Diabetic Ketoacidosis****

Question 1

What is it?

Answer 1

An acute, severe manifestation of insulin deficiency, usually due to type 1 diabetes

Question 2

Pathophysiology:

How does a lack of insulin effect:

• glucose
• ketones
• pH
• HCO3-

Why do they get dehydration?

Answer 2

Hyperglycaemia

High ketones

Low pH - acidosis - hence ketoacidosis

Due to polyuria and vomiting leading to renal impairment

Question 3

Causes:

The main way they present?

Other causes?

Answer 3

Those unknown to be diabetic

Poor diabetic control
Illness - infection, surgery, MI
Insulin pump failure

Question 4

Severity classification:

Under what pH is classed as severe?

Under what pH is classed as mild?

Answer 4

<7.1

<7.3

Question 5

Symptoms:

Symptoms:

Why do they get N&V?

Why do they get abdo pain?

Why do they polydipsia and polyuria?

Answer 5

As ketones accumulate in the blood, more ketones will be passed in the urine, taking sodium and potassium salts out with them. Over time, levels of sodium and potassium salts in the body become depleted, which can cause nausea and vomiting.

Ketones are acidic chemicals that are toxic at high concentrations. In diabetic ketoacidosis, ketones build up in the blood, seriously altering the normal chemistry of the blood and interfering with the function of multiple organs. They make the blood acidic, which causes vomiting and abdominal pain.

With hyperglycemia, this mechanism is overwhelmed and glucose “spills” into the filtrate, and pulls water with it. For these reasons, polyuria is a common feature of DKA. Because the hyperglycemia causes a rise in serum osmolarity, extreme thirst with polydipsia is also common.

Question 6

Symptoms:

Why do they get lethargy?

Why may they have reduced level a consciousness?

Answer 6

They are unable to process the carbs in their food which is needed for energy.

Due to severe dehydration

Question 7

Signs:

Obs signs of dehydration? - 2

What type of breathing may they have? Why does it happen?

What may you notice on their breath?

Answer 7

Hypotension
Tachycardia

Kussmaul breathing - lookup
Very deep breathing at a normal or increased rate.

Compensates for acidosis

Sweet-smelling breath - smells of acetone

Question 8

Diagnosis:

3 parts of the criteria needed to make a diagnosis?

Answer 8

Hyperglycaemia
Ketosis/ketonuria
Acidosis

To remember triad, just think about the name - diabetes (glucose), keto (ketosis) and acidosis (acidosis)

Question 9

Diagnosis:

Fill the gaps:

(1) Capillary glucose >__ mmol/L or ______
(2) Capillary/serum ketones >__ or urine dip ____
(3) Venous pH

Answer 9

(1) Capillary glucose >11 mmol/L or known diabetic
(2) Capillary/serum ketones >3 or urine dip 2+
(3) Venous pH<7.3 or HCO3-<15

Question 10

Investigations:

Bloods:
- Why are U+E’s done?

What happens to the anion gap on ABG?

Why do you not need an ABG until hypoxic and reduced GCS?

What blood cell is raised even in the absence of infection?

What protein in the blood tends to be raised?

Answer 10

Electrolytes are usually altered - usually lost in the urine

Raised as added acid

A venous blood gas is less painful
There is no need to pO2 and pCO2 as this is a metabolic issue.

WBC

Amylase

Question 11

Management:

Step 1 - Fluids:

• What type of fluid is used?
• Under what systolic is this used?

Step 2 - Insulin IV:

• How many units are given per kg per hour?
• What do you want the insulin to do? - 2
• What is done if insulin is not enough?
• IV insulin can cause hypokalaemia. Why does this happen? What sort of monitoring needs to be done?

Answer 11

Normal saline through a large-bore cannula

<90 mmHg

=====
0.1 units/kg/hr

Reduce ketones
Raise bicarbonate

Increase dose by 1 unit/hr

Insulin causes potassium to move into cells which increase the risk of developing hypokalaemia.

Cardiac monitoring for the first phase of treatment

FL;UIDS BEFORE INSUILIN AS THEY ARE SEVEREL;Y DEHYDATED

Question 12

Management:

Step 3 - Fluids are continued - if/when >90 mmHg:

• How are the fluids prescribed?
• Why is rehydration done slowly?

Potassium replacement:

- Why does potassium need to be monitored closely and replaced?
- After how many bags of fluid is K added?

Answer 12

1L in 1 hr then
1L in 2 hr then
1L in 4 hr then
1L in 8 hr

Potassium falls as Rx starts as they begin to enter cells

Insulin causes potassium to move into cells which increase the risk of developing hypokalaemia. It is added to the 2nd one

Question 13

Management - Monitoring:

What continuous monitoring is needed?

How often are capillary blood glucose and ketones checked?

How often is a VBG done?

Answer 13

O2 and ECG

Every hour

2hr, 4hrs, 8 hrs, 12 hrs, and 24 hrs

Question 14

Management:

Hypoglycaemia needs to be avoided. What is started once glucose <14 mmol/L?

Resolution:

• Once eating and drinking, what type of insulin should the patient be switched to?
• How many units of insulin should be given per kg per day?
• Why is LMWH considered or administered?

Answer 14

10% glucose at 125ml/hr to run alongside saline

SC insulin overlapping 30 mins with IV

0.5 units/kg/hr

Risk of MI, stroke and PE to hypovolaemia

Question 15

Pitfalls in DKA:

There is often no fever in infection. What investigations should be done for infection?

Why does creatinine not reflect true renal function if measured?

Why do they get hyponatraemia?

Answer 15

MSU
Blood cultures
CXR
Broad-spec antibiotics

Serum assays for creatinine cross-react with ketone bodies, so plasma creatinine may not reflect true renal function.

Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia.

Question 16

Pitfalls in DKA:

Ketonuria doesn’t always mean ketosis. What could cause ketones in the urine?

Why should you not end insulin infusion once blood glucose is back to normal?

Acidosis without hyperglycaemia could be from an overdose or ________ acidosis (in elderly diabetics). Fill the blank

Answer 16

Alcohol

You get lack of clearance of ketones and can recurrent ketoacidosis

Lactic acidosis

Question 17

Complications from DKA itself:

Why are they at risk of VTE and PE?

Answer 17

Because patients with both DKA and hyperosmolar coma share the features of significant dehydration and some degree of hyperosmolarity, the finding of a significantly higher risk of developing VTE

Question 18

Complications - Iatrogenic:

Why are patients at risk of cerebral oedema which is increased with fast rehydration?

What are some S+S of cerebral oedema?

Why is hypertonic saline used to treat it?

MANNITOL can also be used!!!!1

Answer 18

The osmolar gradient caused by the high blood glucose results in water shift from the intracellular fluid (ICF) to the extracellular fluid (ECF) space and contraction of cell volume.

Headache 
Altered mental status 
Pupillary/oculomotor abnormalities 
An unexpected rise in BP and low HR 
Apnoea - compression of resp centres

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Hypertonic saline and mannitol are effective because they do not cross the blood-brain barrier (much), and thereby draw cerebrospinal fluid out of the cranium and fluid out of the injured brain, reducing pressure and further injury.

Hypertonic saline is used in the hospital to reduce brain swelling by increasing the sodium levels in the bloodstream. This high sodium level will “pull fluid out” of the swollen brain.