ventilation, ?circulatory support - Broad spec Abx 1st, NBM with IV fluids + total parenteral nutrition (NG to drain gas + fluid from stomach + intestines) - Surgical emergency > laparotomy for perforation
34
JAUNDICE What is jaundice?
- Abnormally high levels of bilirubin in the blood
35
JAUNDICE What is the physiology relating to jaundice?
RBCs contain unconjugated bilirubin, they breakdown + release it into blood, conjugated in liver + excreted via biliary system (GI tract) or urine
36
JAUNDICE What are some risk factors for jaundice?
- LBW - Breastfeeding - Prematurity - FHx - Maternal diabetes
37
JAUNDICE Jaundice can be split into 3 aetiological time categories. What are these?
- <24h = always pathological, usually haemolytic disease - 24h–2w = common - >2w = also bad
38
JAUNDICE What are some causes of jaundice <24h after birth?
- Haemolytic diseases #1 = rhesus or ABO incompatibility, G6PD, spherocytosis - Congenital infection (TORCH), sepsis
39
JAUNDICE What are some causes of jaundice 24h–2w after birth?
- Physiological + breast milk jaundice (common) - Infection (UTI, sepsis) - Haemolysis, polycythaemia, bruising - Crigler-Najjar syndrome (rare inherited disorder with no UGT enzyme)
40
JAUNDICE What are some causes of jaundice >2w after birth?
- Unconjugated = physiological or breast milk, UTI, hypothyroid, high GI obstruction (pyloric stenosis), Gilbert syndrome - Conjugated (>25umol/L) = bile duct obstruction (biliary atresia), neonatal hepatitis
41
JAUNDICE How does jaundice present? When would you worry about jaundice persisting?
- Yellow skin/sclera (may be more visible when outside in sunlight) - Persistent or prolonged jaundice worrying (>2w full term, >3w preterm)
42
JAUNDICE What is physiological jaundice?
- High concentration of RBCs in neonate which are more fragile with shorter life - Less developed liver - Foetal RBCs breakdown more rapidly releasing lots of bilirubin > normal rise in bilirubin = mild jaundice from 2–7d
43
JAUNDICE How is physiological jaundice diagnosed? How is physiological jaundice managed?
- Only when all other causes excluded - Usually completely resolves by 10d, most babies otherwise healthy
44
JAUNDICE What might cause breast milk jaundice?
- Components of breast milk inhibiting liver to process bilirubin - Increased bilirubin absorption - Inadequate feeds > slow passage of stools
45
JAUNDICE What is Gilbert's syndrome? How does it present?
- AR deficiency of UDP-glucuronyltransferase = defective bilirubin conjugation - Unconjugated hyperbilirubinaemia (not in urine), jaundice may only be present if ill, exercising or fasting
46
JAUNDICE What investigations would you perform in neonatal jaundice?
- FBC + blood film (polycythaemia, G6PD, spherocytosis) - Bilirubin levels - Blood type testing of mother + baby for ABO/Rh incompatibility - Direct Coombs (antiglobulin) test for haemolysis - TFTs, LFTs + urine MC&S
47
JAUNDICE When measuring bilirubin levels what are you looking for? How would you measure bilirubin levels depending on age?
- Split bilirubin = unconjugated (extra-hepatic) or conjugated (hepatobiliary) - >24h old = transcutaneous bilirubin meter if high, serum to confirm within 6h - <24h old = serum bilirubin within 2h
48
JAUNDICE What is the main complication of jaundice? What is it?
- Kernicterus - Bilirubin-induced encephalopathy caused by unconjugated bilirubin deposition in brain (basal ganglia + brainstem nuclei) as baby's BBB are not well developed
49
JAUNDICE What increases the risk of kernicterus?
- Prematurity as immature liver
50
JAUNDICE How does kernicterus present? What are the outcomes?
- Lethargy, poor feeding > hypertonia, seizures + coma - Permanent damage = dyskinetic cerebral palsy, LD + deafness
51
JAUNDICE What is the management of jaundice?
- Bilirubin Tx threshold charts, plot age of baby against total bilirubin level + treat once at threshold - Phototherapy (450mm wavelength blue-green band) - Exchange transfusion if severe
52
JAUNDICE What is phototherapy?
- Converts unconjugated bilirubin > water-soluble pigment that can be excreted in urine, cover infant's eyes
53
JAUNDICE What are some side effects of phototherapy?
- Temp instability, - macular rash, - bronze discolouration
54
HIE What is hypoxic ischaemic encephalopathy (HIE)?
- In perinatal asphyxia, gas exchange, either placental or pulmonary is compromised or ceases resulting in cardiorespiratory depression
55
HIE What happens as a result of cardiorespiratory depression?
- Hypoxia, hypercarbia + metabolic acidosis - Compromised cardiac output reduces tissue perfusion > hypoxic ischaemic injury to brain
56
HIE What are the causes of HIE?
Anything leading to asphyxia = - maternal shock, - intrapartum haemorrhage, - prolapsed or nuchal cord, - placental abruption
57
HIE What is used to stage the severity of HIE? What are the stages?
Sarnat staging – - Mild = poor feeding, generally irritable + hyperalert, resolves in 24h - Moderate = poor feeding, lethargic, hypotonic, seizures, can take weeks to resolve - Severe = reduced GCS, apnoeas, flaccid + reduced/absent reflexes, half die
58
HIE What is the main complication of HIE? How common is it?
- Permanent brain damage > cerebral palsy - Moderate = 40%, - severe = 90%
59
HIE What is the acute management of HIE?
MDT resus – - Dry baby, APGAR, resp support - Treat seizures, EEG - Treat hypotension by volume + inotropes - Monitor + treat electrolytes
60
HIE What is the main therapeutic management of HIE?
- Therapeutic hypothermia to protect brain from hypoxic injury - Cooled to PR temp 33–34 for 72h to reduce brain damage
61
NEONATAL HYPOGLYCAEMIA What is neonatal hypoglycaemia?
- No agreed definition but <2.6mmol/L often used
62
NEONATAL HYPOGLYCAEMIA What are some risk factors for neonatal hypoglycaemia?
- Preterm + intrauterine growth restriction (IUGR) = lack of glycogen stores - Maternal DM = infantile hyperinsulinaemia - LGA, polycythaemia or ill - Transient hypoglycaemia common in first hours after birth
63
NEONATAL HYPOGLYCAEMIA How does neonatal hypoglycaemia present?
- Jitteriness, irritability, apnoea - Lethargy, drowsiness + Seizures - Long-term may cause permanent neuro disability
64
NEONATAL HYPOGLYCAEMIA What is the management of neonatal hypoglycaemia?
- Regular bedside BM - Prevent by early + frequent feeding - IVI 10% dextrose (central venous catheter if higher concentration of dextrose to prevent skin necrosis) to maintain glucose >2.6mmol/L
65
TORCH What are the TORCH conditions?
Main congenital conditions - Toxoplasmosis, - Other (HIV), - Rubella, - CMV, - Herpes + Syphilis
66
TORCH What are the characteristic features of toxoplasmosis?
- Cerebral calcification, chorioretinitis + hydrocephalus
67
TORCH What is CMV? How is it contracted?
- Most common congenital infection - Herpes simplex virus via personal contact
68
TORCH How is CMV managed?
No therapy so no screening
69
TORCH What is the clinical presentation of CMV?
- 90% normal at birth - 5% = hepatosplenomegaly, petechiae at birth, growth issues, neurodevelopmental disabilities (cerebral palsy, epilepsy, microcephaly) - 5% = problems later in life, mainly sensorineural hearing loss
70
TORCH How does herpes simplex virus present?
- Herpetic lesions on skin or eye, encephalitis or disseminated disease
71
TORCH How is herpes simplex virus managed?
Aciclovir, high mortality in disseminated
72
TORCH How does syphilis present?
- Rash on soles of feet + hands - Hutchinson's triad = keratitis, deafness, small + pointed teeth
73
TORCH How is syphillis managed?
- If fully treated ≥1m before delivery = no treatment - Any doubts = benzylpenicillin
74
MECONIUM ASPIRATION What is meconium aspiration?
- Meconium may be passed due to foetal hypoxia + at birth these infants may inhale it - Lung irritant resulting in mechanical obstruction + chemical pneumonitis + predisposing to infection
75
MECONIUM ASPIRATION What are some risk factors for meconium aspiration?
- Post-term deliveries at 42w - Maternal HTN or pre-eclampsia - Smoking or substance abuse - Chorioamnionitis
76
MECONIUM ASPIRATION What is the clinical presentation of meconium aspiration?
- Presence of meconium or dark green staining of amniotic fluid - Respiratory distress
77
MECONIUM ASPIRATION What investigation would you do in meconium aspiration?
- CXR = hyperinflation, accompanied by patches of collapse + consolidation - High incidence of air leak > pneumothorax
78
MECONIUM ASPIRATION What is a complication of meconium aspiration? What are some other risk factors for that complication?
- Persistent pulmonary HTN of the newborn due to high pulmonary vascular resistance - RDS, sepsis, congenital diaphragmatic hernia, maternal SSRI use, maternal NSAID use in 3rd trimester (early closure of DA)
79
MECONIUM ASPIRATION | What is the management of meconium aspiration?
- Artificial (positive pressure) ventilation with oxygenation - Suction if no breathing
80
CLEFT LIP AND PALATE What is a cleft lip?
- Split or open section in upper lip, can go up to the nose
81
CLEFT LIP AND PALATE What causes a cleft lip?
Failure of fusion of the frontonasal + maxillary processes
82
CLEFT LIP AND PALATE What is a cleft palate?
- Defect in hard or soft palate at roof of mouth which leaves an opening between the mouth + nasal cavity
83
CLEFT LIP AND PALATE What causes it?
Failure of the palatine processes + nasal septum to fuse
84
CLEFT LIP AND PALATE What are some causes of cleft lip + palate?
- Chromosomal disorder or maternal AED therapy
85
CLEFT LIP AND PALATE What are some complications?
Issues feeding, milk aspiration, speech delay + conductive hearing loss, recurrent otitis media (cleft palate)
86
CLEFT LIP AND PALATE What is the management of cleft lip + palate?
- MDT = plastic + ENT surgeons, paeds, orthodontist, SALT - Cleft lip repair ≤3m - Cleft palate repair 6-12m
87
OESOPHAGEAL ATRESIA What is oesophageal atresia?
- Upper + lower oesophagus in 2 sections + does not connect
88
OESOPHAGEAL ATRESIA What is it associated with?
- Tracheo-oesophageal fistula + polyhydramnios
89
OESOPHAGEAL ATRESIA What is the clinical presentation of oesophageal atresia?
- Persistent salivation + drooling from mouth after birth - May cough + choke when fed + have cyanotic aspiration - Some have other congenital malformations (VACTERL association)
90
OESOPHAGEAL ATRESIA What is the management of oesophageal atresia?
- Wide calibre feeding tube passed + checked by XR if reaches stomach - Continuous suction applied to tube passed into oesophageal pouch to reduce aspiration of saliva + secretions > neonatal surgical unit
91
GASTROSCHISIS What is gastroschisis?
- Bowel protrudes through congenital defect in anterior abdominal wall, adjacent to umbilicus but with no covering sac
92
GASTROSCHISIS What is gastroschisis associated with?
- Socioeconomic deprivation (smoking, mum <20y)
93
GASTROSCHISIS What is an investigation for gastroschisis?
- USS shows free loops of bowel in amniotic fluid antenatally
94
GASTROSCHISIS What is a complication of gastroschisis?
Higher risk of dehydration + protein loss – - Wrap infants in several layers of clingfilm to minimise fluid + heat loss - NG tube passed + aspirated frequently - IVI dextrose + colloid support for protein loss
95
GASTROSCHISIS What is the management of gastroschisis?
- May attempt vaginal delivery - Urgent repair (theatre within 4h)
96
BRONCHOPULMONARY DYSPLASIA What is chronic lung disease of prematurity, or bronchopulmonary dysplasia?
- Premature babies often <28w diagnosed when infant requires oxygen therapy after they reach 36w gestation
97
BRONCHOPULMONARY DYSPLASIA What is the pathophysiology of bronchopulmonary dysplasia?
- Reduced lung volume + reduced alveolar surface area > diffusion defect
98
BRONCHOPULMONARY DYSPLASIA What happens to babies with bronchopulmonary dysplasia at birth?
Suffer with RDS, need oxygen therapy or ventilation + intubation at birth
99
BRONCHOPULMONARY DYSPLASIA What is the clinical presentation of bronchopulmonary dysplasia?
- Increased work of breathing (tachypnoea, nasal flaring, recessions, low SpO2) - Crackles + wheezes on auscultation - Poor feeding + weight gain - Increased susceptibility to infection
100
BRONCHOPULMONARY DYSPLASIA What investigations would you do for bronchopulmonary dysplasia?
- CXR = widespread areas of opacification, cystic changes, fibrosis - Formal sleep study to assess SpO2 during sleep supports Dx + guides Mx
101
BRONCHOPULMONARY DYSPLASIA How can bronchopulmonary dysplasia be prevented?
- Corticosteroids to mothers in premature labour <34w - CPAP rather than intubation where possible - Use caffeine to stimulate resp effort - Do not over oxygenate
102
BRONCHOPULMONARY DYSPLASIA What is the management of bronchopulmonary dysplasia?
- Some babies go home with low dose oxygen, weaned over first year - Monthly IM palivizumab for RSV (+ bronchiolitis) protection
103
DUODENAL ATRESIA What is duodenal atresia?
- Congenital absence or complete closure of duodenum This causes intestinal obstruction
104
DUODENAL ATRESIA What is the clinical presentation?
- most appear well at birth - when they atart to feed they are sick (vomit is green) - jaundice - not pass meconium in first day
105
DUODENAL ATRESIA What can confirm it?
- AXR shows 'double bubble' from distension of stomach + duodenal cap
106
DUODENAL ATRESIA What is it associated with?
- Third have Down's
107
DUODENAL ATRESIA What is the management?
- Correct fluid + electrolyte depletion - surgical management is required to remove the narrowed part of bowel and reattach the ends.
108
EXOMPHALOS What is exomphalos, or omphalocele?
- Abdominal contents protrude through umbilical ring, covered with a transparent sac formed by the amniotic membrane + peritoneum
109
EXOMPHALOS What is exomphalos associated with?
- Other major congenital abnormalities, antenatal Dx
110
EXOMPHALOS What is the management?
C-section at 37w, staged repair as primary closure difficult
111
GROUP B STREP INFECTION how do babies become infected?
- it can be passed on from the mother during pregnancy - it can be passed from the mother's genital tract during birth
112
GROUP B STREP INFECTION which babies are at more risk of becoming infected with group B strep?
- preterm labour - premature rupture of membranes - a long time between rupture of membranes and birth - internal foetal monitor - fever - past pregnancy with baby who had strep B - african-american/hispanic - group B strep in urine during pregnancy
113
GROUP B STREP INFECTION what are the symptoms of group B strep infection in newborns?
- being fussy, sleepy + having breathing problems (signs of sepsis) - breathing fast + making grunting noises (signs of pneumonia) - breathing problems + periods not breathing - change in BP - convulsions
114
GROUP B STREP INFECTION what are the symptoms of group B strep infection in babies are a week old?
- decreased movement in arm or leg - pain with movement of arm or leg - breathing problems - fever - red area on face or other part of the body
115
GROUP B STREP INFECTION what are the symptoms of group B strep infection in pregnant women?
- having to urinate often - having a sudden urge to urinate - pain when urinating - fever - nausea and vomiting - pain in side or back - uterus or belly is sore - fast heart rate
116
GROUP B STREP INFECTION what are the investigations?
- blood cultures - lumbar puncture - sputum culture
117
GROUP B STREP INFECTION? what is the management?
- IV antibiotics - NICU admission
118
GROUP B STREP INFECTION what are the possible complications in pregnancy?
- chorioamnionitis - infection of the amniotic fluid, sac and placenta - endometritis - postpartum infection - preterm labour
119
GROUP B STREP INFECTION what are the possible complications in newborns?
- meningitis - pneumonia - sepsis
120
GROUP B STREP INFECTION? how can newborn infection be prevented?
- test for group B strep at 35-37 weeks of pregnancy (vaginal + rectal swab, urine sample) - if test is positive, have IV antibiotics during labour - may be given antibiotics for certain risk factors - previous pregnancy with strep B infection - premature rupture of membranes/premature labour - fever during labour - rupture of membranes >18hrs before delivery
121
LISTERIA INFECTION How do babies become infected?
- It can be acquired in the womb or during/after delivery - pregnant women can become infected by eating contaminated food - soft cheese, seafood, unpasteurised dairy etc
122
LISTERIA INFECTION what is the clinical presentation?
symptoms are similar to sepsis - listlessness, irritable, poor feeding - Early onset = low birth weight, obstetric complications, evidence of sepsis soon after birth - late onset = usually full-term, previously healthy neonates, present with meningitis/sepsis
123
LISTERIA INFECTION what is the prognosis?
- 10-50% of newborns with listeria infection die - the death rate is higher in those with early onset listeriosis
124
LISTERIA INFECTION what is the prevention?
- pregnant women should avoid eating unpasteurised dairy, soft cheeses, raw veg, deli meats, meat spreads and smoked seafood
125
LISTERIA INFECTION what is the management?
ampicillin + aminoglycoside (gentamycin)

My Phase 3a Revision (27 decks)

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