Diabetic ketoacidosis is an acute complication of Diabetes Mellitus. There are two types of Diabetes Mellitus. Type 1 which is an Insulin dependent diabetes mellitus. Type 2 which is a Non- Insulin Dependent Diabetes Mellitus. In the books I read, Diabetes Ketoasidosis or DKA mostly happens in Type 1 Diabetes Mellitus.
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. DKA may be the first symptom of previously undiagnosed diabetes, but it may also occur in known diabetics due to a variety of causes, such as intercurrent illness or poor compliance with insulin therapy. Vomiting, dehydration, deep gasping breathing, confusion and occasionally coma are typical symptoms.
Diabetic ketoacidosis develops when you have too little insulin in your body. Without enough insulin, sugar (glucose) can’t enter your cells for energy. Your blood sugar level rises, and your body begins to break down fat for energy. This produces toxic acids known as ketones. Left untreated, diabetic ketoacidosis may cause you to lose consciousness. Eventually, untreated diabetic ketoacidosis can be fatal.
Symptoms and signs of DKA include those of hyperglycemia with the addition of nausea, vomiting, and—particularly in children—abdominal pain. Lethargy and somnolence are symptoms of more severe decompensation. Patients may be hypotensive and tachycardic from dehydration and acidosis; they may breathe rapidly and deeply to compensate for acidemia (Kussmaul’s respirations). They may also have fruity breath due to exhaled acetone. Fever is not a sign of DKA itself and, if present, signifies underlying infection. In the absence of timely treatment, DKA progresses to coma and death.
DKA management :
Resuscitation
* Always begin with resuscitation of the patient.
* So begin by assessing airway, breathing and circulation.
* Remember the airway may be compromised if the patient is drowsy or obtunded.
Initial monitoring and management
* Put patient on SaO2 monitor, continuous ECG monitor and BP/HR monitor.
* Obtain large-bore peripheral i-v access or insert central venous catheter.
* Urinary catheterisation is usually carried out to monitor urine output and will also allow urinalysis.
There are 4 key aspects in the subsequent management of DKA:
1. Correct dehydration – this will improve the acidosis (along with insulin and thus bicarbonate not required)
2. Insulin – this will reduce the glucose level and improve the acidosis (aim for a steady fall in glucose of approximately 4 mmol/L/hr)
3. Potassium supplementation
4. Treatment of any precipitating illness
Correct dehydration
* Assess severity of dehydration e.g. capillary refill time, dry mucous membranes, tachycardia, hypotension, oliguria.
* If severely dehydrated or shocked – administer a colloid infusion.
* Otherwise begin with N. saline 0.9% (with or with out potassium – see below).
* One example of a regimen is as follows – 1 litre of normal saline over the first 30 mins, followed by 1litre per hour over the next two hours and then 1litre over 2 hours.
* At this point the patient and their blood results and observations should be reviewed and then further intravenous fluids prescribed.
* Repeat U & E’s should also be sent at this time.
Replace potassium
* There is always depletion in total body potassium, however the initial serum K+ values may not be low, instead they can be normal to high reflecting the transcellular shift caused by the ketoacidosis.
* This masks the deficit which is uncovered once insulin has commenced.
* Potassium should be checked immediately – the arterial blood gas will provide a quick result.
* Potassium replacement therapy should be started immediately if the patient is hypokalaemic – but only if potassium level is<5.0-5.5 mmol/L and the patient is passing urine.
* Very rarely potassium replacement therapy may need to be given before insulin if the patient is profoundly hypokalaemic to begin with e.g. K+ <3.5 mmol/L.
* If the patient is hyperkalaemic do not give potassium therapy – recheck after 30 minutes.
Replace insulin
* Treatment with insulin will not only return the blood sugar level to normal but also prevent further lipolysis and ketogenesis.
* Start intravenous insulin sliding scale - see local guidelines for regimen.
* If there is any delay in starting IV insulin and K+ is >3.3 mmol/L then a bolus of 10U may be given by SC or IM routes (bear in mind that absorption may be variable due to poor perfusion).
* After an initial, often sizeable, drop in blood glucose from rehydration the aim is to reduce the blood glucose by <= 4 mmol/L/hr.
* When the blood glucose falls to <12 mmol/L change fluids to 5% dextrose.
* If the blood glucose rises reduce the amount of glucose infused and if necessary increase the insulin infusion.
Treat any precipitating illness
* Measures to actively detect a precipitating cause should be pursued.
* One clue to the possibility of an unrecognised underlying cause is if the pH and anion gap fail to improve despite the aforementioned measures. In this case review insulin therapy and consider other further investigations e.g. serial ECGs in silent cardiac ischaemia.
* If an underlying cause is identified then it should also be treated as appropriate.
* If there are reasonable clinical grounds to suspect infection as the precipitant then appropriate antibiotic therapy should be given (usually broad-spectrum blind treatment); routine antibiotics are not advised.
Other measures to consider:
* Low molecular weight heparin and TED® stockings are given prophylactically (but see local guidelines). It should be considered for those who are obtunded or comatose, or have other risk factors for venous thromboembolism, although as yet there are no concrete trial data to support this approach.
* In unconscious, drowsy or vomiting patients consider passing a nasogastric tube.
Monitoring
* Patients should ideally be managed in a HDU type setting or even ITU if they are severely unwell.
* Electrolytes and venous bicarbonate must be checked at least every 1-2 hours for the first 2–4 hours and then 2-4 hourly thereafter (frequency will depend upon the individual clinical scenario).
* Monitor hourly fluid balance.
* Monitor capillary blood glucose every hour with an aim to reduce plasma glucose by 3–5 mmol/hr.
* Plasma glucose should also be checked regularly as capillary blood glucose may be inaccurate in DKA.
* If capillary/plasma glucose has not fallen by at least 4 mmol/L in the first hour, then check adequacy of rehydration and patency of infusion lines; if these are not at fault then double the dose of insulin for the next hour.
* When plasma glucose is <12 mmol/L then replace normal saline with 5% dextrose to prevent over-rapid correction of blood glucose and hypoglycaemia.
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