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Year 4 > Paeds > Flashcards

Paeds Flashcards

1
Q

def live attenuated vaccine

A

version of living microbe that has been weakened

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2
Q

def inactivated vaccine

A

killed microve

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3
Q

when should you not administer a vaccine

A
  • below age set
  • acutely unwell
  • anaphylaxis reaction to drug previously
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4
Q

different classification of children by age group

A
  • neonates: birth- 1m
  • infants: 1m-2y
  • young child: 2-6y
  • child: 6-12y
  • adolescent 12-18y
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5
Q

red flags of child development

A

not:

  • smiling by 8 weeks
  • following objects/face by 3 months
  • holdinh head up and turning to sound by 4 months
  • reaching for toys by 6 months
  • babbling by 8 months
  • transfer toys from one hand to another by 9 months
  • sitting without support by 9 months
  • wave goodbye by 10 months
  • mature pincer grip by 12 months
  • first word by 15 months
  • walking and feeding themselves by 18 months
  • symbolic play not reached by 2-2.5y
  • talking in sentences by 36 months
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6
Q

causes of stridor

A
  • croup
  • epiglottitis
  • bacterial tracheitis
  • foreign body (laryngeal or oesophageal)
  • anaphylaxis
  • inhalation of smoke
  • trauma
  • retropharyngeal abscess
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7
Q

epidemiology of croup

A

usually 6months to 6years

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8
Q

causes of croup

A

viral:

  • parainfluenza
  • adenovirus
  • RSV
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9
Q

presentation of croup

A
  • sudden onset, seal like barking cough
  • stridor: harsh, rasping
  • chest wall and/or sternal indrawing
  • typically worse at night and increase with agitation
  • hoarse voice
  • prodomal: 12-49h prior: non specific URTI
  • in moderate to severe cases: child showing signs of resp distress or failure
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10
Q

investigations for croup

A

clinical diagnosis but

CXR: subglottic narrowing

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11
Q

management of croup

A
  • analgesia
  • consider admission if moderate to severe illness or resp rate high with fever
  • dose of oral dexamethasone
  • emergency: nebulised adrenaline and high flow O2
  • safenetting (cant talk, drooling, wants to sit instead of lying, skin between ribs being pulled in, child pale/blue/grey for more than few sec)
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12
Q

cause of epiglottitis

A

haemophilus influenzae type B (Hib vaccine)

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13
Q

features of epiglottitis

A
  • rapid onset
  • high T, generally unwell
  • stridor: soft, whispering
  • drooling of saliva
  • ‘tripod’ position
  • voice: muffled, reluctant to speak
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14
Q

investigations for epiglottitis

A
  • direct visualisation

- XRAY if worried about foreign body: thumb sign, swollen epiglottitis

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15
Q

management of epiglottitis

A
  • immediate senior involvement
  • DO NOT EXAMINE THROAT (if so, make sure facilities for immediate intubation)
  • oxygen
  • IV antibiotics
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16
Q

presentation of foreign body inhalation

A
  • sudden onset resp distress

- associated with choking/gagging, coughing, stridor, vomiting

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17
Q

management of foreign body inhalation

A

assess severity
do they have effective/ineffective cough?
- if effective: encourgae cough
- if ineffective: 5 back blows/5 thrusts (if conscious), open airways 5 breats and start CPR (if unconscious)

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18
Q

what is anaphylaxis

A

type 1 hypersensitivity reaction

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19
Q

presentation of anaphylaxis

A
  • wheeze
  • stridor
  • pallor and sweating
  • hypotension, tachycardia
  • generalised pruritis
  • rash
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20
Q

management of anaphylaxis

A
  • adrenaline pen
  • antihistamines
  • advice on allergen avoidance
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21
Q

haemangioma

A
  • slowly progressive airway obstruction/stridor since birth
  • can have capillary haemangiomas (strawberry marks)
  • natural course: enlarge over first 12-24 months of life
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22
Q

presentation of GORD in infants

A
  • intermittent breathing difficulties with symptoms of stridor, episodes of colour changes and/or recurrent chest infections
  • reduced feeding
  • crying on or after feeding or on lying flat
  • vomiting
  • green faeces
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23
Q

treatment of GORD in infants

A
  • small regular feeds
  • correct feeding/burping technique
  • meds: carobel feed thickened, gaviscon, omeprazole
  • surgery
    (tends to resolve with weening)
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24
Q

which groups are high risk for GORD

A
  • neurological or muscular problems
  • pre-term
  • severe allergy
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25
Q

which sign points towards upper resp tract infection compared to LTRI

A

wheeze: lower
stridor: upper

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26
Q

signs of increased work on breathing

A 
tracheal tug 
recession 
increased resp rate 
abdominal breating 
cyanosis
'tripod' position
- stridor/hoarse voice/drroling ig upper airway obstruction
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27
Q

def acute, chronic and reccurent cough

A

acute <3 weeks

chronic: 4-8 weeks
reccurent: 2+ times a year

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28
Q

differentials of cough in children

A
  • congenital heart disease
  • asthma
  • infection (ie pneumonia)
  • pneumothorax (mainly teenagers)
  • sarcoidosis
  • foreign body inhalation
  • CF
  • parental cig smoking
  • functional ie tics, anxiety
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29
Q

def asthma

A

reversible, paroxysmal inflammation of the airwyas, accompanied by wheezing, coush, SOB and exacerbated at night and early morning

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30
Q

pathophysiology of asthma

A
  • airway obstruction
  • smooth muscle hyperplasia and hyperactivity
  • inflammation (histamine bvia IgE mediated allergens: increase mucus prod)
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31
Q

def status asthmaticus

A

asthma attack that does not respond to immediate medical treatment and is life threatening

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32
Q

types of asthma

A
  • atopic/extrinsic: allergic reaction from extrinsic source

- non-atopic/intrinsic: drug related, exercise, stress, occupational

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33
Q

precipitants of asthma

A
  • cold air and exercise
  • emotion
  • allergens
  • pollution and irritant dust, fumes, vapours
  • drugs (NSAIDs, beta blockers)
  • diet
  • infection, smoking
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34
Q

asthma: grading severity

A

Moderate:

  • PEFR > 50-75% best or predicted with normal speech
  • with no features of acute severe or life threatening asthma

Acute Severe:

  • PEFR 33-50% best predicted OR
  • Resp rate > 5-10 resp/min of normal for each age group OR
  • increased HR OR
  • inability to complete sentences OR
  • inability to feed in infants w/ O2sats > 92%

Life Threatening:

  • PEFR < 33% best or predicted OR
  • O2sats < 92% OR (any of the following individually
  • altered consciousness, exhaustion, cardiac arrhythmias, hypotension, cyanosis, poor resp effort, silent chest, confusion
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35
Q

what are predicters of good control of asthma

A
  • no day symptoms
  • no night waking
  • no rescue meds
  • no asthma attacks
  • normal lung function
  • minimal side effects
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36
Q

management of asthma (chronic)

A
  • control of asthma: treat when needed and decrease treatment when control is good, check asthma technique
  • non pharmacological (quit smoking, lose weight, breathing exercises, avoid allergens, info and support advice, assess for depression and anxiety)
  • pharmacological: SABA (PRN), ICS (if use SABA/have symptoms > 3*week, wake up at night at least once a week due to symptoms), LTRA (added to ICS), LABA (if LTRA not controlling it, replace LTRA with LABA)
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37
Q

management of acute exacerbation of asthma

A
  • O2: maintain 94-98%
  • SABA: 1 puff every 30-60s, up to 10 puffs, repeat 10-20s (if life threatening or hypocis: nebulised 5mg) (monitor K+)
  • ipratropium bromide nebs if poor response to salbutamol
  • IV magnesium sulfate (monitor BP)
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38
Q

following acute exacerbation of asthma, what is the discharge plan

A
  • any current change in meds
  • review by GP 48h later, weaning off plan
  • clinic appointment 2 months later
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39
Q

diagnosis of asthma

A
  • under 5s: clinical
  • spirometry with bronchodilator reversibility test (BDR)
  • FeNO (fractional exhaled nitric oxide): levels rise in inflammatory cells
  • check not occupational
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40
Q

assessment of child with suspected pneumonia

A
  • severity assessment: PEWS, physical exam, degree of agitation and consciousness (signs of hypoxia), signs of exhaustion and hydration status
  • refer to hospital if seriously ill
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41
Q

epidemiology of CF

A
  • autosomal recessive condition
  • most common in caucasians
  • affects 1:2500 births
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42
Q

pathophysiolofy of CF

A

abnormal ion transport across epithelial memebranes:

  • in airways: reduction of airway surface liquid layer
  • dysregulation of inflammation and defence against infecction
  • sweat glands, pancreatic ducts, intestine affected
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43
Q

which organisms colonise CF patients

A
  • staphylococcus aureus
  • pseudomonas aeruginosa
  • burkholderia cepacia
  • aspergillus
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44
Q

diagnosis of CF

A
  • screening; heel prick test: raised immunoreactive trypsinogen
  • check common CF gene mutations: if 2 present:
  • sweat test to confirm diagnosis
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45
Q

clinical features of CF

A
  • lungs: thick, sticky mucus buildup, bacterial infection and widened airways
  • skin: salty sweat
  • sinusitis
  • blocked biliary ducts (cirrhosis and portal hypertension)
  • blocked pancreatic ducts (DM)
  • maldigestion and absoprtion (pancreas insufficiency) + mecomium ileus and distal intestinal obstruction
  • vas deferens and fallopian tube blockage: sterility
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46
Q

Management in CF

A
  • ohysio x2 daily for airway clearance and postural drainage
  • high calorie diet (including fat intake), vit supplements and pancreatic enzyme supplements with each meal
  • prophylaxis oral antibiotics
  • minimise contact with other CF patients
  • nebulised d>Nase or hypertonic saline helps with mucus viscosity
  • lung transplant
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47
Q

different types of Heart problems in children

A
  • congenital: acynotic cyanosis
  • aquired: myocarditis, rheumatic heart disease
  • Inherited: HOCM, Marfan’s syndome
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48
Q

types of acynotic congenital heart disease

A
  • septal defect (ventricular and atrial)
  • aortic/pulmonary stenosis
  • coarctation of the aorta
  • patent ductus arteriosus
  • mitral/tricuspid stenosis
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49
Q

types of cyanotic congenital heart disease

A

5Ts

  • Fallot’s Tetralogy
  • TGA (transposition of great arteries)
  • complete atrio-venTricular septal defect
  • tricuspid atresia
  • truncal arteriosus
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50
Q

non specific symptoms in CHD

A
  • poor feeding/weight loss
  • SOB/increased work on breathing
  • clammy when breathing
  • increased sleepiness
  • irritability
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51
Q

non specific signs of CHD

A
  • cyanosis
  • tachycardia
  • tachypnoea
  • murmurs
  • enlarged liver
  • crackles
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52
Q

specific symptoms/signs in coarctation of the aorta

A
  • cold feet/legs
  • femoral pulse weak/Absent
  • systolic hypertension of upper limbs, BP arms&raquo_space;> legs
  • headaches and abdo/leg cramps
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53
Q

specific signs in patent ductus arteriosus

A
  • bounding pulses

- increased systolic BP

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54
Q

Fallot’s tetralogy parts

A
  • ventricular septal defect
  • large overriding aorta
  • right ventricular hypertrophy
  • pulmonary artery narrowing
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55
Q

specific signs of Fallot’s tetralogy

A

clubbing

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56
Q

TGA presentation

A

central cyanosis at birth

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57
Q

tricuspid atresia problem

A

no tricuspid valve: no blood flow from RA to RV

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58
Q

truncus arteriosus problem

A

connection between aorta and pulmonary artery

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59
Q

risk factors for CHD

A
  • maternal factors: anti seizure meds or lithium during pregnancy, uncontrolled DMT1, lupus, rubella in T1
  • FH
  • chromosomal abnormalities (trisomy 13 or 18, Down’s syndrome, turner’s, Karageners, DiGeorge, cri du chat)
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60
Q

management of CHD

A
  • oxygen if cyanotic
  • digoxin, diuretics
  • adequate nutrition (if poor feeding)
  • catherisation or surgical repair
  • prostaglandin with TGA and prostaglandin inhibitors with PDA
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61
Q

neonatal blood spot screening

A
  • congenital hypothyroidism
  • CF
  • sickle cell disease
  • phenylketonuria
  • MCADD (medium chain acyl-CoA dehydrogenase deficiency)
  • maple syrup urine disease (MSUD)
  • isovaleric acidaemi
  • glutarix aciduria type 1
  • homocysturia (HCU)
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62
Q

risk factors involved in child maltreatment

A

child:
- younger, increased needs, low birth weight, multiple births

parental:
- younger, mental illness, drug/alcohol abuse, domestic violence, low SES, parents were abused, criminal hx, chaotic/socially isolated families, vulnerable/unsupported parents, previous child maltreatment in other member of family, known maltreatment of animals

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63
Q

what is the toxic trio of maltreatment

A
  • domestic violence/abuse
  • parental mental illness
  • parental substance misuse
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64
Q

elements in Hx pointing towards NAI

A
  • no mechanism offered/mechanism not consistent with injury
  • delay in reporting the injury/seeking medical attention
  • inconsistent Hx from parents
  • inappropriate reaction from parents
  • recurrent injuries
  • injury inconsistent with child’s age, development, mobility
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65
Q

NAI fractures presentation

A
  • metaphyseal fractures
  • posterior rib fractures
  • fractures of different ages
  • complex skull fractures
  • long bone shaft fractures in non-mobile child
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66
Q

NAI bruises presentation

A
  • face, back, buttocks (soft tissues)
  • bruises outline particular object
  • pattern of bruising ie fingertips
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67
Q

NAI burns presentation

A

uniform shape

glove-stocking distribution

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68
Q

presentation of NAI in a baby

A
  • irritability
  • poor feeding
  • increased head circumference
  • seizures
  • reduced GCS
  • full frontanelle
  • anaemia
  • retinal haemorrhage
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69
Q

fabricated or induced illness presentation

A
  • often background of existing disease
  • bizzare illness events
  • strnage new symptoms
  • parental reportage out of keeping with physical signs
  • symptoms not witnessed by others
  • unneeded operations
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70
Q

management of fabricated or induced illness

A

FII (fabricated or induced illness) pathway

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71
Q

neglect presentation

A
  • failure to thrive
  • inadequate hygiene
  • poor development or emotional attachment to child’s caregiver
  • delay in development in speech and language
  • poor attendance in school and health appointments
  • failure to supervise/unsupervised young children at home
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72
Q

how to do child protection medical assessment

A
  • must be done by registar + level paediatrician and have named consultant on sheet
  • full Hx, exam, growth chart, obs, body map, photography, investigations as appropriate
  • child must be questions away from carers
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73
Q

differentials to NAI bruising

A
  • accidental injury
  • mongolian blue spots
  • leukaemia or aplastic anaemia
  • platelet and coag pb: immune thrombocytopaenic purpura, haemophilia A, vWd, chrismas disease
  • meningococcal septicaemia, Henoch schonlein purpura
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74
Q

differentials to broken bone

A
  • NIA
  • accidental injury
  • osteogenesis imperfecta
  • copper, vit D or vit C deficiency
  • ehler danlos or other hypermobility syndromes
  • JOBs syndome
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75
Q

differentials for abdo pain and diarrhoea

A

common:

  • constipation
  • infectious gastroenteritis
  • acute appendicitis
  • UTI
  • abdominal trauma
  • primary dysmenorrhea
  • pneumonia
  • functional (IBS or abdominal migraine)
  • coeliac disease

less common

  • intussusception
  • Merkel’s diverticulum
  • mesenteric adenitis
  • Hirschprung’s disease
  • IBD
  • small/large bowel obstruction
  • volvulus
  • necrotising enterocolitis
  • peptic ulcer disease
  • GORD
  • DKA
  • neoplasm: neurobladtoma or Willms nephroblastoma
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76
Q

differentials of meleana

A
  • bacterial diarrhoea
  • IBD
  • tearing from anal vein
  • polyp
  • intussusception
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77
Q

presentation of IBD

A
  • diarrhoea (non bloody (crohns) /bloody (UC))
  • abdo pain
  • pyrexia
  • oral ulcers (crohns)
  • abdo mass in RIF
  • PR bleeding (UC)
  • mucus/pus
  • tenesmus
  • perianal disease
  • weight loss
  • malabsorption
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78
Q

coeliac disease presentation

A

symptoms coincide with introduction to cereals

  • failure to thrive
  • diarrhoea
  • abdominal distention and cramping
  • nausea and vomiting
  • anaemia
  • weight loss
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79
Q

Willms nephroblastoma presentation

A
  • abdominal mass (unilateral)
  • painless haematuria
  • flank pain
  • anorexia
  • fever
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80
Q

management of willms nephroblastoma

A
  • refer for paediatric review within 48h

- nephrectomy, chemotherapy, radiotherapy

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81
Q

investigations for IBD

A
  • serum FBC, inflam markers, U&Es, LFTs, TFTs, ferritin, B12, folayte, vit D and coeliac serology
  • stool microscopy and culure (C diff toxin and faecal calprotectin)
  • colonoscopy with biopsies
  • CT for staging (Crohns)
  • AXR if obstruction, absecesses, fistulas and strictures
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82
Q

treatment of Crohns disease

A

may require hospital admission

  • stop smoking
  • oral/IV corticosteroids for flare ups (mesalazine as second line)
  • enteral feeding with elemental diet
  • azathioprine ot mercaptopurine to maintain remission
  • surgery
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83
Q

treatment of ulcerative colitis

A
  • topical (rectal) or oral aminosalicylate

- oral corticosteroids (second line)

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84
Q

investigation of coeliac disease

A
  • serology: tissue transglutaminase (TTG) antibodies (IgA)
  • endoscopic intestinal biopsy (villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina, propria infiltration with lymphocytes)
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85
Q

treatment of coeliac disease

A
  • gluten free diet

- pneumococcal vaccine

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86
Q

pyloric stenosis presentation

A
  • projectile non bile stained vomiting at 4-6 weeks of life
  • FH
  • males> females
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87
Q

intussusception presentation

A
  • 6-9 months of age
  • colicky pain, diarrhoea and vomiting
  • suasage shape mass, red jelly stool
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88
Q

when do you need to worry about refeeding syndrome

A

if patient has not eaten in > 5 days

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89
Q

cause of refeeding syndrome

A

switch from gluconeogenesis (catabolic state) to insulin release: stimulates glycogen, fat and protein synthesis (anabolic state) results in rapid intracellular uptake of cofactors of potassium, magnesium and phosphate
–> electrolyte imbalance can be fatal

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90
Q

clinical features of refeeding syndrome

A
  • electrolyte abnormalities (hypophosphotaemia, hypokalaemia, hypomagnesaemia, hyponatraemia, metabolic acidosis, thiamine deficiency
  • clinical manifestations: muscle weakness, seizures, peripheral oedema, cardiac arrhythmias, hypotensionn delirium
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91
Q

management of refeeding syndrome

A
  • replacement of fluid and electrolytes
  • start feeding cautiously
  • frequent electrolyte monitoring
  • thiamine replacemtn (to avoid beri beri delirium)
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92
Q

what are the risk of rapid weight loss

A
  • refeeding syndrome
  • hypoglycaemia
  • risk of infection
  • cardiac arrythmias
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93
Q

aetiology of anorexia nervosa

A
  • genetic factors
  • events around puberty
  • cultural promotion of thinness
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94
Q

presentation of anorexia nervosa

A

behavioural/psychological:

  • pre occupied with food
  • dysmorphia/feeling fat
  • wont eat in front of others
  • hiding food
  • may be compulsive exerciser

clinical features:

  • low BMI
  • amenorrhea
  • headaches
  • cool peripheries/hypothermia
  • constipation
  • dry skin
  • hair loss
  • fainting/dizziness/hypotension
  • lethargy
  • bradycardia
  • peripheral oedema
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95
Q

what are the significant mortality in anorexia nervosa

A
  • sudden cardiac death
  • suicide
  • chronic emaciation and pneumonia
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96
Q

issues with laxative abuse

A

short term:

  • K+ and Na+ de^pletion
  • severly dehydrated
  • cardiac arrest

long term:
- loss of bowel motility

if try to stop:
- oedema due to refeeding syndrome: CHF and psychological distress of weight gain

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97
Q

diagnosis of anorexia nervosa

A
  • restriction of energy intake relative to requirements leading to low BMI
  • intense fear of gaining weight
  • dysmorphia
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98
Q

management of anorexia nervosa

A

physical stabilisation

  • commence vitamins (thiamine, vit B complex, multivitamins)
  • if not drinking: IV 10% dextrose
  • diet plan: aim for 0.5-1kg weight gain a week

MDT apprach:

  • child psychiatrist
  • dietatictian
  • therapists
  • paediatrician

relapse prevention:

  • transitional phases (ie uni)
  • 3rd sector ie BEAT charity
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99
Q

diagnosis of bullimia nervosa

A
  • recurrent episodes of bing eatinf
  • sense of lack of control
  • recurrent inappropriate compensatoery mechanisms to prevent wieght gain (self vomiting, misuse of laxatives, diuretics)
  • binge eating and comensory mechanisms occur at least once a week for 3 months
  • self evaluation is influenced by body shape and weight
  • disturbance does not occur excusively during episodes of anorexia nervosa
100
Q

management of bullimia nervosa

A
  • refer to specialist

- bulimia nervosa focused family therapy

101
Q

differentials of rapid weight loss

A
  • coeliac diease
  • IBD
  • oesophageal pb ie achalasia
  • T1DM
  • hyperthyroidsim
  • malignancy
  • anorexia nervosa
  • severe depression/OCD/autism
  • juvenile arthritis
  • addisons
102
Q

risk factors for dehydration

A
  • low birth weight
  • <1 year
  • 2+ vomiting episodes and more than 5 diarrhoeal episodes in previous 24h
  • malnourished children
103
Q

presentation of dehydration

A
  • sunken anterior fontanelle
  • dry mucus membrane
  • tachycradia
  • reduced cap refill
  • reduced skin turgor
104
Q

causes of gastroenteritis

A

viral:

  • rotavirus
  • adenovirus
  • calcivirus
  • astrovirus

bacteria:

  • campylobacter
  • C diff
  • E coli
  • salmonella
  • shigella
  • cholera

parasite:

  • giardia lambia
  • cryptosporidium
105
Q

what pathogens are associated with blood in stool in gastroenteritis

A
  • campylobacter
  • shigella
  • e coli
  • rotavirus
  • salmonella
106
Q

main causes of gastroenetiritis in young children

A

rotavirus

adenovirus

107
Q

causes of food poisoning

A
  • campylobacter (found in raw/uncooked meat esp poultry)
  • salmonella (raw/uncooked meat, raw eggs, milk
  • listeria (chilled, ready to eat foods)
108
Q

cows allergy presentation

A
  • failure to gain weight
  • abdominal pain and crying
  • diarrhoea and vomiting
  • rash and wheeze
109
Q

differentials of poor feeding

A
  • difficulty latching on
  • infection (resp)
  • physical malformations
  • neurological (swallowing pb)
  • cardiovascular (congenital cardiac conditions)
  • cows milk allergy/lactose intolerance
  • GORD
110
Q

abdominal migraine presentation

A
  • sudden onset episodic midline abdominal pain lasting between 1 and 72h
  • anorexia, nausea, vomiting, pallor and other vasomotor symptoms are common
111
Q

what additional symptoms do you have in viral gastroenteritis

A
  • fevers
  • headaches
  • chills
  • fatigue
112
Q

modes of transmission of gastroenteritis

A

viral:

  • contaminated water/food
  • contact with vomit/fomites (faecal/oral)

bacterial:

  • as above
  • improperly prepareed and stored food
113
Q

E coli presentation

A
  • associated with diarrhoea with blood in stools and HUS

- occurs in clusters after ingestion of contaminated food

114
Q

complications of gastroenteritis

A
  • dehydration
  • HUS
  • post infective IBS
  • IBD
  • reactive arthritis
115
Q

causes of secondary (typical) HUS

A
  • E coli
  • pneumocooccal infection
  • HIV
  • rare: SLE, drugs, cancer
116
Q

presentation of haemolytic uraemix syndrome

A

triad:

  • microangiopathic haemolytic anaemia
  • thrombocytopaenia
  • renal insufficiency

symptoms:

  • abdo pain
  • bloody diarrhea
  • fever
  • seizures
  • lethargy
117
Q

what investigations to do when suspected HUS

A

FBC: anaemia, thrombocytopaenia, fragmented blood film

  • U&Es: AKI
  • stool culture: STEC infection and shiga toxin (from E coli)
118
Q

management of HUS

A
  • supportive treatment (fluids, blood transfusion, dyalisis)
  • no antibiotics needed
  • plasmapharesis/IVIG
119
Q

management of gastroenteritis

A
  • rehydration (fluids or ORS)
  • education about infection control (4Cs: cleaniless, cooking, chilling, cross contamination)
  • stool culture
  • do not attend school until 48h after last episode of D&V
  • notify healthprotection team if due to food
  • explain that D can last up to 2 weeks and V up to 3 days
  • specific treatment with campylobacter, C diff, shigela
120
Q

red flags for dehydration

A
  • becomes suddenly unwell
  • pale/mottled
  • persistent vomiting
  • decreased urine output/wet nappies
  • irritable/lethargy
  • cold extremities
121
Q

severly ill child red flags

A
  • fever >38 (if aged <3 months), or > 39 (if aged 3-6 months)
  • colour: pale, mottled, cyanosed
  • level of consciousness reduced, stiff neck, bulging fontanelle, status epilepticus, focal neurological signs or seizures, rash
  • significant resp distress (grunting, nasal flarring, use of acc muscles, tachypnoea)
  • bile stained vomiting
  • severe dehydration/shock
122
Q

causes of bacterial meningitis by age group

A

0-3 months:

  • group B strep (neonates)
  • E coli
  • listeria monocytogenes

3 months- 6 years

  • neisseria meningitidis
  • streptococcus peumonia
  • haemophilus influenzae B

6 years above:

  • neisseria meningitidis
  • streptococcus pneumlonia
123
Q

causes of viral meningitis

A
  • enterovirus (coxsachie and echovirus)
  • adenovirus
  • mumps
  • EBV
  • CMV
  • varicella zoster
  • herpes simplex
  • HIV
124
Q

risk factors for meningitis

A
  • low family income
  • children with facial cellulitis, periorbital cellulitis, sinusitis and septic arthritis
  • asplenia
  • basal skull fracture
  • attendance at day care/overcrowding
  • maternal infection and pyrexia at time of delivery
125
Q

epidemiology of meningitis in paeds

A
  • neonates

- adolescents

126
Q

presentation of meningitis in neonates

A 
poor feeding 
lethargy
irritability
apnoea
listlessness
fever
hypothermia
seizures
jaundice
pallor
bulging fontanelle
high pitched cry 
floppiness
127
Q

presentation of meningitis in infants/young children

A 
fever
lethargy
irritability
nausea and vomiting 
bulging fontanelle
neck stiffness
altered consciousness
opisthotonus
poor apetite
seizures
hypothermia
128
Q

presentation of meningitis in older children

A 
fever
headache
nausea/vomiting
neck stiffness
photophobia
altered alertness
seizures
poor apetite
opisthotonus
hypothermia

positive kernig’s sign (pain on lowering leg extension with hip flex) and brudzinski’s sign (involuntary flexion of knees and hips with neck flexion)

129
Q

investigations in suspected meningitis

A
  • bloods: FBC, CRP, coagulation screen
  • blood culture
  • urine culture
  • blood glucose
  • blood gas
  • LP for CSF
130
Q

diagnosis of meningitis

A
  • clinical: symptoms § pos kernig and brudinski sign

- CSF results

131
Q

management of meningitis

A

ANTIBIOTICS

  • under 3 months: IV cefotaxime and amoxicillin/ampicin
  • over 3 months: IV ceftriaxone and vancomycin (if recent abroad travel)

IM if before hospital transfer

VIRAL:
- antiviral

  • dexamethasone: adjuvent to antibiotics to reduce incidence of neuro and audio complications (MUST be given before or with first dose of antibiotics)

prophylaxis offered to household

audiology assesmment as follow up

132
Q

complications of meningitis

A

acute:

  • seizures
  • raised ICP
  • metabolic disturbances
  • coagulopathy
  • anaemia
  • coma
  • death

long term:

  • hearing impairement
  • psychological problems
  • epilepsy
  • developmental/learning difficulties
  • neurological impairement
133
Q

septic sceen

A
  • blood cultures
  • urine sample
  • bloods: FBC, CRP, lactate

if indicated:

  • CXR
  • LP
  • rapid antigen screen on blood/CSF/urine
  • meningococcal and pneumococcal PCR on blood/CSF
  • PCR for viruses in CSF
134
Q

risk factors for sepsis (general to paeds)

A
  • congenital heart failure
  • chronic steroid dependency
  • burns
  • asplenia
  • neonates
  • presence of central line or vascular access device
  • malignancy or bone marrow transplant or impaired immune function
  • neutropaenia
  • complex urogenital anatomy or repair
  • neuro impairement
  • technology dependent (ie ventilated)
135
Q

red flag sepsis for children

A
  • hypotension
  • tachycardia
  • high lactate
  • prolonged cap refill
  • pale/mottled/cyanoses or rash
  • O2 needed to maintain O2sats > 92%
  • resp rate > 60 min or grunting
  • AVPU: V, P or U
  • dry nappies, lack of response to social cues, decreased activity, high pitched or continuous cry
136
Q

management of neonatal sepsis

A
  • IV benzypenicillin with gentamicin
  • maintain adequate O2, fluid and elctrolytes
  • prevent/manage hypoglycaemoa and metabolic acidosis
137
Q

prevention of group B strep infection in neonates

A

give antibiotics to mother during mabout if :

  • previous group B strep baby
  • group B strep in urine during pregnancy
  • fever during labour
  • goes into labour before 37 weeks
138
Q

prevention of meningitis

A

vaccination
MenB at 2, 4 and 12 months
Hib/menC at 12 month
MenACWY at 14 years

139
Q

kawasaki disease presentation

A
  • usually in under 5s
  • persistent (>5days) fever
  • lymphadenopathy
  • bright red cracked lips
  • strawberry tongue
  • bilateral non infective conjunctivitis
  • desquamating rash
140
Q

third generation cephalosporin examples

A

cefotaxime
cefixime
cedtazidime
ceftriaxone

141
Q

side effects of penicillins

A
  • D&V, nausea
  • hypersensitivity
  • skin reaction
  • thrombocytopaenia

rare but important:
- agranulocytosis, angioedema, haemolytic anaemia, neutropaniea, seizures, SCARs

142
Q

what class of drugs does vancomycin belong to

A

glycopeptide antibacterials

143
Q

SE of vancomycin

A

back pain, bradycardia, cardiac arrest, cardiogenic shock , chest pain, dyspnoea, hearing loss, hypotension, nephrotoxicity

agranulocytosis, dizziness, drug fever, oesinophilia, hypersensivity

144
Q

presentation of transient synovitis

A
  • acute onset limp, with or without pain
  • reduced hip movements
  • child systemically well, self limiting
  • often preceded by viral inf (URTI or gastroenteritis)
145
Q

epidemiology of transient synoviitis

A

boys > girls

age 4-8

146
Q

management of transient synovitis

A
  • self limiting
  • rest
  • analgesia (OTC)
147
Q

septic arthritis/osteomyelitis persentation

A
  • acute onset pain
  • non weight bearing
  • extreme pain on movement
  • erythema and heat over site
  • fever
  • systemic upset
148
Q

fracture presentation

A

acute onset pain
reduced/non weight bearing
typical: 0-3 y

149
Q

perthes disease epidemiology

A

boys > girls

age 4-8

150
Q

presentation of perthes disease

A
  • gradual onset limp
  • painless
  • stiffness and reduced hip movements
  • can be bilateral
151
Q

pathophysilogy of perthes disease

A
  • avascular necrosis due to interrupted blood flow to femoral epiphysis
  • remodelling occurs but can result in deformity
152
Q

epidemiology of slipped upper femoral epiphysis (SUFE)

A

boys > girls

age > 10

153
Q

risk factors for SUFE

A
  • obesity

- hypothyroidism

154
Q

presentation of SUFE

A

different presentation

  • sudden onset pain and non weight bearing or
  • gradual onset vague pain that may be referred to knee and a limp
155
Q

cause of SUFE

A

proximal femoral growth plate becoming unstable

epiphsis and diaphysis can slip

156
Q

development dysplasia of the hip presentation

A

girls > boys

usually detected at birth

157
Q

risk factors for DDH

A 
female
breech position 
positive FH 
firstborn children 
oligohydramnios
birth weight > 5 kg
congenital calcaneovalgus foot deformity
158
Q

presentation of DDH

A
  • asymmetrical skin folds
  • leg length disparity
  • buttocks flattened
  • walking with affected leg in external rotation
  • older children: fradual onset of painless limp
159
Q

management of DDH

A

-ultrasound to confirm diagnosis
(if child > 4.5 months: XRay)
- spontaneous stabilisation by 3-6 weeks of age
- Pavlik harness in children < 4-5 months
- surgery in older childrenn

160
Q

SUFE management

A
  • AP and lateral views Xray (frog legs)

- internal fixation

161
Q

Perthes disease management

A
  • plain Xray or technetium bone scan or MRI
  • if less than 6: observation, or cast or brace to keep femoral head in acetabulum.
  • older: surgical management
162
Q

septic arthritis management

A
  • joint aaspiration for culture, blood culture, bloods

- antibiotics, joint washout, arthrotomy

163
Q

types of juvenile idiopathic arthritis

A
  • oligoarthritis (<5 joints affected in 6/12, ANA pos)
  • polyarthritis (>5 joints affected in 6/12, can be RH pos or neg)
  • enthesitis related arthritis (inflam where tendons attach to bone)
  • psoriatic arthritis (mainly fingers and toes + dactilitis and psoriasis)
  • systemic onset JIA (fever and rash)
  • undifferentiated arthritis (symptoms don’t fit with anything else)
164
Q

JIA management

A

referral to rheumatology

  • NSAIDs
  • corticosteroids
  • methotrexate
165
Q

presentation of JIA

A

<16y, >3months duration

  • join pain and swelling (usually medium sized jointss)
  • limp
166
Q

indications for specialist assessment

A

Pain waking the child at night
○ Malignancy
Redness, swelling or stiffness of the joint or limb
○ Infection or inflammation
Weight loss, anorexia, fever, night sweats or fatigue
○ Malignancy, infection or inflammation
Unexplained rash or bruising
○ Haematological or inflammatory joint disease or child maltreatment
Limp and stiffness worse in the morning
○ Inflammory joint disease
Unable to weight bear or painful limitaion of range of motion
○ Trauma or infection
Severe pain, anxiety, agitation afrer traumatic injury
○ Neurovascular compromise or impending compartment syndrome
Palpable mass
○ Malignancy or infection

167
Q

epidemiology of UTI

A

girls > boys
highest incidence in first year life (boys>girls)
e coli most common pathogen

168
Q

presentation of UTI in children <3 months

A

most common to least common

  • fever, vomiting, lethargy, irritability
  • poor feeding, failure to thrive
  • abdominal pain, jaundice, haematuria, offensive urine
169
Q

presentation of UTI in children > 3months

A

from most common to least common:

preverbal:

  • fever
  • abdominal pain, loin tenderness, vomiting, poor feeding
  • lethargy, irritability, haematuia, offensive urine, failure to thrive

verbal:

  • frequency, dysuria
  • dysfunctional voiding, changes in continence, abdo pain, loin tenderness
  • malaise, fever, vomiting, haematuria, offensive cloudy urine
170
Q

risk factors for underlying pathology in UTI

A
  • poor urine flow, dysfunctional voiding
  • Hx of previous UTI
  • recurrent fever of uncertain origin
  • antenatally diagnosed renal abnormality
  • FH of vesicouretic reflux or renal disease
  • constipation
  • enlarged bladder
  • abdominal mass
  • spinal lesion
  • poor growth
  • high BP
171
Q

management of UTI

A
  • if <3 months, urgent paeds referral
  • for upper UTI/cystitis: reconsider referral and start on oral cefalexin or co-amoxiclav
  • for lower UTI/cystitis: trimethoprim or nitrofurantoin
172
Q

further investigations for UTI

A
  • USS: if recurrent UTI > 6months, atypical infection, >6 months and first UTI that responds to treatment
  • DMSA scan (renal function and scarring) if <3y with typical or reccurent UTI or >3y with reccurent UTI
  • MCUG (micturating cystogram) to identify VUR, bladder abnormalities or posterior urethral valves if <6m with atypical/reccurent UTI or >6m if dilation on ultrasound, poor renal flow, no E coli inf of FH VUR
173
Q

pathogen of UTI in children

A
  • E coli
  • proteus mirabilis (mainly boys)
  • staphylococcus saprophyticus (adolescents)
  • pseudomonas (in urinary tract malformation or dysfunction)
  • klebsiella aerogenes and enterococcus species
  • adenovirus (rare)
  • cadidal UTI (immunocompromised)
174
Q

def vesicoureteric reflux (VUR)

A

abnormal backflow of urine from bladder into ureter and kidneys

175
Q

epidemiology of VUR

A
  • found in 30% of children presenting with UTI

- 35% will develop renal scarring

176
Q

pathophysiology of VUR

A
  • ureters are displaced laterally, entering bladder perpendicular fashion
  • shortened intramural course
  • vesicoureteric junction cannot function adequately
177
Q

presentation of VUR

A
  • antenatal period (hydronephrosis on USS)
  • recurrent childhoof UTI
  • reflux nephropathy (chronic pyelonephritis secondary to VUR)
178
Q

investigations when suspecting VUR

A
  • voiding cystourethrogram (VCUG)

- DMSA scan to look for renal scarring

179
Q

treatment of VUR

A
  • self improvement

- surgery to remove blockage or repair valve

180
Q

what are the different co ngenital abnormalities of kidney and urinary tract in childhood

A
  • renal hypoplasia, dysplasia and agenesis
  • infantile polycystic kidney disease (IPKD), ADPKD, ARPKD
  • pelvic kidney/horseshoe kidney/ renal fusion
  • posterior urethral valves
  • ectopic kidney
181
Q

def Henoch Schonlein purpura

A

IgA mediated small vessel vasculitis: inflammation and leaking of blood

182
Q

which organs does HSP affect

A

kidneys
GIT
skin

183
Q

which organs does HSP affect

A

kidneys
GIT
skin
joints

184
Q

features of HSP

A
  • palpable purpuric rash (with lov
185
Q

features of HSP

A
  • palpable purpuric rash (with localised oedema) over buttocks and extensor surface of arms and legs (non blanching, severe: ulceration and necrosis)
  • abdominal pain (severe: haemorrhage, intussusception and bowel infarction)
  • polyarthritis: mostly knees and ankles
  • features of IgA nephropathy: haematuria, renal failure, proteinuria
186
Q

investigations for HSP

A

BLOODS

  • FBC and film (exclude thrombocytopenia, sepsis, leukaemia)
  • CRP and blood cultures (sepsis)
  • renal function
  • albumin
  • urine sample and protein:creatinine ratio
  • BP
187
Q

differentials of HSP

A
  • meningococcal septicaemia
  • leukaemia
  • idiopathic thrombocytopenic purpura
  • HUS
188
Q

diagnosis of HSp

A

palpable purpura with one of the following:

  • difuse abdo pain
  • arthritis and arthralgia
  • IgA deposits on histology
  • proteinuria/haematuria
189
Q

treatment of HSP

A
  • analgesia for arthritis
  • supportive for nephropathy
  • monitoring (urine dip for renal impairement and BP for hypertension)
190
Q

complications of HSP

A

intussusception
pancreatitis
acute renal impairement
arthritis/arthralgia esp knees and ankles

191
Q

prognosis of HSP

A
  • self limiting condition: 4-6 weeks
  • 1/3 patients relapse
  • some develop end stage renal failure
192
Q

def of immune thrombocytopenic purpura (ITP)

A

immune mediated reduction in platelet count

193
Q

epidemiology of ITP

A
  • more acute than with adults
  • equal sex incidence
  • may follow infection/vaccination
  • usually self limiting course: 1-2 weeks
194
Q

symptoms of ITP

A
  • assymptomatic
  • purpura
  • frequent mucosal bleeding (if severe) ie epixtasis
195
Q

diagnosis of ITP

A
  • clinical/diagnosis of exclusion

- isolated thrombocytopenia

196
Q

treatment of ITP

A
  • if asymptomatic: observed

- symptomatic: corticosteroids and IVIG, platelets transfusion

197
Q

def intussusception

A

invagination of one portion of bowel into lumen of adjacent bowel

198
Q

epidemiology of intussusception

A

infants 6-18 months
boys > girls
- associated conditions: CF, HSP, crohns, coeliac, abnormal intestinal formation at birth

199
Q

features of intussusception

A
  • paroxysmal abdominal colic pain
  • draws knees up and turns blue
  • vomiting
  • blood stained stool (red current jelly)
  • sausaged shaped mass in RUQ
200
Q

def testicular torsion

A

twist of spermatic cord resulting in testicular ischemia and necrosis

  • most common in 10-30 year olds
  • peak incidence: 13-15y
201
Q

symptoms of testicular torsion

A
  • pain (severe, sudden onset, can be referred to lower abdomen, elevation of testes does not ease the pain)
  • nausea and vomiting
  • swollen, tender testis, retracted upwards
  • reddened skin
  • cremasteric reflex is lost
202
Q

management of testicular torsion

A

urgent surgical exploration of both testis

203
Q

def epididymo-orchitis

A

infection of epididymis +/- testes resulting in pain and swelling

204
Q

cause of epididymo-orchitis

A

local spread of infection from genital tract or bladder

205
Q

features of epididymo-orchitis

A
  • unilateral testicular pain and swelling
  • urethral discharge may be present
  • gradual onset
206
Q

management of epididymo-orchitis

A

antibiotics
if organism unknown:
-ceftriaxone and doxycycline

207
Q

when do yu send a stool for MS&C

A

If diarrhoea AND

  • suspect septicaemia
  • blood or mucus in stool
  • child is immunocompromised
  • Hx of travel
  • diarrhoea > 7days
  • uncertain about diagnosis of gastroenteritis
208
Q

diagnosis Kawasaki disease

A

clinical

209
Q

treatment of Kawasaki disease

A
  • high dose aspirin
  • IVIG
  • coronary angiography to check for aneurysms
210
Q

presentation of Lyme’s disease

A
  • early: fever, arthralgia, malaise, rash
  • second stage (weeks later): aseptic meningitis, facial palsy, arthritis, carditis
  • third stage (couple of years later): neuropsychiatric manifestations, chronic fatigue
211
Q

treatment of lyme’s disease

A

cefuroxime and amoxicilin

212
Q

differentials of prolonged fever

A

INFECTIVE:

  • localised infection (ie osteomyelitis)
  • bacterial infection
  • deep absecess
  • infective endocarditis
  • TB
  • nontuberculous mycobacterial infections
  • viral infections (EBV, CMV, HIV)

NONINFECTIVE

  • systemic onset juvenile idiopathic arthritis
  • SLE
  • vasculutis
  • IBD
  • sarcoidosis
  • malignancy
  • macrophage activation syndromes
  • drug fever
  • FII
213
Q

epidemiology of febrile seizure

A
  • aged 6 months- 5 years
  • occurs during febrile illness
  • most common seizure disorder in childhood
214
Q

presentation of simple febrile seizure

A
  • short (<15min) generalised seizure
  • not recurring within 24h
  • not resulting from acute disease of CNS
215
Q

presentation of complex febrile seizure

A
  • focal or generalised and prolonged seizure
  • duration 15-30 mins
  • reccuring more than once in 24h and/or
  • associated with postictal neurological abnormalities ie todds palsy
216
Q

def febrile status epilepticus

A
  • complex febrile seizure w/ duration > 30min OR

- shorter serial seizures witout regaining consciousness at interictal state

217
Q

what treatment to give in acute management of generalised seizures

A
  • buccal midazolam
  • rectal diazepam
  • IV lorazepam
  • IV phenytoin

do not give more than 2 doses of benzos

218
Q

diagnosis of epilsepsy

A
  • primarily from Hx from child and eyewitnesses video
  • triggers aand impairementq (educational, psychological, social)
  • clinical exam: skin markers of neuro-cutaneous syndrome/neuro pb
  • EEG
  • MRI for structural abnormalities
  • ECG (convulsive syncope)
219
Q

challenges of long term management in seizures

A
  • avoid swimming unsupervised and deep baths due to life threatening consequences
  • driving, contraception and pregnancy an issue
  • alcohol and poor sleep routines can precipitate seizures
  • do less well educationally, socially and in future employment
220
Q

def inborn errors of metabolism

A

disorders of enzymatic reactions that degrade, synthesise, or interconvert molecules within cells

221
Q

epidemiology of IEM

A
  • commonly affects the brain

- autosomal recessive inheritance

222
Q

different categories of neonatal sepsis

A
  • early-onset (within 72h of birth)

- late-onset: between 7-28 days of life

223
Q

cause of neonatal sepsis

A
  • GBS and Ecoli are most common
  • early onset sepsis: GBS
  • late onset: staphylococcus epiderlidis, pseudomonas aeruginosa, Klebsiella, enterobacter
224
Q

investigations in neonatal sepsis (and how to differentiated between different causes)

A
  • blood culture
  • urine MS&C: rarely pos for EOS, more useful for LOS
  • LP
225
Q

how does IEM present

A
  • screening
  • unexpectedly severe presentation of an otherwise common illness
  • significant metabolic acidosis
  • unexplaied resp alkalosis
  • hypoglycaemia
  • cardiac failure/cardiomyopathy
  • hepatomegaly/hepatosplenomegaly/liver dysfunction
  • unexplained drowsiness, coma or irritability
  • early onset seizures
  • dysmorphic features
  • developmental regression or loss of skills
  • sudden unexplained death
226
Q

problem in pheylketonuria

A

unable to convert phenylalanine inro tyrosine due to enzyme deficiency : excess phenylalanine which is toxic to the brain (developmental delays + regression or loss of skills) + decreased tyrosine

227
Q

management of PKU

A

very low protein diet
supplements of all amino acids except PHE
- monitoring of blood PHE levels

228
Q

outcomes of PKU

A
  • good
  • women with PKU need strict diet for pregnancy, or bad outcomes
  • but as adults, can come off diet
229
Q

def global development delay

A

significant delay in milestones in + areas

230
Q

what are the main causes of profound disability in paeds

A
  • chromosomal abnormalities
  • genetic factors (microduplications, deletions)
  • cerebral palsy
  • IEM
231
Q

what investigations for developmental delays

A
  • observation of child
  • neuro and ear exam
  • genetic blood test ( CGH microarray and karyotype)
  • standard blood test (TFTs, CK, urate, chloride, FBC and ferritin, U&Es, LFTs, calcium, lactate, ammonia)
232
Q

differentials of fever

A
  • meningococcal disease
  • bacterial meningitis
  • herpes simplex encephalopathy
  • Kawasaki disease
  • UTI
  • septic arthritis
  • pneumonia
233
Q

def cerebral palsy

A

group of lifelong conditions of motor and coordination dysfunction (tone, posture, movement) caused by non progressive brain lesion in developing brain

234
Q

risk factors for cerbral palsy

A
  • prematurity/low birth weight
  • intrauterine infections: TORCH
  • multiple gestations
  • complications in pregnancy (thrombophilias, haemorrhage, preeclampsia)
  • birth asphyxia
  • complicated labour and delivery
  • kernicterus (from neonatal jaundice)
  • NAI/head trauma
  • meningitis/encephalitis
  • cardiac-pulmonary arrest
235
Q

presentation of cerbral palsy

A
  • delays in reaching developmental milestones
  • hypotonia/hypertonia
  • weakness in limbs
  • fidgety, clumsy, jerky mvnt
  • walking on tiptoes
  • dysphagia
  • learning disability
  • fisting
236
Q

treatment of cerbral palsy

A
  • physio
  • speech therapy
  • occupational therapy
  • meds for stiffness: baclofen, diazepam, botulin toxin
  • surgery: orthopaedics and neurosurgical
237
Q

prevention of cerebral palsy

A
  • phototherapy for neonatal jaundice (kernicterus)
  • vaccinations
  • buckle children into car seats
238
Q

prognosis of cerebral palsy

A
  • most children live into adulthood
  • can limit activities/independance
  • may need special school
  • can cause strain on body
  • can cause psychiatric pb ie depression
239
Q

presentation of autism

A
  • social communication pb
  • social understanding and interaction pb
  • social imagination

young childre: tandrums, active, difficult to engage with

older children: difficult making/maintaining relationship

  • social cues diff
  • difficult taking turns
  • edge of groups
240
Q

suumptoms of ADHD

A
  • inattention
  • impulsivity
  • hyperactivity
241
Q

clinical features of DMT1

A 
hyperglycaemia
polyuria
polydipsia
weight loss
excessive tiredness

secondary nocturnal enureis
skin sepsis
candida and othe infections

242
Q

management of DMT1

A
  • insulin theray (one long acting and short acting before meals OR continuous subcutaneous insulin infusion with insulin pump therapy)
  • monitoring ( at least 5 cap blood glucose test per day and HbA1c 4x/year)
  • hypos: fast acting glucose by mouth or IM glucagon)
243
Q

complications of diabetes type 1

A
  • increase risk of hypothyroidism, addison’s disease, coeliac disease, rheumatoid arthritis
  • diabetic retinopathy, kidney disease, neuropathy
  • hypertension
244
Q

symptoms of DKA

A
  • smell of acetones on breath
  • vomiting
  • dehydraarion
  • abdo pain
  • hyperventilation
  • hypovolaemic shock
  • drowsiness
  • coma and death
245
Q

diagnosis of DKA

A
  • symptoms
  • acidosis (blood pH<7.3 or high bicarb)
  • ketanaemia
246
Q

management of DKA

A

fluids

insulin

Year 4 (13 decks)

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