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Year 4- Paediatrics > Emergency > Flashcards

Emergency Flashcards

1
Q

What is meant by Bell’s palsy?

A

Acute, unilateral, idiopathic facial nerve paralysis

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2
Q

When would you normally see Bell’s palsy?

A

Peak incidence is 20-40 years and the condition is more common in pregnant women.

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3
Q

What are the features of Bell’s palsy?

A

Lower motor neuron facial nerve palsy- forehead is affected

Patients may also notice post auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis.

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4
Q

What is the treatment for Bell’s palsy?

A

Prednisolone 1mg/kg for ten days should be prescribed within 72 hours of onset of Bell’s palsy
Eye care is also important and therefore artificial tears and eye lubricants should be considered

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5
Q

How would you be able to tell whether Bell’s palsy is an upper or lower motor neuron lesion?

A

an upper motor neuron lesion would spare the upper face

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6
Q

What are the reversible causes of cardiac arrest?

A

4Ts
Tamponade, toxins, thrombus,

4Hs
Hypoxia, hypovolaemia, hypo/hyperkalaemia, hypo/hyperglycaemia, hypothermia

4Ts
Thrombosis (coronary or pulmonary), tension pneumothorax, tamponade (cardiac), toxins

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7
Q

What questions should you ask about dehydration?

A

Is the child producing wet nappies?
Is the child thirsty
Do they produce tears when they cry

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8
Q

What are the clinical features of dehydration?

A

The clinical features can be split into interstitial volume depletion and intravascular volume depletion.

Interstitial volume depletion…

Sunken anterior fontanelle 
Dry mucous membranes 
Dry tongue 
Sunken eyes and decreased tears 
Reduced skin turgor (pinch the skin on abdomen or thigh)

Intravascular volume depletion

Altered consciousness/ responsiveness 
Reduced urine output 
Tachypnoea 
Tachycardia +/- weak pulse pressure 
Increased cap refill time 
Falling blood pressure
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9
Q

When sending a child home who is at risk of progression to hypovolaemic shock, it is important to make parents aware of the features that the child is moving to this point, what would you tell them to look out for?

A 
. Pale/ mottled skin 
Cool extremities 
Weak peripheral pulses 
Increased capillary refill time 
Hypotension (lastly)
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10
Q

Where does an epistaxis originate from?

A

Kiesselbachs plexus, located in Littles area, this is an area of the nasal mucosa at the front of the nasal cavity which has lots of blood vessels. when the mucosa is disrupted in this area the blood vessels are exposed and are prone to bleeding.

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11
Q

What are the causes of epistaxis?

A

Allergic rhinitis
Picking the nose
URTI
Foreign body

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12
Q

When would you consider posterior bleeding in epistaxis?

A

If there is bleeding from both nostrils.

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13
Q

What advise would you give to a parent who’s child is having a nose bleed?

A

Sit up and tilt the head forwards
Squeeze the soft part of the nostrils together for 10-15 minutes
Spit out any blood In the mouth rather than swallowing

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14
Q

What should be done if a nosebleed does not stop after 10-15 min/is severe/both nostrils?

A

Nasal packing using nasal tampons or inflatable packs

Nasal cautery using silver nitrate sticks

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15
Q

What May you consider prescribing after an acute nosebleed?

A

Naseptin four times daily for ten days, this reduces inflammation/crusting/infection

Contraindicated in peanut or soya allergy

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16
Q

What are febrile convulsions?

A

Type of seizure that occur in children with a high fever. They are not caused by epilepsy or other underlying neurological pathology such as meningitis or tumours
By definition febrile convulsions only occur between ages of 6 months and 5 years

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17
Q

What are simple febrile convulsions?

A

Generalised tonic clonic seizures, last less than 15 mins and only occur once during a single febrile illness.

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18
Q

What is a complex febrile convulsions?

A

This is when they consist of partial or focal seizures, they last more than 15 mins or occur multiple times during the same febrile illness

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19
Q

How do you diagnose a febrile convulsions?

A 
In order to make a diagnosis of febrile convulsions, other neurological pathology must be excluded 
. Epilepsy 
. Encephalitis 
. Meningitis 
 . Trauma
. Electrolyte abnormalities 
. Syncopal episode
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20
Q

What is a typical presentation of a complex febrile child?

A

The first stage is to identify and manage the underlying source of infection and control the fever with simple analgesia such as: paracetamol and ibruprofen.

Parental advice if further seizure:
. Put the child in a safe place like a carpeted floor or a pillow under their head
. Place them in the recovery position and away from potential sources of injury
. Dont put anything in their mouth
. Call an ambulance if the seizure lasts for more than 5 minutes

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21
Q

What is the risk of developing epilepsy after a febrile convulsions?

A

1.8% for the general population
2-7.5% for a simple febrile convulsions
10-20% after a complex febrile convulsion

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22
Q

What is the pathophysiology of hypothermia?

A

Neonates have thin skin, little adipose tissue and a large body surface area comparative to their body weight and therefore they are very susceptible to heat loss and consequently hypothermia.

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23
Q

What are the risk factors for hypothermia?

A

Prematurity
Systemic illness
Low birthweight
Diabetic mother

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24
Q

How do you manage hypothermia?

A

Using incubator Warm mattress/skin to skin with mum
. Keeping room temp warm and avoiding droughts
. Wrapping baby, including hats and socks

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25
Q

What are the symptoms of hypoglycaemia in the newborn?

A 
Jitteriness
Irritability 
Apnoea 
Lethargy
Drowsiness 
Seizures
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26
Q

Hypoglycaemia is particularly likely in the first 24 hours of life, what are the reasons for it?

A 
IUGR 
Preterm 
Born to mothers with diabetes mellitus 
Large for dates 
Hypothermic, polycythaemic or ill for any reason
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27
Q

Why would growth restricted babies have hypoglycaemia?

A

Growth restricted and preterm infants have poor glycogen stores

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28
Q

Why would babies with diabetic mothers have low glucose levels?

A

Hyperplasia of the islet cells in the pancreas causes high insulin levels.

29
Q

How can hypoglycaemia be prevented?

A

Early and frequent milk feeding. In infants at increased risk of hypoglycaemia the blood glucose is regularly monitored at the bedside.

30
Q

What would you do if the infant has two low blood glucose levels, one very low blood glucose level or is symptomatic?

A

Glucose is given by IV infusion aiming for mIntain the glucose level over 2.6mmol/l

The concentration of the IV dextrose may need to be increased from 10% to 15% or even 29%
Abnormal blood glucose results should be confirmed in the lab
High concentration IV infusions of glucose should be given via. A central venous catheter

If there is a difficulty or delay in starting the infusion, or a satisfactory response is not achieved then glucagon can be given

31
Q

How does malnutrition result normally?

A

Combination of anorexia, malabsorption and increased energy requirements because of infection or inflammation.

Malnutrition in older children and adolescents may also result from eating disorders

32
Q

How do you assess the nutritional status of a child?

A

Dietary assesment
. Parents are asked to record the food the child eats during several days

Anthropometric (the study of body proportions)
Weight and height are key measurements
Skinfold thickness of the triceps reflects subcutaneous fat stores and can be measured with callipers

Lab investigations can be done to detect early physiological adaptation to malnutrition

33
Q

What are the consequences of malnutrition?

A

Immunity is impaired
Wound healing is delayed
Operative morbidity and mortality increased
Malnutrition worsens outcome of an illness
Malnourished children are less active and more apathetic
Profound malnutrition can cause permanent delay in intellectual development

34
Q

What is enteral nutrition?

A

Involving or passing through the intestine, either naturally via the mouth and oesophagus or through an artificial opening.

35
Q

When would you use enteral nutrition?

A

Used when the digestive tract is functioning, as it maintains gut function and is safe.
Feeds are given either nasogastrically, gastrostomy, or via. Feeding tube in the jejunum

Gastrostomies can be created endoscopically or surgically

If long term enteral nutrition is required (>6 weeks), a gastrostomy is preferred as it avoids repeated replacement of NG tubes which is distressing for the child.

36
Q

What are the components of a nutritional assesment?

A

Anthropometric- weight, height, mid upper arm circumference, skinfold thickness

Lab
Low plasma albumin
Low concentration of specific minerals and vitamins

Food intake
Dietary recall, dietary diary

Immunodeficiency
Low lymphocyte count
Impaired cell mediated immunity

37
Q

When is a PEG tube used?

A

In a child with severe neuro disability who is unable to eat by mouth.

38
Q

When is parenteral nutrition used?

A

Can be used exclusively or as an adjunct to enteral feeds to maintain and/ or enhance nutrition.

39
Q

What is the aim of parenteral nutrition?

A

To provide a nutritionally complete feed in an appropriate volume of IV fluid. Energy is given as glucose together with a fat emulsion. Electrolytes, full range of vitamins, micronutrients and trace elements are also given

Clinical deficiencies (such as zinc deficiency, causing erythematous rash around the mouth and anus) may occur and monitoring is required.

40
Q

Who might require parenteral feeding long term?

A

Short bowel syndrome
Loss of bowel from complicated gastroschisis
Volvulus
Long segment Hirschsprung’s

41
Q

How would a child with marasmus present?

A

Child would have a wasted, wizened appearance. Oedema is not present and affected children are often withdrawn and apathetic.

42
Q

How does a child present with kwashiorkor?

A

Generalised oedema as well as severe wasting.
Because of the oedema the weight may not be as severely reduced as in marasmus.
In addition there could be:

Flaky paint skin rash with hyper keratosis and desquamatiom

Distended abdomen and enlarged liver

Angular stomatitis

Hair which is sparse and depigmented

Diarrhoea, hypothermia, bradycardia, hypotension

Low plasmin albumin, potassium, glucose, magnesium

43
Q

What are the normal Resp rates for infants, young children and older children?

A

Infants= 30-40
Young children= 25-35
Older children= 20-25

44
Q

What is the normal HR for infants, young children and older children?

A

Infants= 110-160
Young children = 95-150
Older children= 80-120

45
Q

How can you rapidly assess the level of consciousness in the child?

A 
You can use AVPU/GCS
A= alert 
V= responds to Voice 
P= responds to Pain 
U= unresponsive

A score of P means that the child’s airway is at risk and will need to be maintained by a manoeuvre or adjunct.

46
Q

How do you measure the capillary refill time of a child?

A

Press on the skin of the sternum or a digit at the level of the heart
Should apply pressure for five seconds
Measure the time for blush to return
A prolonged cap refill time is >2s

47
Q

What are the indicators of moderate resp distress in infancy?

A 
Tachycardia 
RR>50bpm 
Nasal flaring 
Use of accessory muscles 
Intercostal and subcostal recession 
Head retraction 
Unable to feed
48
Q

What are the signs of severe resp distress?

A 
Cyanosis 
Getting tired 
Reduced conscious level 
Sats<92% despite O2 
Rising partial pressure of CO2
49
Q

What is the supportive therapy given for resp distress?

A

Oxygen (face mask or nasal cannula)
Noninvasive ventilation - CPAP/ BIPAP
Endotracheal intubation and mechanical ventilation

50
Q

Why are children more susceptible to shock?

A

Higher surface area to volume ratio

Higher basal metabolic rate

51
Q

What is severe acute malnutrition defined as?

A

Weight for height more than 3 standard deviations below the median on the standard WHO growth chart

MUAC less than 115 mm in children 6 months- 5 years old

Bilateral oedema

52
Q

How do you treat severe acute malnutrition if the child is alert?

A

If the child is alert and has an appetite then they can be managed with ready to use therapeutic food which has revolutionised its treatment, the treatment is based on peanut butter mixed with dried skimmed milk and vitamins and minerals, it is consumed directly by the child.

53
Q

How do you treat acute severe malnutrition in children with no appetite, severe oedema, medical complication or being less than 6 months old?

A 
. Treat or prevent hypoglycaemia 
. Treat or prevent hypothermia 
. Treat or prevent dehydration (avoid fluid overload) 
. Correct electrolyte imbalance 
. Treat infection 
. Correct micronutrient deficiency 
. Initiate feeding
54
Q

How is vitamin D derived?

A

It is derived from synthesis in the skin (D3) following exposure to ultraviolet light or the diet (D2/D3)

55
Q

What are the functions of vitamin D?

A

Regulation of calcium and phosphate metabolism, it is essential for bone health as well as regulation of immune system.

56
Q

What happens if vit D deficiencies are present in childhood?

A

Rickets and osteomalacia will develop

57
Q

What is the pathophysiology behind low vit D levels and osteomalacia?

A

Lack of Vit D causes a low serum calcium, this then triggers secretion of parathyroid hormone and normalises the serum calcium but demineralises the bone. PTH also causes renal loses of phosphate and consequent.y low serum phosphate levels, further reducing potential for bone calcification.

58
Q

How does vitamin D deficiency usually present?

A

Bony deformity and the classical picture of rickets
It can also present without bone abnormalities but with symptoms of hypocalcaemia- seizures, neuromusclar irritability causing muscle spasm of the hands and feet (tetany), Apnoea, stridor, cardiomyopathy.

59
Q

What is the difference between rickets and osteomalacia?

A

Rickets is the failure in mineralization of the growing bone or osteoid tissue.

Failure of the mature bone to mineralize is osteomalacia

60
Q

What are the causes or rickets?

A

Nutritional vit D deficiency due to inadequate intake of insufficient exposure to direct sunlight.
. Living in northern latitudes
. Dark skim
. Decreased exposure to sunlight
. Maternal vit D deficiency
. Diets low in calcium, phosphorus and vit D

. Intestinal malabsorption (coeliac/ pancreatic insufficiency in CF)

. Chronic liver disease

. Chronic kidney disease

61
Q

What drugs can lead to vit D deficiency?

A

Anticonvulsants- phenobarbital and phenytoin (anticonvulsants) interfere with vit D metabolism and may also cause rickets.

62
Q

What are the clinical manifestations of rickets?

A

Earliest sign is a sensation similar to pressing a ping pong ball elicited by firmly pressing over the occipital or posterior psrietal bones.
Costochondral junctions mahbe palpable
Ankles and wrists may be widened
Horizontal depression fo the lower chest
Legs may become bowed

63
Q

What investigation results would show a diagnosis or rickets?

A

Low plasma calcium and phosphate
High alkaline phosphatase and parathyroid hormone
Very low vit D

64
Q

What is harrisons sulci?

A

Occurs in rickets

Is indentation of the softened lower ribcage at the side of attachment of the diaphragm.

65
Q

What are the clinical symptoms of paracetamol overdose?

A

Early= Abdominal pain, vomiting

Later (12-24h) liver failure

66
Q

What might you expect if someone has taken a paracetemol overdose on their blood results?

A

High ALT

Deranged clotting

67
Q

What is the mechanism behind paracetamol poisoning?

A

Initially there is gastric irritation

Then you get a build up of NAPQI (N acetyl p benzoquinone imine) due to liver metabolism being reduced.

68
Q

How do you manage paracetamol overdose?

A

Risk is assessed by measuring plasma paracetamol concentration

Treat with IV acetyl cysteine if concentration is high or liver function is abnormal.

Year 4- Paediatrics (21 decks)

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