OSCE emergencies (Paediatrics) Flashcards

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1
Q

resuscitation fluids for children

A

10 mL/kg over <10 minutes

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2
Q

managment of hypoglycaemia

A

<4mmol
- Encourage drink of sweet drink e.g. lucozade
- IV dextrose 10%
- IM glucagon

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3
Q

investigations for overdose

A

Bedside
- BM
- 12 lead ECG
- Capillary blood gas

Laboratory
Bloods
- Full blood count
- Urea and electrolytes
- Liver function tests
- Clotting
- Blood conc of toxin

Urine
- Toxocology screen

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4
Q

examination for overdose

A
  • A-E assessment
  • AVPU
  • Neuro examination
  • Pupillary reflexes
  • Height and weight
  • specific signs
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5
Q

great resource for overdose

A

TOXBASE

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6
Q

management of paracteamol

A
  • <1 hour give activated charcoal
  • Serum conc (4h post ingestion)
  • <8 hours: N-acetylcysteine infusion
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7
Q

aspirin overdose management

A
  • acitvated charcoal
  • fluid replacment
  • urine alkalinisation with sodium bicarbonate
  • benzos for seizures
  • haemodialysis if severe
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8
Q

iron overdose management

A
  • metabolic acidosis - sodium bicarbonate (large flush before and after due to irritation of vein)
  • Desferrioxamine
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9
Q

benzodiazepine management

A
  • fluids
  • <1 hour activated charcoal
  • Flumenzenil
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10
Q

maagement of button batteries

A

Surgical removal

  • mucosal ulceration -> necrosis -> haemorrhage -> perforation
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11
Q

management of pneumothorax

A

if not breathlessness and <2cm
- no treatment

if breathless and/or >2cm rim of air on chest x-ray

  • Aspiration - large bore cannula into 2nd intercost space midclavicular line
  • When aspiration fails twice, a chest drain is required- triangle of safety - 5th intercostal spcae midaxillary line (above the rib)
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12
Q

pleural effusion management

A

Conservative management
- small effusions
- supportive

Pleural aspirtation
- 2nd intercostal space midclavicular line
- chest drain - 5th intercostal space mid axillary line

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13
Q

severity of asthma attach

A
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14
Q

management of mild asthma attack

A

Mild cases can be managed as an outpatient with regular salbutamol inhalers via a spacer (e.g. 4-6 puffs every 4 hours).

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15
Q

Moderate to severe asthma attack

A

cases require a stepwise approach working upwards until control is achieved

  1. Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours
  2. Nebulisers with salbutamol / ipratropium bromide
  3. Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days)
  4. IV hydrocortisone
  5. IV magnesium sulphate
  6. IV salbutamol
  7. IV aminophylline
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16
Q

A typical step down regime of inhaled salbutamol is

A
  • 10 puffs 2 hourly
  • then 10 puffs 4 hourly
  • then 6 puffs 4 hourly
  • then 4 puffs 6 hourly.
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17
Q

asthma attack discharge

A

discharge can be considered when the child well on 6 puffs 4 hourly of salbutamol.

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18
Q

Presentation of DKA
x

A

The patient will present with symptoms of the underlying hyperglycaemia, dehydration and acidosis:

  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Weight loss
  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered consciousness
  • Symptoms of an underlying trigger (i.e. sepsis)
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19
Q

Diagnosing DKA

A

Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:

  • Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
  • Ketosis (i.e. blood ketones > 3 mmol/l)
  • Acidosis (i.e. pH < 7.3)
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20
Q

management of DKA

A
  1. Correct dehydration evenly over 48 hours. This will correct the dehydration and dilute the hyperglycaemia and the ketones. Correcting it faster increases the risk of cerebral oedema.
  2. Give a fixed rate insulin infusion. This allows cells to start using glucose again. This in turn switches off the production of ketones.

Other important principles:

  • Avoid fluid boluses to minimise the risk of cerebral oedema, unless required for resuscitation.
  • Treat underlying triggers, for example with antibiotics for septic patients.
  • Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l.
  • Add potassium to IV fluids and monitor serum potassium closely.
  • Monitor for signs of cerebral oedema.
  • Monitor glucose, ketones and pH
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21
Q

clinical featues of kawasaki

A

A key feature that should make you consider Kawasaki disease is a persistent high fever (above 39ºC) for more than 5 days. Children will be unhappy and unwell. The key skin findings are a widespread erythematous maculopapular rash and desquamation (skin peeling) on the palms and soles.

Other features include:

  • Strawberry tongue (red tongue with large papillae)
  • Cracked lips
  • Cervical lymphadenopathy
  • Bilateral conjunctivitis
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22
Q

kawasaki investigations

A
  • Full blood count can show anaemia, leukocytosis and thrombocytosis
  • Liver function tests can show hypoalbuminemia and elevated liver enzymes
  • Inflammatory markers (particularly ESR) are raised
  • Urinalysis can show raised white blood cells without infection
  • Echocardiogram can demonstrate coronary artery pathology
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23
Q

Management of kawasaki

A

There are two first line medical treatments given to patients with Kawasaki disease:

  • High dose aspirin to reduce the risk of thrombosis (dont worry about Reyes syndrome)
  • IV immunoglobulins to reduce the risk of coronary artery aneurysms
  • Patients will need close follow up with echocardiograms to monitor for evidence of coronary artery aneurysms.
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24
Q

pyloric stenois

A

progressive hypertrophy of the smooth muscle fo the pyloric sphincter

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25
Q

presentation of pyloric stenosis

A

occurs in first few weeks of life

  • failing to thrive
  • projective vomiting (non- bilious)
  • feels like a large olvie
  • can often see peristalsis
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26
Q

blood gas for pyloric stenosis

A

hypochloremic hypokalaemic metabolic alkalosis

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27
Q

diagnosis of pyloric stenosis

A

US

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28
Q

management of pyloric sten “Ramstedt’s operationosis

A

Ramstedt’s operation- laparoscopic pyloromyotomy

29
Q

management of bronchiolitis

A

think RSV

  • ensure adequate intake e.g. with NG or IV fluids
  • Saline nasal drtops and nasal suctioning to clear secretions
  • Supplementary oxygen
  • Ventilatory support as required e.g. high flow humidified oxyegn or CPAP or intubation
30
Q

management of croup

A

think parainfluenza - swelling of the larynx - barking cough

Stepwise options in severe croup to get control of symptoms:

  • Oral dexamethasone
  • Oxygen
  • Nebulised budesonide
  • Nebulised adrenalin
  • Intubation and ventilation
31
Q

management of epiglottitis

A

Think HiB (ask about vaccination)
- - IV antibiotics (e.g. ceftriaxone)
- Steroids (i.e. dexamethasone)

32
Q

presentation of intussusception

A
  • Severe, colicky abdominal pain
  • Pale, lethargic and unwell child
  • “Redcurrant jelly stool”
  • Right upper quadrant mass on palpation. This is described as “sausage-shaped”
  • Vomiting
  • Intestinal obstruction
33
Q

management of intussusception

A

diagnosis: US or contrast enema
conservative

  • therapeutic enema

surgical
- reduction
- if bowel is gangrenous -> surgical resection to prevent perforatioa nd ifnection

34
Q

most common cause of haemolytic uraemic syndrome

A

a toxin produced by the e. coli 0157 bacteria, called the shiga toxin. Shigella also produces this toxin.

35
Q

Presentation of HUS

A

E. coli 0157 causes a brief gastroenteritis, often with bloody diarrhoea. The symptoms of haemolytic uraemic syndrome typically start around 5 days after the onset of the diarrhoea.

Signs and symptoms of HUS may include:

  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdominal pain
  • Lethargy and irritability
  • Confusion
  • Oedema
  • Hypertension
  • Bruising
36
Q

HUS management

A

HUS is a medical emergency and has a 10% mortality. It needs to be managed by experienced paediatricians under the guidance of a renal specialist. The condition is self limiting and supportive management is the mainstay of treatment:

  • Urgent referral to the paediatric renal unit for renal dialysis if required
  • Antihypertensives if required
  • Careful maintenance of fluid balance
  • Blood transfusions if required
  • 70 to 80% of patients make a full recovery.
37
Q

general management of sickle cell crisis

A
  • Have a low threshold for admission to hospital
  • Treat any infection
  • Keep warm
  • Keep well hydrated (IV fluids may be required)
  • Simple analgesia such as paracetamol and ibuprofen (NSAIDs should be avoided where there is renal impairment)
  • Penile aspiration is used to treat priapism
38
Q

Splenic Sequestration Crisis

A

Splenic sequestration crisis is caused by red blood cells blocking blood flow within the spleen. This causes an acutely enlarged and painful spleen. The pooling of blood in the spleen can lead to severe anaemia and circulatory collapse (hypovolaemic shock)

39
Q

management of splenic sequestration crisis

A

Supportive
- Blood transfusiona nd fluid resus for anaemia and shock
- Splenectomy to prevent sequestration crisis

40
Q

aplastic crisis most commonly triggered by

A

parvovrius B19 (slapped cheek)

41
Q

management of aplastic crisis

A

supportive with blood transfusions if necessary. It usually resolves spontaneously within a week.

42
Q

A diagnosis of acute chest syndrome requires:

A
  • Fever or respiratory symptoms, with:
  • New infiltrates seen on a chest xray
43
Q

management of acute chest syndrome

A

high flow oxygen
* Antibiotics or antivirals for infections
* Blood transfusions for anaemia
* Incentive spirometry using a machine that encourages effective and deep breathing
* Artificial ventilation with NIV or intubation may be required

44
Q

presentation of constipation

A
  • Less than 3 stools a week
  • Hard stools that are difficult to pass
  • Rabbit dropping stools
  • Straining and painful passages of stools
  • Worse when eating
  • Abdominal pain
  • Holding an abnormal posture, referred to as retentive posturing
  • Rectal bleeding associated with hard stools
  • Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
  • Hard stools may be palpable in abdomen
  • Loss of the sensation of the need to open the bowels
45
Q

secondary causes of constipation

A

such as Hirschsprung’s disease, cystic fibrosis or hypothyroidism.

46
Q

conservative management of constipation

A

Lifestyle Factors
There are a number of lifestyle factors that can contribute to the development and continuation of constipation:

  • Habitually not opening the bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)
47
Q

Complications of constipation

A
  • Pain
  • Reduced sensation
  • Anal fissures
  • Haemorrhoids
  • Overflow and soiling
  • Psychosocial morbidity
48
Q

management of constipation

A
  • Correct any reversible contributing factors, recommend a high fibre diet and good hydration
  • Start laxatives (movicol is first line)
  • Faecal impaction may require a disimpaction regimen with high doses of laxatives at first
  • Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.
49
Q

management of appendicits

A

Supportive
- pain relief
- antiemetic
- broad spectrum antibiotics

Surgical
- laparoscopic appendicetomy

50
Q

Complications of Appendicectomy

A
  • Bleeding, infection, pain and scars
  • Damage to bowel, bladder or other organs
  • Removal of a normal appendix
  • Anaesthetic risks
  • Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
51
Q

principles of neonatal rescus

A

1) Warm the baby -> vigorous drying stimulates breathing
2) Calculate APGAR
3) Stimulate breathing - check for airway obstruction e.g. meconium
4) Inflation breaths: two cycles of five inflation breathes
5) If no response chest compression (<HR 60)
6) if risk of HIE therapeutic hypothermia

52
Q

Hypoxic ischaemic encephalopathy (HIE)

A

occurs in neonates as a result of hypoxia during birth.

  • Hypoxia is a lack of oxygen
  • Ischaemia refers to a restriction in blood flow to the brain
  • Encephalopathy refers to malfunctioning of the brain
53
Q

Suspected HIE in neonates when

A
  1. there are events that could lead to hypoxia during the perinatal or intrapartum period,
  2. acidosis (pH < 7) on the umbilical artery blood gas
  3. poor Apgar scores, features of mild, moderate or severe HIE (see below) or evidence of multi organ failure.
54
Q

Causes of HIE

A

Anything that leads to asphyxia (deprivation of oxygen) to the brain can cause HIE. For example:

  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
55
Q

management of HIE

A
  • Neonatal resus
  • Optical ventilation and circulatory support, nutrion and acid balance
  • Treatment of seixures
  • Therapeutic hypothermia
56
Q

therapeutic hypothermia

A

Cooling blankets
- Target of between 33 and 34°C, measured using a rectal probe.
- This is continued for 72 hours, after which the baby is gradually warmed to a normal temperature over 6 hours.

57
Q

Necrotising enterocolitis (NEC)

A

is a disorder affecting premature neonates, where part of the bowel becomes necrotic. It is a life threatening emergency. Death of the bowel tissue can lead to bowel perforation. Bowel perforation leads to peritonitis and shock.

58
Q

risk factors for developing NEC:

A
  1. Very low birth weight or very premature
  2. Formula feeds (it is less common in babies fed by breast milk feeds)
  3. Respiratory distress and assisted ventilation
  4. Sepsis
  5. Patient ductus arteriosus and other congenital heart disease
59
Q

Presentation of NEC

A
  • Intolerance to feeds
  • Vomiting, particularly with green bile
  • Generally unwell
  • Distended, tender abdomen
  • Absent bowel sounds
  • Blood in stools
60
Q

Investigations
for NEC

A

Blood tests:

  • Full blood count for thrombocytopenia and neutropenia
  • CRP for inflammation
  • Capillary blood gas will show a metabolic acidosis
  • Blood culture for sepsis

Imaging
- Abdominal xray (dilated loops of bowel, thickened wall, gas in bowel wall, pneumoperitoneum)

61
Q

management of NEC

A

Supportive
- Nill by mouth
- IV fluid
- NG decompression
- TPN
- Antibitoics

Surgery
- excision of dead bowel (may get short bowel syndrome)

62
Q

pathophysiology of respiratory distress syndrome

A

Inadequate surfactant leads to high surface tension within alveoli. This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand. This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.

63
Q

management of RDS

A

Antenatal steroids (i.e. dexamethasone) given to mothers with suspected or confirmed preterm labour increases the production of surfactant and reduces the incidence and severity of respiratory distress syndrome in the baby.

Premature neonates may need:

  • Intubation and ventilation to fully assist breathing if the respiratory distress is severe
  • Endotracheal surfactant, which is artificial surfactant delivered into the lungs via an endotracheal tube
  • Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing
  • Supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates
64
Q

complications of RDS

A

Complications
Short term complications:

  • Pneumothorax
  • Infection
  • Apnoea
  • Intraventricular haemorrhage
  • Pulmonary haemorrhage
  • Necrotising enterocolitis

Long term complications:

  • Chronic lung disease of prematurity
  • Retinopathy of prematurity occurs more often and more severely in neonates with RDS
  • Neurological, hearing and visual impairment
65
Q

Management meconium aspiration syndrome?

A
  • The use of a ventilator.
  • Surfactant or antibiotics to open their lungs and clear any infection.
  • Extracorporeal membrane oxygenation (ECMO).
  • A radiant warmer to help control your baby’s temperature.
  • Continuous positive airway pressure (CPAP).
66
Q

investigations for septic arthritis

A

Aspirate the joint prior to antibiotics and send the sample for gram staining, crystal microscopy, culture and antibiotic sensitivities

67
Q

management of septic arthritis

A

Empirical IV antibiotics should be given until the sensitivities are known. Antibiotics are usually continued for 3 – 6 weeks in total. Choice of antibiotic depends on the local guidelines. Example regimes are:

Flucloxacillin plus rifampicin is often first line

68
Q

Peritonsillar abscess presentation

A
  • Sore throat
  • Painful swallowing
  • Fever
  • Neck pain
  • Referred ear pain
  • Swollen tender lymph nodes

Additional symptoms that can indicate a peritonsillar abscess include:

  • Trismus, which refers to when the patient is unable to open their mouth
  • Change in voice due to the pharyngeal swelling, described in textbooks as a “hot potato voice”
  • Swelling and erythema in the area beside the tonsils
69
Q

management of quinsy

A

Management
- needle aspiration or surgical incision and drainage to remove the pus from the abscess.
- Co-amoxiclav
- Clarithromycin if penicillin allergic

Some ENT surgeons give steroids (i.e. dexamethasone) to settle inflammation and help recovery, although this is not universal.