Diabetic ketoacidosis (DKA)

Ketoacidosis results from a lack of insulin. 

Causes:
1• stopping insulin or reducing the dose either in error or
deliberately
2• resistance to insulin during infections or other intercurrent
illness
3• the unrecognised onset of Type 1 diabetes.

The clinical onset of ketoacidosis occurs over hours or days.
Symptoms of uncontrolled diabetes are always present.

Vomiting in Type 1 diabetic patients is always serious. Patients
usually consult their doctors during the preceding days, but the
presence of uncontrolled diabetes is frequently overlooked.
Diabetic control should always be assessed if a diabetic patient
becomes unwell for any reason.

Many cases of ketoacidosiscould be prevented.
 
Preventing ketoacidosis:
 sick day rulesDuring any illness or infection the blood glucose concentration
tends to increase and diabetic control deteriorates. Most
patients then need a larger dose of insulin than usual, and
some who normally take tablets may need insulin just during
the illness.  

The increased need for insulin occurs even when
the appetite declines or vomiting begins.
Every insulin treated patient should understand that insulin
should never be stopped. Stopping or even reducing insulin
during the course of an illness often leads to diabetic
ketoacidosis.

When a diabetic person is ill the normal insulin dose
should be continued, carbohydrate taken in some palatable
fluid form, and the blood tested regularly—four times a day if
necessary.

If blood glucose readings greater than 15 mmol/l are
obtained the dose of insulin should be increased. Additional
doses of insulin (about 8 units) may also be given at noon or
bedtime when control is very poor. It is preferable to make
these adjustments with short acting (soluble) insulin if this is
available. If vomiting continues without remission for more
than a few hours, admission to hospital for treatment with
intravenous fluids and insulin is advisable to prevent
ketoacidosis.

Assessment of blood or urine ketones during illness is
helpful. Using the new blood ketone meters, readings of
1·0-3·0 mmol/l taken in conjunction with the blood glucose
reading usually indicate the need for additional insulin;
readings should be repeated within two to four hours. If they
persist or increase above 3·0 mmol/l, specialist advice is
required from the hospital clinic staff. Ketonuria can be
detected using Ketostix, which are readily available.
 
Recognising ketoacidosis
Dehydration is the most obvious clinical feature of patients with
ketoacidosis. They are also drowsy, but rarely unconscious—
“diabetic coma” is an inappropriate description; they are often
overbreathing, but not usually breathless; their breath smells of
acetone (though many people cannot smell this); and many
also have the gastric splash. In more severe cases patients are


hypothermic (even in the presence of infection) and
hypotensive. Hyperosmolar non-ketotic (HONK) patients are
usually grossly dehydrated but without overbreathing or the
smell of acetone. Inexperienced clinicians often have difficulty
in recognising patients with this condition, especially when they
seem deceptively well.

Diagnosis:-
The diagnosis of ketoacidosis is confirmed by laboratory tests.
• Blood glucose concentrations may range from slightly
increased to extreme hyperglycaemia. The blood glucose
concentration itself does not usually indicate the severity of
the illness, although most patients are seriously unwell when
it is greater than 30 mmol/l.
• Blood acid-base status pH ranges from 6·9 to normal. The
bicarbonate level is depressed.
• Plasma ketones are easily detectable with a ketone meter and
exceed 3·0 mmol/l.
• Urine test shows heavy glycosuria and ketonuria.
• Electrolytes: the serum potassium concentration is either
normal or raised, and very rarely low. This measurement is
vital, and life-saving treatment is needed to maintain
potassium values in the normal range. The sodium
concentration is normal or reduced, and urea and creatinine
concentrations are often raised through dehydration.

• Blood count:
if a blood count is performed the white cell
count is often spuriously raised to 15-20
109/l even in the
absence of infection.
Serum amylase is sometimes moderately elevated in
patients with diabetic ketoacidosis: it is of salivary origin and
need not be indicative of pancreatitis
 
Treatment
Patients should be treated in an area where there they can be
observed regularly, preferably by staff familiar with managing
this condition, in a high dependency area, or if very ill in
intensive care.
• Insert a nasogastric tube if consciousness is impaired. Do not
allow any fluids by mouth; if patients are thirsty they may
suck ice.
• Give intravenous fluids. The regimen needs to be modified
according to age, weight, and the presence of cardiac disease.
In seriously ill patients and all those with cardiac disease a
catheter for measuring central venous pressure is essential.
A suitable regimen for most patients is shown in the box;
0·9% saline is used.
• The fluid should be changed to 10% dextrose once the
blood glucose concentration has fallen to less than
10 mmol/l. The rate of infusion is determined by individual
need but at this stage should probably be about one litre
every eight hours.
• Start intravenous soluble insulin immediately. If there is any
delay in obtaining intravenous access. Soluble insulin
(20 units) can be given immediately intramuscularly.
Insulin treatment
Intravenous insulin:
soluble insulin is diluted in 0·9% saline in
a syringe, at the concentration of 1 unit/ml. It is given by
infusion pump at 6 units/h (0·1 units/kg/h for children) until
the blood glucose concentration is less than 10 mmol/l. Blood
glucose should fall at a rate of about 5·0 mmol/l/h, and plasma
ketones should fall at the same time. When the blood glucose is
less than 10 mmol/l, the dose may be reduced to 3 units/h.

Higher infusion rates are rarely needed; when they are needed
in insulin resistant patients the rate should be doubled or
quadrupled, etc. If the patient is not responding, medical staff
should check the equipment for pump failure, blockage or
leakage. The insulin infusion is continued until the patient is
well enough to eat. The changeover to subcutaneous insulin
should be made before breakfast.

Preprandial subcutaneous
soluble insulin is then given and intravenous insulin
discontinued after the meal. Intravenous insulin should
not be stopped before subcutaneous insulin has been given

Intramuscular insulin
is used only when an infusion pump
is not available. Soluble insulin 20 units is given as a loading
dose, than 6 units every hour until blood glucose is less than
10 mmol/l, then continued at two hourly intervals. As with
intravenous insulin, higher doses are rarely needed.
Potassium and sodium bicarbonate

Potassium chloride administration should usually start at about
the second hour, preferably not before the serum potassium
concentration is known. It should be withheld in exceptional
cases of oliguria or anuria, or if the serum potassium value
remains above 5·0 mmol/l. After the second hour, or earlier if
the initial serum potassium value is normal or less than
4·0 mmol/l, 20mmol potassium chloride should be added to
each litre of saline. If the serum potassium value falls below
3·5 mmol/l, 40mmol should be used in each litre. The exact
amount should be determined by serial serum potassium
measurements—every two hours at first, then every four hours—
and serum potassium maintained between 4·0 and 5·0 mmol/l.

An electrocardiographic monitor should be set up; however,
there is no substitute for serial potassium measurements.
Sodium bicarbonate is not normally beneficial and is not
given unless the blood pH value is less than 7·0 or the patient is
shocked. If it is needed, aliquots of sodium bicarbonate (500 ml
of 1·26%) with added potassium chloride (15 mmol) should be
given.
This can be repeated if there is no response within one
hour and if the patient’s condition remains serious.
Note: Never use sodium bicarbonate 8·4% concentration.
 
Treatment of the underlying condition
 Underlying disease should be sought, especially respiratory or
urinary infections, which may not be obvious at the onset.

Blood culture, culture of the midstream specimen of urine, and
chest radiography are performed. There is no need to give
antibiotics routinely. Abdominal pain may occur, especially in
young patients with severe ketoacidosis. It is vital to discover
whether there is indeed an intra-abdominal cause needing
attention if the pain does not resolve rapidly.

HONK patients
Blood glucose in these patients can be extremely high without
ketosis or acidosis.

Management is the same as that for
ketoacidosis, except that 0·45% saline is given if the serum
sodium value is greater than 150 mmol/l, and a lower rate of
insulin infusion (3 units/h) is often sufficient. In shocked and
dehydrated patients prophylactic, low dose, subcutaneous
heparin is considered.
Lactic acidosis

These patients are profoundly ill and the cause of the acidosis
must be sought and rigorously treated. They are often very
insulin resistant due to serious intercurrent illness, and need
large amounts of sodium bicarbonate.

Absence of a raisedplasma ketone level excludes ketoacidosis as the cause of the
metabolic acidosis. Metformin induced lactic acidosis should be borne in mind