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Year 4 - Paediatrics > Paeds - Altered Conciousness > Flashcards

Paeds - Altered Conciousness Flashcards

1
Q

To what extent is T1DM genetic?

A

Twin studies have shown concordance of 30-40%

Thus there is a notable genetic component but not a significant as T2DM (~ 80% concordance)

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2
Q

What causes T1DM?

A

Often molecular mimicry between an environmental trigger and an antigen on the surface of pancreatic β­-cells

Environmental triggers:

  • Enteroviral infections
  • Cow’s milk proteins
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3
Q

T1DM has 2 peaks in the age of presentation, what are they?

A

1) Pre-school
2) Teenagers

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4
Q

How do children often present with T1DM?

A

Hx of a few weeks of:

  • Classic triad:
    1. Polyuria
    2. Polydipsia
    3. Weight loss or excessive tiredness
  • Hyperglycaemia (random plasma glucose > 11.1 mmol/L)
  • Secondary nocturnal enuresis (young children)
  • Candida infection (mouth, genitalia, feet)
  • DKA:
    • Acetone breath
    • Abdominal pain
    • Hyperventilation due to acidosis (Kussmaul breathing)
    • Vomiting
    • Dehydration
    • Hypovolaemic shock
    • Drowsiness
    • Coma / Death
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5
Q

How does diabetic ketoacidosis present?

A
  • Polyuria
  • Polydipsia
  • Acetone breath
  • Abdominal pain - correlates with degree of acidosis
  • Hyperventilation due to acidosis (Kussmaul breathing)
  • Vomiting
  • Dehydration - dry mucous membranes, poor skin turgor, sunken eyes, ↑ HR, ↓ BP
  • Hypovolaemic shock
  • Drowsiness
  • Coma / Death
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6
Q

Define Diabetes Mellitus

A

Diabetes Mellitus = a reduction in insulin action sufficient to cause a level of hyperglycaemia that, over time, will result in diabetes specific microvascular pathology and macrovascular pathologies

Microvascular pathologies:

  • Retinopathy
  • Nephropathy
  • Neuropathy

Macrovascular pathologies:

  • Stroke
  • MI
  • Renovascular disease
  • Limb ischaemia
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7
Q

What are the 3 mechanisms by which ↓ insulin action occurs in Diabetes Mellitus?

A
  1. ↓ insulin production
  2. ↓ insulin sensitivity of target organs
  3. Overwhelming ↑ in catabolic hormones
    • The anabolic effect of insulin is balanced against 4 main ‘catabolic hormones’ e.g. catecholamines, cortisol, glucagon and growth hormone
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8
Q

Describe Non-diabetic hyperglycaemia (NDH) also called pre-diabetes (for patients) and impaired glucose regulation (for healthcare staff).

A

NDH = insulin action ↓ is sufficient to cause hyperglycaemia but not sufficient enough to cause microvascular damage

There are 2 main types of impaired glucose regulation:

  1. Impaired fasting glucose (IFG) - due to hepatic insulin resistance
    • Fasting glucose 6.1 - 6.9 mmol/L
    • Pts with IFG should have an OGTT to rule out diabetes - if ≥ 7.8 but < 11.1 then pt has IGT
  2. Impaired glucose tolerance (IGT) - due to muslce insulin resistance
    • Fasting glucose < 7.0 mmol/L + OGTT 2-hour ≥ 7.8 but < 11.1
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9
Q

What is HbA1c?

A

HbA1c = glycated haemoglobin

  • It is an indication of the previous 3-month average plasma [glucose]
  • Test is limited to 3-month average as lifespan of RBCs is 120 days i.e. 4 months
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10
Q

What is DKA (Diabetic Ketoacidosis)?

A

DKA = acute metabolic complicationof T1DM

it is characterised by the triad of:

  1. Hyperglycaemia
  2. Ketonaemia
  3. Acidaemia
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11
Q

What are the 3 most common events precipitating DKA?

(Besides new presentation of T1DM as DKA)

A
  1. Inadequate insulin therapy (e.g. missed insulin dose)
  2. Infection (causes ↑ in bodies metabolic demands, for which there is insufficient insulin to accommodate for i.e. not enough to move enough glucose into cells)
    • Pneumonia and UTI are most common
  3. MI - cardiovascular events can stim release of counter-regulatory hormones that precipitate DKA (catecholamines, cortisol, glucagon, growth hormone)

The following are other known risk factors for precipitating DKA:

  • Pancreatitis
  • Acromegaly (↑ GH production due to benign pituitary adenoma)
  • Hyperthyroidism
  • Cushing’s Syndrome
  • Drugs affecting carbohydrate metabolism e.g. corticosteroids, thiazides, anitipsychotics
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12
Q

What is the mechanism underpinning the development of DKA?

A
  • Foundation is a combination of:
    • ↓ net effective insulin
    • ↑ counter-regulatory hormones (e.g. glucagon, catecholamines, cortisol and growth hormone)
  • ↓ net effective insulin –> hyperglycaemia (as body is unable to move glucose into cells)
  • The ↑ plasma [glucose] results in ↑ glucose in kidney nephrons –> this increases osmotic pressure (lowers H2O potential) causing solutes and H2O to move into the nephrons –> this is called osmotic diuresis
  • ​Osmotic diuresis causes:
    • Polyuria
    • Dehydration
    • Polydipsia
    • Electrolyte loss/disturbances
  • ↓ glucose moving into cells also causes ↑ lipolysis –> releasing fatty acids, which are converted by beta-oxidation (in the liver) into ketone bodies; acetoacetate and β-hydroxybutyrate
  • Ketone bodies are used as an energy source in starvation (i.e. absence of carbohydrate energy sources fat stores are used) –> however they turn blood acidic
  • The body initially buffers the ketoacidosis with bicarbonate (HCO3-), but is overwhelmed
  • The body hyperventilates (respiratory compensation) to lower blood CO2 (reduce acidity)
    • Kussmaul Breathing – is a form of hyperventilation involving deep + laboured breathing and associated with metabolic acidosis
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13
Q

How is DKA diagnosed from tests (excluding examination)?

A
  1. Hyperglycaemia - blood glucose > 11.0 mmol/L or known diabetes mellitus
  2. Ketonaemia - > 3.0 mmol/L
    • Urinary ketones NOT used anymore (worse predictor of DKA)
  3. Acidaemia:
    • Bicarbonate (HCO3-) < 15.0 mmol/L and/or
    • Venous pH < 7.3
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14
Q

What tests/investigations might be useful in a patient suspected of DKA?

A
  • Blood glucose > 11.1 mmol/L
    • 5-10% of DKA patients present as being euglycaemic
  • Blood ketones - > 3.0 mmol/L
  • Lactate - taken to exclude lactic acidosis (result should be normal in DKA)
  • Blood glucose
    • 5-10% of DKA patients present as being euglycaemic
  • VBG / ABG - severe metabolic acidosis
    • Generally VBG is easier, lower risk, and can be used to diagnose and determine response to treatment
    • VBGs can also provide glucose + potassium
    • ABG (gold standard for metabolic disturbances) is more accurate for determining hypercapnia and hypoxia
  • U+Es:
    • Serum K+ often ↑ but total body K+ ↓
    • Na+, Cl-, Mg2+ and Ca2+ are normally ↓
  • Urine Dipstick:
    • +ve for leucocytes in UTI (can precipitate DKA)
    • +ve nitrites (infection)
    • +ve for glucose
    • +ve for ketones
  • FBC:
    • Leucocytosis (↑ WBC) occurs during hyperglycaemic state and in infection
  • Blood culture - looking for infective pathogen
  • ECG - to identify MI as precipitant or examine cardiac effects of electrolytes disturbances (Hyperkalaemia = tall-tented T-waves and widened QRS, hypokalaemia = U-waves)
  • CXR - if pneumonia thought to be precipitant of DKA
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15
Q

What 3 things are done to mange DKA?

A
  1. Fluid replacement:
    • Typical fluid deficit in DKA ~100ml/Kg e.g. 70kg = 7 litres
    • Always consider age, gender and concomitant medication and co-morbidites when replacing fluid
    • Caution when replacing fluid in following; Young adults (18-25yrs), elderly, pregnant, HF or kidney failure or if taking mediation for BP
  2. Fixed rate Insulin infusion:
    • IV fixed rate infusion pump - made of up of 50 units insulin made up to 50ml with 0.9% saline –> infuse at rate of 0.1 unit/kg/hr
    • When blood glucose < 15 mmol/l an infusion of 5% dextrose should be started
    • Continue pts long-acting insulin at usual dose + times in diabetic patients
    • Only give bolus (stat) dose of IM insulin (0.1 unit/kg) if there is delay in setting up infusion
  3. K+ replacement - correction of hypokalaemia (caused by insulin)
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16
Q

What is the fluid replacement regime for DKA?

A

Fluid replacement

  1. Insert 2 large-bore cannula (one in each arm ideally)
  2. If systolic BP < 90 mmHg (and no concomitant HF or sepsis):
    • 500ml 0.9% sodium chloride (Saline) over 10-15 mins
    • If BP doesn’t improve then another 500ml over 10-15 mins + contact senior
    • If BP remains low –> contact ICU
  3. If/once systolic BP > 90 mmHg:
    • See image
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17
Q

What are the potassium cut-offs which dictate potassium replacement during DKA?

A

Hypokalaemia and hyperkalaemia can occur in DKA:

  • K+ is normally ↑ on admission (even though the total body K+ is ↓)
  • But will ↓ post insulin treatment
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18
Q

How is T1DM diagnosed in children?

A
  1. Symptoms of DKA:
    • Hyperglycaemia
    • Ketonaemia - > 3.0 mmol/L or significant ketonuria (more than ++ on urine dipstick)
    • Acidaemia
  2. Symptoms typical of T1DM in children:
    • Polyuria
    • Polydipsia
    • Weight loss
  3. Hyperglycaemia:
    • Random blood glucose > 11.1 mmol/L
    • Fasting blood glucose > 7 mmol/L
    • Raised HbA1c > 6.5% or 48 mmol/mol
  4. Glycosuria
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19
Q

What features of a Hx might indicate a child has T2DM as opposed to T1DM?

A
  • Family history of T2DM
  • Child is black or from indian subcontinent
  • Severly obese
  • Signs of insulin resistance:
    • Acanthosis nigricans - velvety dark skin on the neck or armpits
    • Skin tags
    • Polycystic ovaries in females
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20
Q

What are the classifcations / types of insulin - based on their profile of action/duration?

A
  1. Rapid-acting insulin analogues
    • Onset = 5 mins
    • Peak = 1 hour
    • Duration = 3-5 hours
  2. Short-acting insulin (also called soluable insulin)
    • Onset = 30 mins
    • Peak = 3 hours
    • Duration = 6-8 hours
  3. Intermediate-acting insulin
    1. Onset = 2 hours
    2. Peak = 5-8 hours
    3. Duration = 12-18 hours
  4. Long-acting insulin analogues
    1. Onset = 1-2 hours
    2. Peak = flat profile
    3. Duration = 24 hours
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21
Q

What is a basal-bolus regime for Insulin?

A

It is the combination of:

  1. Rapid/short-acting ‘bolus’ insulin before meals
  2. Intermediate/long-acting ‘basal’ insulin once or twice daily
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22
Q

Name some examples of the following Insulin types:

  1. Rapid-acting insulin analogues
  2. Short-acting insulins
  3. Intermidate-acting insulins
  4. Long-acting insulin analogues
A
  1. Rapid-acting insulin analogues:
    • Insulin Aspart (Novorapid)
    • Insulin Lispro (Humalog)
  2. Short-acting insulins:
    • Actrapid
    • Humulin S
  3. Intermidate-acting insulins:
    • Isophane insulin
  4. Long-acting insulin analogues:
    • Insulin determir (Levemir) - once or twice daily
    • Insulin glargine (Lantus) - once daily
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23
Q

What are ‘Premixed’ preparations of Insulin composed of?

A

Combinations of intermediate acting insulin + either a rapid-acting insulin analogue or short-acting insulin e.g.

  • Novomix 30:
    • 30% insulin aspart (rapid-acting)
    • 70% insulin aspart protamine (intermediate-acting)
  • Humalog Mix 25:
    • 25% insulin lispro (rapid-acting)
    • 75% insulin lispro protamine (intermediate-acting)
  • Humalog Mix 50:
    • 50% insulin lispro
    • 50% insulin lispro protamine
24
Q

Is Insulin typically administered; subcutaneously, intramuscularly, IV or oral?

A

Subcutaneously

25
Q

What localised side effect can insulin injection cause?

A

Lipohypertrophy

small lump under skin due to fat accumulation at injection sites (insulin causes fat hypertrophy)

26
Q

What factors can cause blood glucose to go up vs down?

A

Raise blood glucose:

  • Omission of insulin
  • Food (especially refined carbs e.g. white bread, white pasta, white rice, sweets etc)
  • Illness - but lack of eating during illness can cause varied blood glucose (best to monitor BMs closely and respond appropriately)
  • Menstruation (shortly before onset)
  • Growth hormone
  • Corticosteroids
  • Sex hormones at puberty
  • Surgery

Lower blood glucose:

  • Insulin
  • Exercise
  • Alcohol
  • Anxiety / excitement
  • Medication
27
Q

How is DKA in a child managed?

A

This regimen is initiated IF the child is:

  1. vomiting or
  2. has reduced conciousness level or
  3. clinically dehydrated

(otherwise only subcut insulin is required)

  1. Fluids
    • If in shock –> resus with 0.9% saline, insert central venous line + urinary catheter
    • If vomiting or reduced conciousness –> NG tube (to reduce risk of aspiration)
    • Rehydrate over 48-72h (rapid rehydration can cause cerebral oedema)
    • 40 mmol/L of potassium - ensure all fluids given to children /w DKA contain 40 mmol/L of K+
    • Don’t stop IV fluid therapy until ketosis is resolving + alert + oral fluids without vomiting
    • Monitor:
      • Fluid input + output
      • U+Es, creatinine and blood gas
      • Neurological state
  2. Insulin
    • Do not give bolus
    • Insulin infusion 0.05-0.1 U/kg/hr - start 1-2hr after IV fluid therapy
    • Monitor BMs regularly - aim for gradual reduction of 2 mmol/hr
    • Change to 0.9% saline with 5% dextrose and 40 mmol/L potassium chloride (KCl) when blood glucose < 14 mmol/L to avoid hypoglycaemia
    • Don’t change IV insulin to subcut insulin until ketosis is resolving + alert + oral fluids without vomiting
    • Start subcut insulin 30-60 mins before stopping IV insulin
  3. Potassium
    • Initially hyperkalaemia but will fall with insulin
    • Start K+ replacement as soon as urine is passed
    • Continuous ECG monitoring (to avoid hyperkalaemia)
  4. Acidosis
    • This will correct with fluids + insulin
    • Only give bicarbonate if in shock and note responding to therapy
28
Q

Which human leukocyte antigens (HLA) are associated with T1DM?

A

HLA-DR3 and HLA-DR4

29
Q

What kidney condition is diabetes

the commonest cause of?

A

End Stage Renal Disease (ESRD)

30
Q

What conditions can cause diabetes?

A
  • Cushing’s syndrome
  • Acromegaly (GH excess)
  • Gestational diabetes
  • Chronic pancreatitis
  • Cystic fibrosis (features of both T1DM / T2DM in that it exhibits reduced insulin production but reduced insulin sensitivity)
31
Q

How would you rule out cerebral oedema due to iatrogenic treatment of DKA?

A

CT head + senior review

32
Q

Which population are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA management?

A

Children and young adults

33
Q

When does cerebral oedema usually occur in the treatment of DKA?

A

4-12 hours after treatment

but can present at any time

34
Q

Under what conditions / circumstances is DKA likely to occur?

A
  1. At diagnosis (pts with T1DM can not present to doctors until DKA)
  2. Illness e.g. viral / bacterial infection
  3. Growth spurt / puberty
  4. Insulin omission (for any reason)
  5. Malfunctioning insulin pump (pump doesn’t give any long-acting insulin, so without short-acting supply, DKA can develop)
35
Q

If a child presents with:

  1. polydipsia
  2. polyuria
  3. and unexplained weight loss or excessive tiredness
  • and any of the following:
    • nausea / vomiting
    • abdo pain
    • hyperventilation
    • dehydration
    • reduced level of consciousness

What investigation should be done immediately?

A

Caillary blood glucose

> 11 mmol/L + symptoms of DKA = suspect DKA & send to hospital

36
Q

When DKA is suspected in a child with known T1DM

what blood test should be done?

A

Blood ketones

If elevated –> send to hospital

37
Q

What should your initial actions be when you suspect / diagnose a child with DKA?

A
  1. Inform responsible senior clinician
  2. Explain to child / young person / family what DKA is and the care required
  3. Record:
    • consciousness level
    • vital signs; HR, BP, temp, RR (Kussmaul)
    • Hx of nausea or vomiting
    • clinical evidence of dehydration
    • body weight
38
Q

If a child has DKA and is NOT:

  1. vomiting or
  2. has reduced conciousness level or
  3. clinically dehydrated

how are they managed?

A
  1. Oral fluids
  2. Subcut insulin
  3. Monitor ketonaemia + acidosis via blood ketones & blood gases
39
Q

What 3 things (that are normal in adult DKA management) are not normally given in child DKA management?

A
  1. Fluid bolus
  2. Insulin bolus
  3. IV sodium bicarbonate (or any bicarbonate for that matter)
40
Q

When giving IV fluids for DKA in a child how is their total fluid requirement for the first 48hrs calculated?

A

Estimated fluid deficit + fluid maintenance

Estimated fluid deficit:

  • Mild - moderate DKA (pH of 7.1 or above) = 5%
  • Severe DKA (pH of below 7.1 ) = 10%

Maintenance fluids ‘reduced volume’ rules:

  • < 10 kg = 2 ml/kg/hr
  • 10 - 40 kg = 1 ml/kg/hr
  • > 40 kg = fixed volume of 40 ml/hr
41
Q

What monitoring is needed during treatment of DKA in children?

A
  1. Hourly - capillary glucose, ketones, vitals and fluid balance
  2. Every 30 mins - level of conciousness (modified GCS) and HR (to detect bradycardia) - because children are are greater risk of cerebral oedema
  3. Continuous ECG - monitor for hypokalaemia (ST depression and prominent U-waves)
  4. At 2 hours post start of treatment then every 4 hrs:
    • blood glucose
    • blood gas (pH, pCO2)
    • U+Es
    • Face-to-face review
42
Q

What are the early manifestations of Cerebral Oedema in children?

A
  1. Headache
  2. Agitation
  3. Irritability
  4. Unexpected drop in HR & increased BP
  5. Deterioration in level of consciousness
  6. Respiratory pauses
  7. Ocullomotor palsies
  8. Pupil inequality or dilation
43
Q

How do you treat cerebral oedema in children?

A

Mannitol 20%, 0.5–1 g/kg over 10–15 minutes

OR

Hypertonic sodium chloride 2.7% or 3%, 2.5–5 ml/kg over 10–15 minutes

44
Q

What messages should be given to diabetic patients regdarding

Sick Days, so called ‘Sick Day Rules’?

A
  1. Increase frequency of blood glucose monitoring to 4-hourly or more
  2. Encourage fluid intake - aim for at > 3L in 24hrs
  3. If unable/struggling to eat –> keep sugary drinks to maintain blood glucose
  4. Advise pts to keep a box of ‘sick day supplies’ for if they become unwell
  5. Continue to take oral hypoglycaemic medication even if not eating - bodies response to stress is ↑ cortisol –> ↑ glucose
  6. If on insulin –> take doses as normal - if blood glucose + ketones are high –> give corrective insulin dose
    • Rule of thumb: total daily insulin / 6 (max 15 units)
  7. Advise pt to keep access to a mobile phone –> has been shown to reduce progression of ketosis to diabetic ketoacidosis
45
Q

What are the diagnostic criteria for T2DM for each of the following investigations, with symptoms and then without symptoms:

  1. Random plasma glucose
  2. Fasting glucose
  3. Oral glucose tolerance test (OGTT)
  4. HbA1c
A

If patient is SYMPTOMATIC + ONE of:

  • Fasting glucose ≥ 7.0 mmol/L
  • Random plasma gucose ​≥ 11.1 mmol/L
  • Oral glucose tolerance test (OGTT) - ≥ 11.1 mmol/L (2h after 75g glucose given orally)

If patient is ASYMPTOMATIC the above criteria apply BUT must be demonstrated on two seperate occasions!

HbA1c:

  • Diabetes = HbA1c ≥ 48 mmol/mol (6.5%)
  • Pre-diabetes = HbA1c 42-47 mmol/mol
  • Not diabetic = HbA1c ≤ 41 mmol/mol (5.9%)
  • If asymptomatic the test must be repeated to confirm
  • Conditions that affects RBC turnover can produced misleading HbA1c - thus the it can’t be used in the following conditions:
    • Children
    • Pts with symptoms < 2 months
    • Haemoglobinopathies
    • Haemolytic anaemia
    • Untreated iron deficiency anaemia
    • Suspected gestational diabetes
    • HIV
    • CKD
    • Medication that may cause hyperglycaemia (e.g. corticosteroids)
47
Q

What is the risk that gestational diabetes poses?

How can it be diagnosed via fasting glucose or OGTT?

A

↑ foetal morbidity/mortality

  • Fasting glucose ≥ 5.6 mmol/L
  • OGTT ≥ 7.8 mmol/L
48
Q

What test can be done to help confirm T1DM in an ambiguous clinical picture?

A

GAD antibodies test

(Glutamic Acid Decarboxylase autoantibodies)

  • GAD antibiodies +ve in autoimmune style diabetes e.g. T1DM
  • Can be used to distinguish between LADA & T2DM in an adult with low BMI or weight loss (suggestive of autoimmune diabetes pattern)
49
Q

How often should children with T1DM test their blood sugar?

A

~ 5 times per day

(more during illness / symptomatic / physical activity etc)

50
Q

How many times per year should children with T1DM be offered HbA1c measurement?

A

4 times per year

(more frequent if concern about blood glucose control)

51
Q

How is hypoglycaemia in children / young people with T1DM managed?

A

Mild - moderate hypoglycaemia:

  • Fast-acting glucose e.g. 10-20g PO
    • Raises blood glucose within 5-15 mins
    • Glucogel can be rubbed on lips
    • May need to be given in frequent small amounts as hypoglycaemia can cause vomiting
  • Re-check blood glucose within 15 mins
  • Oral complex long-acting carbohydrate - give when symptoms improve / normoglycaemia is achieved (unless about to have a snack)

Severe hypoglycaemia:

  • IF rapid IV access –> 10% IV glucose, max dose of 500 mg/kg
  • IF no rapid IV access –> IM glucagon or concentrated oral glucose solution (e.g. Glucogel)
    • Do not use oral glucose solution is level of consciousness is reduced
52
Q

In the treatment of severe hypoglycaemia in children without IV access what do you give and how much?

A
  • Child < 8-yrs or weigh < 25 kg –> 500 micograms of IM glucagon
  • Child > 8-yrs or weigh > 25 kg –> 1 mg of IM glucagon
53
Q

When can IM glucagon be ineffective in treating hypoglycaemia?

A

In T1DM patients whose hypoglycaemia is due to alcohol consumption

54
Q

Diabetes can involve various complications, what monitoring is done for these?

A
  1. Thyroid disease - TFTs at diagnosis + annually
  2. Diabetic retinopathy - opthalmoscopy annually from 12-yrs
  3. Diabetic kidney disease - ACR of 3-30 mg/mmol (microalbuminuria) tested for annually from 12-yrs
    • Use ‘early morning urine’ sample (first urine sample of day) - reduces risk of false +ve results
  4. Hypertension - BP annually from 12-yrs
55
Q

What are some rare complications of T1DM?

A
  1. Juvenile cataracts
  2. Necrobiosis lipoidica - a necrotising skin condition associated with diabetes and RA
  3. Addison’s disease
56
Q

What does this image show?

A

Necrotising Lipoidica

(severity or control of diabetes does not affect who experiences it)

  • Hardened, raised are under skin
  • Yellow-ish tint to centre with dark pink surrounding
  • Often appears on shins, both legs (can also be on forearms, trunk and hands)
57
Q

What blood glucose level indicates hypoglycaemia?

A

< 4.0 mmol/L

Year 4 - Paediatrics (16 decks)

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