Pt w/ Glucose disturbance Flashcards

1
Q

In which group of patients does DKA occur?

A

T1DM

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2
Q

Pathophysiology of DKA?

What are the clinical features of DKA?

A

Pathophysiology of DKA
-too much glucose>body uses up all insulin>intracellular lack of glucose>break down fatty acids>ketones>acidemia>vomiting (to try and lose H+)>dehydration> electrolyte inbalance

VARIABLE

  • Polyuria and Polydipsia are important hx factors (has lead to dehydration over past few days)
  • Signs of dehydration
  • Sweet smelling breath
  • Weight loss and weakness
  • Hyperventilation - respiratory compensation for the metabolic acidosis - Kussmaul’s respiration (deep and sighing)
  • Abdominal pain (DKA can be an acute abdomen)
  • Vomiting (this makes dehydration worse)
  • Confusion and coma
  • Low BP (due to acidosis and dehydration)
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3
Q

What investigations should you do if you’re considering DKA?

A

Bedside tests

  • Urine (ketones strongly positive. Note may be raised in starvation)
  • Septic screen (urine and blood cultures)
Bloods
BLOOD GLUCOSE (usually high but might be low in severe academia)
ABG - assess degree of metabolic acidosis (↓pH, ↓HCO3-, often  ↓CO2 due to compensation 

Plasma ketones
FBC - WCC might be up in infection
U+E (look for AKI)

Imaging
-CXR (to check for cause

Special tests
-Determine cause

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4
Q

What is required for diagnosis of DKA?

A

D -Diagnosis of diabetes or BG >11mmol/L
K -Ketones (blood finger prick ketone >3mmol/L or urine ++)
A -Acidosis on ABG (<7.3 or bicarb <15)

note: patients on SGLT2 inhibition’s (flozin) may be euglycemic

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5
Q

What are some common precipitants of DKA?

A

Infection, non-compliance with treatment, Newly diagnosed diabetes, stress

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6
Q

What are the two main principles of DKA management?

A

REHYDRATION AND INSULIN THERAPY

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7
Q

Describe DKA management (5 steps)

A

DKA MANAGMENT
Place 2 wide bore cannulas and start fluid replacement through one (0.9% NaCl)
-NG tube (to prevent aspiration-big cause of death)

1) FLUIDS 0.9% NaCl (1,2,2,4)
-Consider initial bolus 500ml if hypotensive BP <90
-When BP over 90 start 1224 Regime:
1L over 1hr → 1L over 2hr → 1L over 2hr → 1L over 4hr

2) INSULIN THERAPY
- IV infusion of insulin ACTRAPID
- soluble insulin mixed with NaCl (e.g. 50U in 50ml)
- concentration of 1 unit/mL
- at fixed rate of 0.1units/kg/hr

3) POTASSIUM
-Add 40mmol KCL AFTER first bag if potassium <5.5mmol/L ‘pre empt’
(NB: must never give >20mmol K+ over 1 hr, thats why you give in 2nd bag-slower 2 hourly rate)

4) GLUCOSE
- once the blood glucose level falls to 14mmol/l, give 10% dextrose (rate of 1L 8 hourly)
- give alongside fluids and insulin (do not stop insulin)

5) TREAT CAUSE
- due to stress (infection/PE/poor compliance/wrong dose insulin)

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8
Q

Why do we need to replace potassium in DKA management?

When do we replace potassium?

A
  • Insulin will cause potassium to shift into intracellular compartment
  • do not give potassium replacement in first litre or if serum potassium is >5.5mmol/L but consider giving after

*can also cause hypomagnesium

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9
Q

What are the targets for the insulin therapy?

How often should you check these targets?

A

TRAGETS DKA

  • Blood ketones should drop by 0.5 mmol/litre/hour -Blood-glucose concentration should fall by at least 3 mmol/litre/hour (Give 10% dextrose when BG<14mmol/L
  • Monitor blood-ketone and blood-glucose concentrations HOURLY and adjust the insulin infusion rate accordingly.
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10
Q

What should you monitor throughout DKA management?

A

Cap glucose, ketones and urine output, serial VBGs

Consider arterial line for regular ABGs

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11
Q

How long do we give IV insulin therapy for in DKA?

What do we do when it is done?

A

STOPPING DKA THERAPY CRITERIA: (different to start)

  • capillary blood ketones <0.6mmol/L
  • Venous pH >7.3
  • AND nd the patient is able to eat and drink

*ideally give SC fast-acting insulin and a meal, and stop the insulin infusion 1 hour later.

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12
Q

What complications are associated with DKA treatment?

A
  • Hypoglycaemia from over-treatment with insulin
  • Cerebral oedema - occurs mainly in children
  • Serum phosphate can fall (moves IC with K+)
  • Serum Mg can fall
  • Hyperchloraemic acidosis can occur
  • Thromboembolism (give prophylaxis)
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13
Q

Who should be assessed for hypoglycaemia?

A

ALL PATIENTS SHOULD HAVE BLOOD GLUCOSE CHECKED especially…

  • those with collapse or reduced consciousness
  • those with infection

ALL UNCONSCIOUS PATIENTS SHOULD BE ASSUMED TO BE HYPOGLYCAEMIC UNLESS PROVEN OTHERWISE

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14
Q

What glucose levels would suggest hypoglycaemia

What level is classed as SEVERE?

A

Glucose <4mmol/L
ALWAYS TAKE A CAPILLARY SAMPLE and then confirm with the LAB

Lab sample:
<2.2mmol/L is defined as SEVERE ATTACK
< 1.5 = coma

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15
Q

How does hypoglycaemia present?

A

The SYMPATHETIC system becomes overactive leading to:

  • Tachycardia
  • Hypertension
  • Shaking
  • Sweating
  • Pallor
  • Palpitations and anxiety

When it becomes severe (plc <2.6mmol/L) neuro sx: (slurred, blurred, confused)

  • Confusion
  • Slurred speech/blurred vision
  • Drowsiness
  • Odd behaviour
  • Focal neurological deficit
  • Coma/siezures

Others
-Nausea and vomiting

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16
Q

In which patient might symptoms of hypoglycaemia not be so clear?

A
  • Patients w/ well controlled diabetes have hypoglycaemia more frequently and so might not be symptomatic as soon
  • Patients on Beta-blockers. These drugs could mask symptoms (tremor and palpitations)
17
Q

What investigations should be done in a hypoglycaemic patient?

A
  • GLUCOSE
  • U+Es (hypoglycaemia is common in diabetic nephropathy)
  • Take C-peptide and serum insulin levels
  • Always take blood BEFORE giving insulin
18
Q

What are some causes of hypoglycaemia?

drugs, organ failure, others

A

Causes of hypoglycemia
Drugs
-Insulin!!!
-Sulphonylureas common (e.g. Glicazides) (any diabetic drug that’s not metformin
-B blockers (suppress sympathetic NS>less gluconeogenesis)
-Salicyclates

Organ failure

  • Hypopituitarism or adrenal failure (normally hypothalamus>pituitary gland (ACTH)> adrenal gland (cortisol)) therefore increase in glucose
  • Myxoedema (hypothyroidism)
  • Acute liver failure e.g. ALCOHOL

Random causes:

  • Sepsis syndrome
  • Malaria
  • Insulinoma
19
Q

What must we measure before giving glucose?

Management of hypoglycaemia for CONCIOUS patients?

A

-Take blood PRIOR to glucose administration (glucose, insulin, C-peptide)

GET THE HYPO BAG!!!!!!
GCS 15 and safe swallow
- 15–20 g oral glucose
-150-200ml fruit juice
-4 or 5 glucose tablets
-2 tubes gel (good for those that cant swallow)
-check 10-15 mins and repeat max 3 times (report if not > 4 mmol)

IF UNRESPONSIVE to previous step
-150ml 10% IV Glucose OR 75ml 20%
or
-IM glucagon (ineffective if depleted glycogen stores)

Then..

  • After blood glucose is above 4 mmol/litre, give starchy long acting carb (brown bread)
  • ADMIT
  • FOLLOW UP (why did this happen)
20
Q

Management of hypoglycaemia for unconscious patients?

A

Patients who are unconscious, having seizures, or who are very aggressive:

  • ABCDEG assessment
  • Stop IV insulin
  • initially treat with glucagon (unless contraindicated)
  • if glucagon is unsuitable/no response after 10 mins>try IV glucose 150ml 10% or 75ml 20%

Then..

  • When they have recovered and blood glucose is above 4 mmol/litre, give starchy long acting carb (brown bread)
  • ADMIT
  • FOLLOW UP (why did this happen)
21
Q

What response should you see to treatment of hypoglycaemia?

A

-Patient should regain consciousness or become coherent within 10mins although complete cognitive recover may take up to 45min

DO NOT GIVE FURTHER BOLUSES WITHOUT REPEATING BLOOD GLUCOSE

22
Q

What patients would glucagon NOT work for? (a.k.a proffered choice is IV glucose)

A

Glucagon ineffective in patients with depleted liver glycogen stores:

  • prolonged fasting (anorexia)
  • adrenal insufficiency
  • T1DM
  • chronic hypoglycaemia
  • alcohol-induced hypoglycaemia
  • taking a sulfonylurea;

**cant give repeatedly (use up reserves)

23
Q

For alcoholics with hypoglycaemia, what should you give in addition to glucose? why?

A

ALCOHOLICS WITH HYPOGLYCAEMIA

-if alcoholic patient-give IV thiamine with or after IV glucose to prevent Wernikes encephalopathy

24
Q

How do you diagnose HHS (hyperosmotic hyperglycaemia state)?

A

Hyperosmotic hyperglycaemia state

1) HYPOVOLEMIA
- cause low Na (water follows glucose and is lost)
2) HYPERGLYCEMIA (blood glucose>30mmol/L)
3) Normal ketones/no academia (ketones <3mmol/L)

With increased osmolality > 320mosmol/kg
-(glucose + urea + 2xNa)

25
Q

Treatment of HHS ? (4 things to think about)

A

Hyperosmotic hyperglycaemia state

  • Mainstay treatment = fluid resuscitation (don’t replace too fast)
  • Consider IV insulin (half as much as in DKA so 0.05units/kg/hr)
  • Correct electrolyte disturbances
  • Prophylactic LMWH (HIGH RISK OF THROMBUS)
26
Q

Throughout DKA treatment, should the patient’s long acting insulin be continued?

A

Long acting insulin and DKA
-Established subcutaneous therapy with long-acting insulin analogues (insulin detemir or insulin glargine) should be continued during treatment of diabetic ketoacidosis.

27
Q

Other things to include in managment of patient with DKA?

A

DKA

  • Catheter – monitor UO, esp. if olguric
  • Abx – if infection is suspected
  • LMWH (Enoxaparin or Dalteparin) – should be given to all diabetic patients as prophylaxis for VTE
28
Q

Differentials for hypoglycaemia

A

Differentials for hypoglycaemia

  • stroke
  • seizures
  • intoxication
29
Q

How do you calculate osmolarity?

What is increased?

A

With increased osmolality > 320mosmol/kg

-(glucose + urea + 2xNa)

30
Q

Symptoms of HHS ?

Signs of HHS?

A

Symptoms of HHS

  • Insidious onset polyuria + polydipsia
  • Severe DEHYDRATION (av fluid loss 8-10L)
  • Transient weakness, leg cramps, visual imp.
  • Confusion
  • ↓Consciousness – degree related to plasma osmolality (>440 = coma)

Signs

  • ↑HR
  • ↓BP (hypo because sugar leaves and water follows)
  • ↑RR
31
Q

Causes of HHS?

A

HHS

  • Acute infections and other medical conditions
  • Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics)
  • Nonadherence to diabetes treatment
32
Q

If a patient has DKA- what do you do with their normal insulin treatment?

A
  • MAINTAIN NORMAL INSULIN in DKA

- EVEN IF NOT EATING/DRINKING

33
Q

When is a DKA patient suitable for critical care review?

A

Critical care for DKA

  • if bicarb <5 or pH <7.1
  • drowsy GCS <12
  • pregnancy
  • heart failure
  • oliguria/anuria
  • sats<92%
  • persistant BP <90 despite 2L fluids
  • potassium <3.5mmol/L
34
Q

When you are stopping DKA treatment, what insulin should they take?

A

Can you eat/drink?

Yes

  • give short acting insulin with meal
  • few hours later> stop the fixed rate

No

  • switch to variable rate insulin (depending on sugars)
  • and reassess (if now yes> follow yes advice)