Altered Conscious Level Flashcards

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1
Q

What is AVPU?

A

Alert
Responds to Voice
Responds to Pain
Unresponsive

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2
Q

What causes tachycardia?

A
  • Hypovolaemia secondary to vomiting
  • Use of salbutamol
  • Anxiety
  • Cardiac arrhythmia - can be secondary to electrolyte imbalances, especially hyperkalaemia
  • Co-exist endocrine conditions
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3
Q

What causes an abnormal respiratory pattern?

A
  • Endocrine e.g. DKA (Kussmaul breathing)
  • Exacerbation of asthma
  • Possible chest infection
  • Cardiac disease - compensating for poor perfusion and hypoxia and also an element of pulmonary oedema i.e. cardiomyopathy, arrhythmia
  • Metabolic conditions with compensatory breathing for metabolic acidosis/alkalosis
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4
Q

What causes agitation?

A
  • Hypoglycaemia due to vomiting
  • Exhausted due to work of breathing and feeding
  • Hypocapnia secondary to hyperventilation
  • Cerebral oedema - irritability and agitation can be an early indication of cerebral oedema in DKA
  • Encephalopathic due to infection - viral and bacterial
  • Encephalopathic due to high ammonia secondary to a metabolic condition
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5
Q

What are differentials for severe difficulty breathing?

A

Clear chest, normal RR + O2, tachycardia, increased CRT, agitation

  • DKA secondary to T1DM
  • Anxiety/panic attack
  • Exacerbation of asthma
  • LRTI
  • Hypoglycaemia
  • Encephalopathy
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6
Q

What causes DKA?

A
  • Occurs due to very low insulin levels - body resorts to uncontrolled lipolysis, results in excess free fatty acids that convert into ketones
  • Most common precipitating factors - infection, missed insulin doses, MI
  • If suspecting DKA (plasma glucose >11mmol/l and DKA smyptoms) - immediate hospital admission
  • LIFE-THREATENING EMERGENCY
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7
Q

When is DKA most likely to occur?

A
  • At diagnosis
  • When ill
  • During a growth spurt/puberty
  • Insulin omission for any reason
  • DKA usually develops over 24hrs but can develop faster particularly in young children or patients on insulin pumps (they have no long acting insulin on board so develop DKA quickly if cannula dislodges)
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8
Q

What are the features of DKA?

A
  • Abdominal pain
  • Polyuria, polydipsia, dehydration
  • Initially tachypnoeic but then deep hyperventilation (Kussmaul breathing) begins as acidosis worsens (to reduce CO2)
  • Acetone smelling breath (‘pear drops’ smell)
  • Reduced consciousness
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9
Q

What is the diagnostic criteria for DKA?

A
  • Glucose >11mmol/l or known diabetes mellitus
  • pH <7.3, severe if <7.1
  • Bicarbonate <15mmol/l
  • Ketones >3mmol/l or urine ketones ++ on dipstick
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10
Q

When would you send a child with DKA to acute paediatric facilities?

A
  • Plasma glucose level >11mmol/l in a child or young person without known diabetes and symptoms suggestive of DKA
  • Ketones are elevated in a child or young person
  • When DKA is suspected in a child or young person with known diabetes and it is not possible to measure ketones
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11
Q

When would you suspect DKA in a child/young person?

A

Children and young people taking insulin for diabetes may develop DKA with only mildly elevated blood glucose levels. Suspect DKA in a child or young person with known diabetes and any of: N+V, abdo pain, hyperventilation, dehydration and decreased level of consciousness.

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12
Q

What is the management for DKA?

A
  • Fluid replacement (most patients depleted by ~5.8L) - isotonic saline initially used (slow infusion over a few hours, not rapid replacement)
  • Insulin - insulin infusion at 0.05-0.1 unit/kg/hr (1-2 hrs after IV fluid started), once blood glucose <14mmol/l then start 5% dextrose infusion
  • Correct hyperkalaemia
  • Continue long acting insulin (stop short acting insulin)
  • NG tube if patient is unconscious and vomiting (reduce aspiration risk) - urgent anaesthetic review
  • Measure obs, GCS, look for Kussmaul’s breathing, history of n+v, clinical evidence of dehydration, body weight
  • Also measure Na, K, urea and creatinine
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13
Q

Why does fluid resuscitation need to be monitored in children?

A

Quick fluid resuscitation carries risk of cerebral oedema (especially kids) - need 1:1 monitoring for signs of this e.g. headache, visual disturbances, irritability. To treat cerebral oedema - mannitol or hypertonic NaCl.

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14
Q

Who should be called to deal with a child with DKA?

A

Inform senior clinician of DKA patient. Children and young people with DKA should be treated on a recognised paediatric high dependency unit. If they are <2yrs or have severe DKA (pH <7.1) discuss with regional PICU.

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15
Q

When should you think about sepsis in a child/young person with DKA?

A
  • Fever or hypothermia
  • Hypotension
  • Refractory acidosis
  • Lactic acidosis
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16
Q

What is the fluid and insulin therapy for DKA?

A
  • Treat DKA with oral fluids and SC insulin only if the child or young person is alert, not n+v and not clinically dehydrated - monitor for resolution of ketonaemia and acidosis
  • Treat DKA with IV fluids and insulin if the child is not alert, n+v or clinically dehydrated
  • Fluid requirement for people with DKA, assume a 5% fluid deficit in mild to moderate DKA (indicated by pH of >/= 7.1) and a 10% deficit in severe DKA (<7.1)
  • Fluid maintenance with DKA: <10kg then 2ml/kg/hr, 10-40kg then 1ml/kg/hr, >40kg then give a fixed volume of 40ml/hr
  • Lower than standard volumes due to increased risk of cerebral oedema, use 0.9% NaCl without glucose for rehydration and maintenance until plasma glucose <14mmol/l
  • Ensure that all fluids (except initial bolus) administered to children with DKa contain 40mmol/ potassium chloride, unless they have renal failure.
17
Q

What are the complications of DKA?

A
  • Cerebral oedema (suspect in any child with decreased consciousness - IV mannitol)
  • Hypokalaemia (need to temporarily suspend insulin, discuss with senior)
  • VTE
  • Gastric stasis
  • Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia - stop insulin infusion if hypokalaemia occurs and give K+
  • Acute respiratory distress syndrome
  • AKI
  • Avoiding future episodes - discuss with family factors leading to episode
18
Q

What are the key features of T1DM in children and young people?

A
  • Hyperglycaemia (random plasma glucose >11mmol/l)
  • Polyuria
  • Polydipsia
  • Weight loss
  • Excessive tiredness
19
Q

What is the WHO diagnostic criteria for T1DM?

A
  • Fasting plasma glucose >/= 7.0mmol/l (126mg/dl) OR

- 2hr plasma glucose >/= 11.1mmol/l (200mg/dl)

20
Q

When would you suspect T2DM in children and young people over T1DM?

A
  • Have a strong FH of T2DM
  • Are obese at presentation
  • Are of black or Asian family origin
  • Have no insulin requirement or have an insulin requirement of <0.5 units/kg body weight/day after partial remission phase
  • Show evidence of insulin resistance e.g. acanthosis nigricans
21
Q

What features would indicate other types of diabetes (insulin resistance syndromes or monogenic/mitochondrial diabetes)?

A
  • Diabetes in the 1st year of life
  • Rarely or never develop ketone bodies in the blood (ketonaemia) during episodes of hyperglycaemia
  • Associated features such as optic atrophy, retinitis pigmentosa, deafness or another systemic illness or syndrome
  • Strong FH of diabetes (T1DM also has genetic component)
22
Q

What is the insulin therapy for T1DM?

A
  • Multiple daily injection basal bolus insulin regimens: injections of short-acting insulin before meals, together with 1 daily injection of long-acting insulin
  • Continuous SC insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid-acting insulin analogue or short-acting insulin) by SC needle or cannula
23
Q

What are the target ranges for blood glucose in T1DM?

A
  • Fasting plasma glucose level of 4-7mmol/l on waking
  • Plasma glucose level of 4-7mmol/l before meals at other times of the day
  • A plasma glucose level of 5-9mmol/l after meals
  • A plasma glucose level of at least 5mmol/l when driving
24
Q

What is the advice on blood glucose monitoring in children and young people?

A
  • Advise children and young people with T1DM and their family members or carers (as appropriate) to routinely perform at least 5 capillary blood glucose tests per day. Sometimes more frequent testing is needed e.g. with physical activity and intercurrent illness.
  • HbA1c target level of
25
Q

How do you treat hypoglycaemia?

A
  • Fast acting glucose (e.g. 10-20g) by mouth: may need to be given in frequent small amounts, because hypoglycaemia can cause vomiting
  • Recheck blood glucose within 15 mins (fast acting glucose should increase blood glucose within 5-15 mins) - as glucose levels restore, give long-acting complex carbohydrates to maintain blood glucose, unless they are about to have a snack/meal receiving continuous SC insulin infusion.
  • Severe hypoglycaemia - treat in hospital with IV 10% glucose. Give max dose of 500mg/kg (5ml/kg). If no IV access - give IM glucagon or conc. oral glucose solution e.g. Glucogel. Don’t give orally if altered consciousness.
26
Q

What do you need to do with drinking alcohol when you have T1DM?

A
  • Eat food containing carbohydrate before and after drinking, monitor blood glucose levels and aim to keep levels in recommended range by eating carbohydrates
  • When alcohol causes or contributes to the development of hypoglycaemia, glucagon may be ineffective in treating hypoglycaemia and IV glucose will be required.
27
Q

What extra monitoring needs to be done in children with T1DM?

A
  • Thyroid disease at diagnosis and annually thereafter until transfer to adult services
  • Diabetic retinopathy - annually from 12yrs
  • Moderately and albuminuria (ACR 3-30mg/mmol; microalbuminuria) to detect diabetic kidney disease annually from 12yrs (first urine sample of the day)
  • HTN - annually from 12yrs
28
Q

What are the rare complications and associated conditions with T1DM?

A
  • Juvenile cataracts
  • Necrobiosis lipoidica
  • Addison’s disease
  • Children with T1DM are screened for coeliac disease at diagnosis
29
Q

What are the features of Maturity Onset Diabetes of the Young (MODY)?

A
  • Also called monogenic diabetes
  • Diabetes caused by a faulty gene (single gene defects, syndromes)
  • Usually presents in people <25, is very rare and often gets mistakenly diagnosed for T1/2DM
  • Similar symptoms to T2DM i.e. asymptomatic hyperglycaemia with progression to more severe complications such as DKA
  • Vertical hx of diabetes
  • IMPORTANT: may not need insulin
  • Consider in diabetes diagnosis of infants <1yr
  • Usually treated with sulphonylureas - stimulate pancreas to produce insulin
30
Q

What treatments are needed in diabetes?

A
  • Insulin is delivered into SC tissue via injection or pump
  • Mealtime boluses 20mins before meal - rapid acting
  • Long acting insulin in evening for nocturnal cover
  • Sick day rules (ACDC)
31
Q

What is a cow’s milk allergy vs lactose intolerance?

A
  • Primary lactose intolerance - diarrhoea from birth on breast milk or cows milk formula
  • Cows milk allergy can be either immediate reactions (rash, wheeze, vomiting) or more commonly delayed with abdominal pain, crying and diarrhoea (might be bloody).
    Cows milk allergy is more common in bottle fed infants, mother can continue to breastfeed if she eats a dairy free diet. Nutramigen is better as the protein has been broken down.
  • Some very sensitive baby’s can respond to maternal dietary intake in breast feeding mother
32
Q

How do you decide on milk for the baby?

A
  • Primary lactose intolerance due to lactase deficiency - rare - use a lactose free milk e.g. SMA lactose free
  • Cows milk allergy (CMA) - can try different types of milk
  • Similac Alimentum (or Aptimil Pepti junior) - a milk where the cows protein is extensively hydrolysed - in most infants with CMD - this is effective
  • Neocate milk - the protein is broken down into a much more elemental form for infants with severe allergy
33
Q

How do you manage GORD in babies?

A
  • Small regular feeds
  • Correct feeding/burping technique
  • Tends to resolve with weaning
  • High risk groups - neurological and muscular problems, pre-term, severe allergy
  • Treatment: carbobel feed thickener, gaviscon, ranitidine, omeprazole, surgery (very serious cases - fundoglycatin)
  • Tests: pH studies, barium swallow
34
Q

How might neurological lesions present in infants?

A
  • May often present as feeding problems
  • May have non-specific symptoms e.g. difficult baby, crying all the time
  • Colicky baby - crying incessantly (draw knees up) - usually due to abdo pain
35
Q

What are the causes of evolving neurological symptoms in infants?

A
  • Cerebral palsy - cause not clear, probable antenatal events
  • Hypoxic ischaemic encephalopathy
  • Neonatal meningitis
  • Trauma e.g. shaken baby syndrome
  • Vascular malformation
  • Metabolic conditions e.g. metachromatic leucodystrophhy, adrenoleucodystrophy
  • Neuronal migration defects
36
Q

What are the investigations for neurological conditions in infants?

A
  • Neuro exam
  • Microarray (chromosomes, syndromes)
  • Bloods - FBC, U+Es, LFTs, TFTs, calcium
  • Vit D, ferritin, Vit B12, folate
  • Anti-TTG
  • MRI brain
  • CK
37
Q

What are the features of lissencephaly?

A
  • Gyri and sulci aren’t there, brain is smooth and featureless (lack of sulcation and smooth brain) - all over, sometimes anterior > posterior
  • In utero, early onset
  • PT (muscle tone), OT, S+L, community paediatrician
  • Early: problems with feeding, visual fixation, head control
  • Later: struggling to move around, sit, walk, crawl (increased tone)
  • Muscle spasms: pain due to increased tone, tx: physiotherapy, baclofen, botox, surgery
38
Q

What is the difference between spasticity and dystonia?

A
  • Spasticity: change on speed of movement

- Dystonia: increased resistance