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Decompensated Cardiac Insufficiency. Thoracic Radiology. Thromboembolism in Cats. Use of Digitalis in the Dog. Critical Care. Acute Adrenocortical Insufficiency.
Acute Renal Failure. Emergency: Respiratory Distress. Cervical and Thoracolumbar Disc Disease. Corticosteroids in Shock. Fluid Therapy in the Critical Patient. Management: Head Trauma. Shock Resuscitation. Acute Pancreatitis. Major Body System Evaluation. Dentistry: Exotic Animals. Dentistry: Emergency.
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In addition, miniature poodles and dachshunds are predisposed to diabetes with ketoacidosis. Although the ketoacidosis is ultimately brought on by the dog's insulin dependency due to diabetes mellitus, underlying factors include stress, surgery, and infections of the skin, respiratory, and urinary tract systems. Concurrent diseases such as heart failure, kidney failure, asthma, cancer may also lead to this type of condition.
He or she will then perform a complete physical examination, as well as a biochemistry profile and complete blood count CBC. The most consistent finding in patients with diabetes is higher than normal levels of glucose in the blood. If infection is present, white blood cell count will also high. Other findings may include: high liver enzymes, high blood cholesterol levels, accumulation in the blood of nitrogenous waste products urea that are usually excreted in the urine azotemia , low sodium levels in the blood hyponatremia , low levels of potassium in the blood hypokalemia , and low levels of phosphorous in the blood hypophosphatemia.
For example, urinalysis may reveal abnormally high levels of glucose in urine glucosuria and ketone bodies ketonuria. If your pet is alert and well hydrated, hospitalization may not be required. Otherwise, it is vital that the dog's bodily fluids and electrolytes are restored immediately, especially if it is lethargic or vomiting.
Diabetic ketoacidosis, a complication of diabetes mellitus, is an important differential for acute collapse in dogs and cats. In this article, Poppy Gant BVSc MRCVS, final-year emergency and critical care resident at the Royal Veterinary College, aims to review the pathophysiology, diagnostics and main aspects of treatment, with particular reference to what can initially be achieved in general practice.
As a result, glucose cannot be transported into cells for production of adenosine triphosphate ATP , leading to hyperglycaemia and glucosuria. Ketone body production itself is a normal attempt of the body to provide an alternative energy source for cells in the absence of glucose. Figure 1 shows how fat stores are mobilised and fatty acids then oxidised by the liver to form ketones which can be transported to extra hepatic tissues.
Increased gluconeogenesis in the liver also depletes intermediates of the citric acid cycle and diverts acetyl-CoA to ketone body production. Bicarbonate is initially used to buffer these hydrogen ions but when ketones are produced beyond the capacity of extra hepatic tissues to utilise them, an acidaemia results. This acidaemia can contribute to the non-specific signs associated with diabetic ketoacidosis DKA , including lethargy, anorexia, vomiting, dehydration and eventual collapse.
Both glucose and ketones are also osmotically active, leading to polyuria and polydipsia and subsequent dehydration, with risk of hypovolaemia. This process most commonly develops in undiagnosed or newly diagnosed diabetics that are not receiving adequate insulin. However, all diabetic patients are at risk, especially if they have or develop comorbidities. Figure 2 gives some of the most common concurrent diseases seen in DKA patients. Triage of the DKA patient Initial assessment of the collapsed patient should focus on the major body systems to determine whether emergency treatment eg.
Cardiovascular assessment Assessment of extravascular dehydration and intravascular hypovolaemia volume depletion:. Once an initial triage has been performed and the patient deemed to be stable, a complete physical examination and further diagnostic tests can be performed.
These should take into consideration the most common comorbidities seen in veterinary patients Figure 2. Diagnosis The history and initial physical examination of patients with DKA is likely to be fairly non-specific. The only clinical finding seen more often in cats with DKA compared to non-acidaemia diabetic cats is hypothermia. Fortunately, there are several diagnostic options available to confirm or at least increase the suspicion of DKA. Useful point of care testing for diagnosis of DKA Blood gas analysis with or without electrolyte analysis Figure 3, eg.
Identify an increased anion gap see below. Point of care glucose analysis eg. Not all point of care glucometers are veterinary specific. This can result in lower blood glucose readings owing to species differences in the distribution of glucose in the plasma and red blood cells. Point of care ketone analysis eg. Only practices with the ability to run blood gas analysis will be able to truly diagnose DKA.
Where this is not available, some studies have tried to investigate the degree of ketonaemia or ketonuria that is consistently associated with acidaemia. In practices without a ketometer, although the urine nitroprusside reagent strips only test for acetoacetate, several studies have shown that using heparinised plasma on urine semi-quantitative test strips can improve the sensitivity of ketone detection.
However, it requires bicarbonate which may not be routinely measured. Figure 7 shows how to calculate the anion gap. The anion gap can also be increased in other disease processes. However, a normal or only mildly increased lactate and creatinine and low risk of toxin exposure makes a diagnosis of diabetic ketosis much more likely. Figure 7: Calculation of the anion gap and representation of a high anion gap.
Extended minimum database Given the high prevalence of concurrent disease, an extended minimum database for all patients should ideally include complete blood count, serum biochemistry with electrolytes ideally with pancreatic lipase serology , urinalysis and culture and thoracic and abdominal imaging.
Additional points Dogs with suspected DKA should not undergo testing for hyperadrenocorticism at the time of emergency presentation, as this is highly likely to result in a false positive result due to being systemically unwell.
Cats, in particular, are at risk of hepatic lipidosis and can often be affected by cholangiohepatitis. If liver enzymes are elevated then ultrasonographic evaluation and possibly aspiration of the liver and biliary system may be indicated. Urinalysis Urine-specific gravity is usually low secondary to osmotic diuresis but concurrent renal disease is also possible, particularly in cats. Cytology: Diabetic patients often have problems mobilising white blood cells to sites of infection and therefore, may have an inactive urine sediment, even with infections.
A urine culture is therefore always recommended. Empirical antimicrobials may be started where there is a concern for a urinary tract infection. Treatment of Diabetic Ketoacidosis DKA in Dogs and Cats Goal of treatment of DKA in dogs and cats is rehydration, drop glucose, normalizing pH, eliminate ketones, manage electrolyte imbalances and address concurrent diseases or underlying disease. Fluid Administration Tips Administration of 0.
Fluids are given for approximately 6 hours before any insulin therapy is attempted because fluids alone will drop glucose concentrations. KPhos can be given as a CRI at 0. Alternatively, can use the other potassium supplementation scale how much mEq to add to 1 L by using half KCl and half KPhos. IM: initial dose of 0.
Then base insulin dose on how much glucose is dropping per hour. Different clinicians will likely have slightly different CRI protocols. Bicarbonate Therapy Bicarbonate therapy is described but is only reserved for severely acidemic patients generally, pH less than 7 after 1 hour of fluid therapy per American Diabetes Association.
Serum Beta-hydroxybutyrate measurement is better than measuring for urine ketones can be ketonemic without being ketonuric.
Differentials for ketonemia include acute pancreatitis, starvation, low-carb diet, persistent hypoglycemia, persistent fever, and pregnancy. Differentials for primary metabolic acidosis include acute kidney injury, lactic acidosis, toxins, severe tissue destruction, renal tubular acidosis, and hyperchloremia. Almost all dogs and only young cats get cataracts associated with diabetes mellitus because glucose enters the lens of the eye and is metabolized by the polyol pathway to sorbitol and fructose, which then promote water to enter the lens causing disruption of lens fibers.
The enzyme responsible is called aldose reductase dogs have high activity of aldose reductase their entire lives where cats tend to lose activity of this enzyme as they age. Hormones that further antagonize insulin include cortisol, glucagon, epinephrine, growth hormone, and progesterone.
Glucagon most implicated…with severe cellular starvation for glucose, glycogenolysis and gluconeogenesis are ramped up which worsens hyperglycemia. Vomiting often occurs due to activation of chemoreceptor trigger zone by ketones.
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