the clinical signs of dehydration are seen . Galloway [ 2 ] suggests that DKA patients are typically 6 – 10 % dehydrated on presentation . For these patients , Vets Now [ 6 ] advises that a 50 % deficit should be replaced within 4 – 6 hours of admission , and the remaining volume during the next 18 – 20 hours .
Hypovolaemia refers to volume depletion within the intravascular compartment , resulting in inadequate tissue perfusion . In cases of ongoing dehydration where cells and interstitial fluid suffer volume loss , fluid is drawn from the intravascular space due to osmosis . Clinical signs that indicate hypovolaemia include tachycardia ( bradycardia or normal heart rate may be observed in feline patients ), pale mucous membranes , prolonged capillary refill time , weak peripheral pulses , a reduction in core temperature and impaired mentation . Blood pressure monitoring may detect hypotension , but it must be remembered that during the compensatory stages of hypovolaemic shock , this may be measured within normal limits . Hypovolaemic patients will require prompt fluid resuscitation to restore blood volume and improve tissue perfusion . This should be initiated using an isotonic crystalloid product such as 0.9 % sodium chloride or lactated Ringer ' s solution ( LRS ).
LRS is suggested as the fluid of choice by many sources for treating metabolic acidosis , due to its buffering ability [ 6 , 7 ] . LRS contains lactate , which is metabolised by the liver into bicarbonate ; this causes an increase in the pH of the blood and therefore decreases its acidity . It is essential to remember that around 10 % of patients could be hyperkalaemic ; in these cases LRS could exacerbate the hyperkalaemia , as it contains potassium [ 8 ] . Conversely , LRS contains levels of electrolytes that may be helpful in patients with deficiencies , which are common in these patients . This demonstrates the need to monitor electrolytes .
Insulin therapy
Reducing blood glucose levels using insulin before replacing intravascular volume could cause a further loss of water from the intravascular space alongside the glucose . Hyperglycaemia causes osmotic diuresis , resulting in large losses of water and electrolytes such as sodium and potassium through urine excretion . Introducing insulin too soon could worsen the hypovolaemic patient and cause a decrease in blood pressure , risking hypoperfusion . It is suggested that insulin therapy is started within 2 – 4 hours of IVFT , and delays of up to 4 hours may allow correction of severely low potassium levels before starting insulin [ 2 ] .
Galloway [ 2 ] indicates that there are two main protocols for the administration of insulin therapy to DKA patients . Patients with systemic signs will require insulin , IVFT and intensive monitoring . Blood glucose , electrolytes and acid – base measurements can change very quickly during the course of stabilisation .
Intramuscular administration
Regular insulin is administered through intramuscular ( IM ) injection , followed by hourly blood glucose measurements . Regular insulin has an onset of action of between 10 and 30 minutes and a duration of action of between 3 and 10 hours , depending on the route of administration . Galloway [ 2 ] suggests that insulin absorption is unpredictable in these patients , due to the likelihood of dehydration . IM administration is also likely to be more time-consuming compared with constant rate infusion ( CRI ), and decreases in blood glucose measurements occur more rapidly with IM than with CRI administration . With either method , serial monitoring of the patient is vital . The administration of insulin aims to prevent further ketogenesis in DKA patients , and initially the focus should not be on lowering blood glucose but on reversing the ketogenesis [ 6 ] .
CRI administration
For administration via CRI , neutral insulin is added to intravenous fluids . Niessen [ 5 ] suggests that insulin will bind to plastic , which can potentially affect the dose the patient receives . Therefore , the infusion line should be run for 30 seconds before attaching it to the patient . Blood glucose is monitored hourly , much like in the IM protocol , and dextrose is administered if glucose readings decrease to < 8 mmol / l .
CRI administration has many advantages over IM administration . Niessen [ 5 ] suggests that better control of serum insulin levels is achieved , along with better predictability and active effect on the patient . CRI administration also has the advantage that if the patient ' s status changes quickly – for example , if blood glucose declines too rapidly – the rate can be altered swiftly to accommodate this . CRIs are less labour-intensive for veterinary staff and much less invasive for the patient .
Panciera [ 9 ] states that the use of smaller doses of insulin administered through CRI is less likely to cause severe hypokalaemia or sudden dips in blood glucose . As repeated doses of insulin are administered to prevent ketogenesis , the addition of 5 % dextrose to the patient ' s fluids is indicated if blood glucose levels decrease to < 8 mmol / l , as a measure to prevent hypoglycaemia during treatment [ 6 ] .
Galloway [ 2 ] advises that the aim should be to decrease the blood glucose levels slowly , by no more than 3 – 4 mmol / l / hour . There is a risk that allowing blood glucose to decrease too rapidly will cause a sudden decrease in osmolality , which has the potential to cause life-threatening cerebral oedema [ 9 ] .
With either protocol , once the patient is bright and eating voluntarily , with ketones decreasing and blood glucose < 15 mmol / l , they can be transferred to longeracting insulin [ 3 ] .
50 Veterinary Nursing Journal