What Complications You Have to Fear in Case Your Cat’s Diabetes is Not Well Controlled
A complication is a disease, an injury or any side effect resulting from the initial disease and that usually aggravates the initial condition.
In the case of cat diabetes, complications are often more severe than the diabetes itself and always occur if the diabetes is not treated. The primary goal of diabetes treatment is to prevent the onset of complications:
- Diabetic ketoacidosis
- Diabetic neuropathy
- Diabetic nephropathy
- Eye Damage
- Increased infection episodes
- Hepatic lipidosis
Diabetes usually occurs in aging cats that have a limited life expectancy at the time they get their diabetes. Thus, complications of human diabetes that takes many years to develop are not usually seen in cats: nephropathy, vasculopathy, coronary artery disease…
Diabetic ketoacidosis (DKA) is a very severe disease, fatal in many cases. It is an unavoidable outcome of untreated diabetes mellitus.
Diabetic ketoacidocis is caused by an excessive amount of ketones in the blood. Ketones are a result of the metabolic process that uses free fatty acids (FFAs) as source of energy when glucose is missing. Insulin is a potent inhibitor of the formation of ketones from FFAs as well as an essential promoter of glucose utilization within the cells. Cats with DKA have an overt insulin deficiency.
The lack of insulin is not the only reason for the development of a diabetic ketoacidosis. Glucagon hormone, catecholamines and epinephrine are believed to have a strong influence in the production of ketones.
The production of ketones is not a problem in itself. In healthy animals, free fatty acids provide the body the energy it needs when food is lacking, and when glucose levels are low. However, in cats with diabetes, there are both production of ketones and high level of sugar in the blood. The ketones and glucose are both eliminated in the urine whose osmolarity dramatically increases. It results in massive water and electrolytes (sodium, potassium, phosphorus…) losses. Eventually, when glucose excretion becomes less effective, the blood osmolarity starts increasing and water shifts out of the cells, causing dehydration.
As the disease progresses, the classic signs of diabetes (i.e., polydipsia, polyuria, polyphagia, weight loss, lethargy) shift towards more severe symptoms that characterize diabetic ketoacidosis: dehydration, depression, weakness, tachypnea (excessively rapid respiration), vomiting, abdominal pain and sometimes a strong odor of acetone on the breath.
The classic signs of diabetes mellitus may have remained unnoticed until the more severe signs of DKA arose, making the treatment more difficult and more expensive.
The diagnosis is based upon the identification of diabetes (see diabetes diagnosis) combined with the presence of ketones in the urine. Ketones can be detected in the urine with reagent strips: KetoStix® for ketones alone and KetoDiastix® for ketones and glucose. Symptoms must be present for ascertaining the diagnosis.
In most cases, cats with diabetic ketoacidosis will require hospitalization. Therapy is based on insulin injections aimed at normalizing both ketones and glucose in the blood. For the more severely ill cats (i.e., with vomiting, anorexia, nausea…), the vet will set up a fluid therapy. It consists of rehydrating the cat and replacing the minerals rejected in the hyperosmolar urine, mainly sodium, potassium and sometimes phosphorus.
Unfortunately, diabetic ketoacidosis is very difficult to manage and fatal outcomes are not rare, especially when ketoacidosis is associated with a concurrent disease (renal, infections…). That is why it is very important that diabetes mellitus can be diagnosed soon enough to avoid the onset of a diabetic ketoacidosis.
The diabetic neuropathy syndrome corresponds to the nervous disorders associated with diabetes mellitus. It is specific to cats and can hardly be found in diabetic dogs.
It corresponds to the neurologic symptoms of weak legs that affect primarily the rear part of the body: stance on the hocks (plantigrade posture), hind limb weakness, loss of the cat’s ability to jump, muscle atrophy, decreased reflexes. It may eventually progress toward the front limbs.
The neuropathy arises as a result of different mechanisms that start with an excess of glucose:
- Decreased blood circulation in the smaller blood vessels close to the nerves
- Nerves conduction disturbed by some nerves structural proteins glycation (glycation = irreversible binding of proteins and glucose to form glycated proteins)
- Increased levels of Protein Kinase C that slows nerves conduction down
- Nerve cells damaged by sorbitol and free-radical molecules
Diabetes affects conduction velocity especially in the longer nerves, which explains why rear limbs are more exposed.
There is no specific therapy for diabetic neuropathy in cats. Symptoms can be improved by achieving a good blood glucose control.
Renal diseases are very frequent in aging cats, even in the absence of diabetes. Renal disease progresses slowly and is often diagnosed late. That is why, in practice, it is difficult to assess the role of the diabetes in the onset and progression of a chronic kidney disease.
The kidneys have three main roles:
- Filter the blood to remove wastes that passes into the urine
- Regulate electrolytic balance in the body
- Produce and release hormones (renin, calcitriol…)
In healthy animals, blood glucose passes in the kidney’s nephrons (small functional kidneys’ subunits that filter blood – there are 400 000 nephrons in a cat), but is reabsorbed back in blood thanks to the glucose transporters in the renal tubules. This is a normal mechanism. No harm is done to the kidney.
In mild diabetic animals, the glucose, present in larger amounts, is still entirely reabsorbed in blood circulation. But renal tissues contain excessive glucose concentrations and kidney’s glucose transporters are “stressed” because of the additional work load.
In cats with more severe diabetes, blood glucose exceeds the 280 mg/L (16 mmol/L) threshold at which not all glucose can be reabsorbed anymore. Part of the glucose passes into the urine. The transporters work at their maximum capabilities and are progressively destroyed. Nephrons are damaged.
Mild to severe diabetes harm the kidneys. It causes glomerulosclerosis (scarring within the renal glomeruli) and renal blood vessels vasoconstriction. They are the main functional impairments that explain the development of renal disease. In addition, diabetes has the same deleterious effects on the kidneys than on the other organs: cells dehydration, impaired cells metabolism…
Cataract is not common in cats. A cataract is a cloudiness or opacity in the normally transparent crystalline lens of the eye. In the case of diabetes, this cloudiness is caused by the accumulation of sorbitol. Sorbitol increases local osmolarity and induces the liquefaction of lens fibers. Cataract may lead to eventual blindness. Fortunately, cataract can be successfully treated by surgery. The cats will recover vision.
Diabetic retinopathy comes from impairment of blood circulation in the eye small vessels caused by diabetes. It causes vision distortions. Ultimately, the blood vessel may bleed and the retina can detach, leading to blindness.
Hypertension, a common condition in cats is another, more frequent, cause of retinopathy.
High sugar concentration in cells boosts bacteria growth and makes it more difficult for the organism to fight against infections. In addition, hyperglycemia both reduces immunity and increases inflammation.
In cats, these infections affect mainly the skin, the lungs, and the bladder. In diabetic cats, infections have to be diagnosed early to improve the success of the treatment.
(Also known as Feline Fatty Liver Syndrome)
A period of a couple of weeks of anorexia in obese cats caused, for instance, by an underlying disease such as diabetes, or a period of stress, may trigger the mechanisms of hepatic lipidosis. A lack of available glucose leads to the transfer of peripheral fatty acids in the liver (peripheral fatty acids = fatty acids located in tissue and especially in the abdomen). These fatty acids are intended to be transformed by the cat’s liver into triglycerides that can be readily be used by the cells as a source of energy. However, the cat is poor at transforming its fatty acids that eventually accumulate in the liver.
Symptoms may seem close to those of diabetes: depression, lethargy, vomiting. Cats may also hypersalivate. At physical examination, they are usually thin but still maintain a high level of abdominal fat. Jaundice is often present.
Lab exams and ultrasound will assess liver function and the presence of a concurrent disease, such as diabetes, that would explain the onset of the disease.
At first, the vet may implement a fluid therapy aimed at rehydrating and correcting electrolyte imbalances. The mainstay of hepatic lipidosis treatment is an aggressive diet therapy with high protein and high caloric content. The cat should have no other choice than eating. It can be forced (food crafted in small balls and provided to the cats like a pill). Alternatively, it can be fed with a liquid diet and through a feeding tube. In this case, the vet will choose among three possibilities:
- Nasogastric tube: the tube passes in the cat nose and the esophagus
- Esophagostomy: the tube is directly inserted in the esophagus (requires short anesthesia)
- Percutaneous gastrostomy: a tube goes directly in the stomach (requires short anesthesia)
In well-treated cats, survival rates range from 60% to 80%.
As a complement to this information, learn more about concomitant diseases in diabetic cats