SIMMAN - Emergency conditions Flashcards

(38 cards)

1
Q

What is the diagnosis?

  • Brief: Pt has T1DM, blurred vision, headache, and lethargy, rapid breathing (Kussmaul), sweet/fruity/acetone breath.
  • (confusion, reduced consciousness, tachycardia, hypotension, abdominal pain and or vomiting)
A

Diabetic ketoacidosis

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2
Q

Investigations for DKA

A
  • Blood glucose: > 11.1 mmol/l
  • Ketones: urine (2+ or more on dipstick), blood (> 3 mmol/l)
  • VBG: metabolic acidosis (low bicarbonate and low pH)
  • U&Es: assess renal function + monitor for any electrolyte imbalances (particularly potassium)
  • Urinalysis: to look for UTI (can be precipitating factor for DKA)
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3
Q

Acute management of DKA

A
  1. Fluid replacement - 0.9% sodium chloride 1L over 1hr

(If hypotensive then give fluid bolus)

  1. IV insulin fixed rate infusion - e.g 50 units ACTRAPID in 50ml 0.9% NaCl (0.1 unit/kg/hour)

(continue long-acting insulin (eg. Lantus, Tresiba), stop short-acting insulin)

  1. Once blood glucose < 14 mmol/L, ADD 10% DEXTROSE AS A SEPARATE IV INFUSION
  2. Potassium replacement - unless K+ > 5.5 mmol/l
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4
Q

SIMMAN - DKA

Why is there a risk of cardiac arrhythmias in a pt with DKA?

A

due to significant electrolyte imbalances (particularly hypokalemia)

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5
Q

SIMMAN - DKA

How would blood glucose lvls be measured in this scenario?

A

point of care testing using a finger prick sample

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6
Q

SIMMAN - DKA

Urine dipstick for ketones or blood testing?

A

blood ketone testing preferred due to greater sensitivity and specificity

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7
Q

SIMMAN - DKA

Triggers for DKA

A
  • non-compliance with insulin treatment
  • acute infections (increases insulin requirements)
  • new-onset diabetes
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8
Q

SIMMAN - DKA

Why is fluid replacement first priority in a DKA patient?

A

dehydration drives hyperglycaemia, worsening ketosis and acidosis

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9
Q

SIMMAN - DKA

Why is insulin given as an infusion and not a bolus?

A

if insulin given too quickly —> rapid glucose drop —> cerebral oedema risk

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10
Q

SIMMAN - DKA

Why is potassium replacement required?

A

insulin drives K+ into cells —> risk of hypokalemia and arrhythmias

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11
Q

SIMMAN - DKA

Why is dextrose 10% given once blood glucose < 14 mmol/l?

A

allows continued insulin administration without causing hypoglycaemia (need to continue insulin infusion to clear ketones and correct acidosis)

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12
Q

SIMMAN - DKA

DKA resolution criteria

A
  • pH > 7.3
  • blood ketones < 0.6 mmol/L
  • bicarbonate > 15.0 mmol/L
    .
    (if this criteria met and pt is eating/drinking again then switch them back to subcutaneous insulin)
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13
Q

What is the diagnosis?

Brief: most likely a diabetic patient, sweating, tachycardia, pallor, tremors, hunger, confused, dizziness

Blood glucose: < 3.3 mmol/l

A

Hypoglycaemia

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14
Q

Acute management of hypoglycaemia

A
  • If pt is alert: oral glucose 10-20g should be given in liquid form or sugar lumps
  • If pt is confused, but conscious: Glucogel or Dextrogel (buccal absorption) - quick-acting carbs
  • If pt is unconscious or unable to swallow: subcut or IM glucagon (1mg)
  • Further management: IV 20% glucose solution

(note: if pt on IV insulin infusion —> STOP)

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15
Q

SIMMAN - hypoglycaemia

Causes of hypoglycaemia in a diabetic patient

A
  • too much insulin
  • sulfonylureas (eg. gliclazide)
  • missed meals/fasting
  • excessive exercise, alcohol, infection
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16
Q

SIMMAN - hypoglycaemia

Why do sulfonylureas increase the risk of hypoglycaemia in diabetic patients?

A

they act by increasing the secretion of insulin from beta-cells

17
Q

SIMMAN - hypoglycaemia

Why can alcohol cause hypoglycaemia?

A

due to its inhibitory effect on gluconeogenesis and glycogenolysis

  • gluconeogenesis = metabolic process that produces glucose in the liver and kidneys (triggered by low blood glucose lvls)
  • glycogenolysis = process of breaking down glycogen into glucose, which the body uses for energy
18
Q

SIMMAN - hypoglycaemia

Diagnosis of hypoglycaemia (Whipple’s triad)

A
  • symptoms/signs of hypoglycaemia
  • low blood glucose
  • resolution of symptoms with correction of blood glucose
19
Q

SIMMAN - hypoglycaemia

What is a ‘HypoKit’?

A

often prescribed to diabetic patients, contains a syringe and vial of glucagon for IM or subcut injection at home

20
Q

SIMMAN - hypoglycaemia

Once hypoglycaemia has been acutely managed, what are your next steps in management?

A

once blood glucose > 4.0 mmol/l, give a long-acting carbohydrate (eg. toast, biscuits) + monitor closely + identify the cause and educate patient on hypoglycaemia

21
Q

SIMMAN - hypoglycaemia

Contraindications for IM glucagon + what should be used instead?

A

glycogen depletion (eg. liver disease) - glucagon requires liver glycogen to raise blood glucose, if stores are depleted it will be ineffective —> use IV glucose instead

22
Q

What is the diagnosis?

  • Brief: fatigue, lack of energy, weight loss, low blood pressure, abdominal pain, vomiting, cramps, skin pigmentation
  • PMH: adrenal insufficiency receiving exogenous steroids and type 1 diabetics
A

Addisonian crisis

23
Q

Investigations in an Addisonian crisis

  • electrolytes
  • blood glucose
  • ABG/VBG
  • BP
  • GCS
A
  • Hyponatraemia and hyperkalaemia
  • Hypoglycaemia
  • metabolic acidosis
  • Hypotension
  • Reduced GCS
24
Q

Acute management of an Addisonian crisis

A
  1. IM or IV hydrocortisone - 100mg STAT, followed by 200mg infusion over 24hrs (need to admit)
  2. IV fluids - fluid resuscitation first if needed
  3. IV 10% dextrose - if hypoglycaemic
  4. Correct underlying cause - eg. infection (antibx for sepsis), supportive care

(monitoring of electrolytes (esp. Na+ and K+) and fluid balance)

25
SIMMAN - Addisonian crisis What causes an Addisonian crisis?
severe adrenal insufficiency, where the absence of steroid hormones leads to a life-threatening emergency - abrupt withdrawal of steroids (eg. pt on long-term steroids and stops/reduces dose by too much) - acute illness/infection (particularly in pts with existing adrenal insufficiency)
26
SIMMAN - Addisonian crisis Why is there hyponatraemia, hyperkalemia, and hypotension in an Addisonian crisis?
due to deficiency in aldosterone, it promotes Na+ reabsorption, K+ excretion, and water retention (via Na+ reabsorption)
27
SIMMAN - Addisonian crisis Why do you get a metabolic acidosis in an Addisonian crisis?
lack of aldosterone also reduces H+ excretion, leading to acidosis
28
SIMMAN - Addisonian crisis Why do you get hypoglycaemia in an Addisonian crisis?
due to cortisol deficiency (impaired gluconeogenesis)
29
Acute management of a thyroid storm (thyrotoxicosis)
1. Carbimazole - *to treat high thyroid function (or propylthiouracil 2nd-line)* (Iodine given 1hr after antithyroid medication to inhibit thyroid hormone release) 2. Propranolol - *to control symptoms (HR and palpitations)* 3. IV paracetamol - *for fever* (supportive care where needed)
30
SIMMAN - Thyroid storm Causes of thyroid storm
infection, trauma, surgery
31
Management of epistaxis (nosebleeds)
1. First aid measures: *sit down, pinch soft part of nose, lean forward* (note: spit out any blood in the mouth, rather than swallowing) . If bleeding does not stop after 10-15 mins, then it is severe: - If anterior bleed and can see bleed point —> *nasal cautery using silver nitrate* - If low*-*volume bleeding, but no obvious bleed point —> *nasal packing (tranexamic acid soaked nasopore pack)* (note: remove pack after 24hrs and reassess —> *nasal examination +/- cautery)* - If high-volume bleeding —> *Rapid Rhino pack* - If bleeding not controlled with these measures —> *Surgery (sphenopalatine artery ligation)* . - DISCHARGE with Naseptin nasal cream (or vaseline)
32
Where does anterior epistaxis arise from
Kiesselbach’s plexus in Little’s area (a vascular network in the anterior part of the nasal septum)
33
Where does posterior epistaxis arise from?
branches of the sphenopalatine artery (tends to be more severe)
34
What is the main risk we are worried about in posterior nosebleeds
higher risk of aspiration of blood
35
Contraindications for Naseptin
peanut or soya allergy
36
Hypercalcaemia symptoms + acute signs
Bones, Stones, Groans, and Moans - acute signs: reduced GCS, muscle weakness, hyporeflexia, nausea/vomiting
37
Management of acute hypercalcaemia
- IV fluids (0.9% NaCl) - IV bisphosphonates (Zolendronic acid) - *inhibits osteoclast activity --> reduces bone resorption*
38
Why is there a metabolic acidosis and ketosis in DKA?
When insulin lvls are low, lipids are broken down rapidly, producing large amounts of ketone bodies (acidic) that then build up in the blood - causing metabolic acidosis and ketosis