829
edits
Changes
no edit summary
===Laboratory Tests===
===Laboratory Tests===
The defining indicator of diabetes mellitus is persistent fasting hyperglycaemia with glycosuria. Single measurements demonstrating hyperglycaemia are not sufficient to make a diagnosis as transient hyperglycaemia frequently occurs after stress, eating or excitement, particularly in cats. Urine glucose is therefore measured to confirm the diagnosis but this test is also not sufficient in isolation because glycosuria may occur independently of hyperglycaemia in a number of other diseases, including Fanconi Syndrome and primary renal glycosuria. If there is any doubt as to the cause of hyperglycaemia, repeated measurements may be made to determine whether it persists over time or blood may be submitted for measurement of fructosamine levels (see below).
The defining indicator of diabetes mellitus is '''persistent fasting hyperglycaemia with glycosuria'''. Single measurements demonstrating hyperglycaemia are not sufficient to make a diagnosis as transient hyperglycaemia frequently occurs after stress, eating or excitement, particularly in cats. Urine glucose is therefore measured to confirm the diagnosis but this test is also not sufficient in isolation because glycosuria may occur independently of hyperglycaemia in a number of other diseases, including Fanconi Syndrome and primary renal glycosuria. If there is any doubt as to the cause of hyperglycaemia, repeated measurements may be made to determine whether it persists over time or blood may be submitted for measurement of fructosamine levels (see below).
A biochemical profile may reveal mildly elevated ALP, ALT and AST due to widespread hepatic hydropic change. Hepatomegaly may also cause slight hepatic cholestasis.
A biochemical profile may reveal mildly elevated ALP, ALT and AST due to widespread hepatic hydropic change and because hepatomegaly may also cause slight hepatic cholestasis. Affected animals may also have elevated serum concentrations of triglyceride and cholesterol due to increased lipolysis.
Animals with DKA are often severely hyperkalaemic and it may be possible to measure serum ketone bodies directly in some laboratories.
Animals with DKA are often severely hyperkalaemic and it may be possible to measure serum ketone bodies directly in some laboratories.
===Other Tests===
===Other Tests===
===Stabilisation===
===Stabilisation===
Animals presenting with DKA are often collapsed, comatose and severely dehydrated. Stabilisation would involve the following aspects of care:
Animals presenting with DKA are often collapsed, comatose and severely dehydrated. Stabilisation would involve the following aspects of care:
*'''Intra-venous fluid therapy''' with a suitable product. Ultimately, the priority of fluid therapy is to hydrate the animal and prevent further damage due to poor tissue perfusion and the exact choice of the fluid product may appear somewhat academic. Some clinicians recommend the use of sodium choride solutions (0.9% saline) as it will not exacerbate the severe hyperkalaemia encountered in animals with DKA. Others prefer to use compound sodium lactate (Hartmann's solution) as it provides some buffering capacity and, because its potassium content is much lower than that of normal plasma, it is unlikely to worsen any hyperkalaemia.
*'''Intra-venous fluid therapy''' with a suitable product. The priorities of fluid therapy are to hydrate the animal and prevent further damage due to poor tissue perfusion and to provide sodium which will have been lost with the osmotic diuresis. With the latter aim in mind, 0.9% sodium chloride solution is recommended. Other clinicians prefer to use compound sodium lactate (Hartmann's solution) as it provides some buffering capacity and, because its potassium content is much lower than that of normal plasma, it is unlikely to worsen any hyperkalaemia. Fluid deficits should be replaced over 24 hours and fluids should not be infused at rates much above twice maintenance to prevent cerebral oedema for occurring due to rapid alterations in electrolyte concentrations. It would also be advisable to measure serum electrolyte concentrations regularly to prevent this effect from occurring.
*'''Insulin''' should be provided to reverse the metabolic changes that have resulted in the crisis. Since the administration of insulin may also have marked consequences for electrolyte status, it is best to administer it gradually as an infusion of soluble insulin. The insulin solution (made up in 0.9% sodium chloride) should be administered through a separate fluid line to that used for conventional fluids and the solution should be run through this line to saturate the bindings sites along the plastic with insulin molecules. Blood glucose concentration should be measured every regularly. Alternatively, intermittent injections of insulin may be used at hourly intervals while also measuring the blood glucose concentration.
It is important that insulin is not administered too quickly because it causes both potassium and phosphate to move intracellularly with glucose. This can result in rebound hypoglycaemia, hypokalaemia, hypophosphataemia and hypomagnesaemia because the total body levels of these cations will probably have been reduced by the enforced osmotic diuresis). Severe hypophosphataemia may result in the development of haemolytic anaemia. Potassium may need to be supplemented from the outset and the rate at which insulin is administered should be reduced if the animal is hypokalaemic on presentation. Other electrolytes should only be supplemented after their serum levels have been measured.
*'''Infections''' occur frequently, either as a cause or effect of DKA. Broad spectrum bactericidal antibiotics are generally recommended in all cases.
*'''Bicarbonate''' therapy is recommended by some clinicians to treat the metabolic acidosis encountered in DKA. Opinions differ as to the use of this drug and many claim that restoration of renal function will result in stabilisation of the acidosis. In any case, bicarbonate should be used with care as it may cause rebound metabolic alkalosis, paradoxical cerebral acidosis and tissue hypoxia due to a left shift of the haemoglobin-oxygen dissociation curve. Paradoxical cerebral acidosis occurs because only carbon dioxide (not bicarbonate) is able to cross the blood brain barrier.
If the animal had previously been receiving insulin therapy, the cause of the instability should be identified and managed.
===Management===
===Management===
The non-ketotic diabetic animal can be managed as an outpatient and a great deal of the monitoring and treatment of the disease will then devolve upon the owner. In dogs, almost all cases of diabetes mellitus are insulin-dependent and insulin is therefore a necessary part of the management regime. Since many cats suffer from non-insulin dependent diabetes mellitus, they can often be managed with a change in diet and oral hypoglycaemic drugs.
==Prognosis==
==Prognosis==
==References==