CLINICAL EFFECTS OF DIABETIC KETOACIDQSIS
Normally, all glucose filtered by the kidney is reabsorbed. With hyperglycemia, this mechanism is overwhelmed and glucose "spills" into the filtrate, and pulls water with it.
Polyuria (frequent urination) is a common feature of DKA. Because the hyperglycemia causes a rise in serum osmolarity, extreme thirst with Polydipsia (increased thirst) is also common. As the acidosis causes a very strong drive to breathe, patients may feel short of breath.
Nausea and vomiting are also common in DKA (cause unknown), as well as a feeling of general malaise. These latter symptoms are often the reason for seeking medical attention. Another fairly common patient report is blurred vision. While the vision problems in diabetic retinopathy result from years of hyperglycemia, blurry vision in DKA results from the rapid movement of water in and out of the orbit, a consequence of the osmotic shifts that occur with 'fluctuating serum glucose levels (iRoeket, 2005).
Inspection is quite valuable in DKA. Immediately upon talking with the patient, one may detect a pungent fruity smell on the patient's breath, a result of the acetone (a ketone) that the body's organs are producing. In addition, people with DKA have Kussmaul breathing (deep and rapid breaths), reflecting the body's attempt to blow off carbon dioxide to compensate for the metabolic (keto) acidosis.
There is also loss of weight and they developed much much lower and they are always found in type 1 diabetics and they increases the risk of long term complication and they typical developed mainly after many years (10-20).
This is related to altherosclerosis of large arteries which are ischemic disease which damages the small blood vessels including Diabetic retinopathy which affect blood vessels formation in the retina and can lead to blindness. And this is the impact of Diabetes of the nervous system.
Finally, because polyuria may cause severe dehydration (especially if the patient does not drink enough replacement fluids), the patient may be tachycardic and even hypotensive, and may show reduced skin turgor. Patients with severe hyperglycemia may exhibit signs of delirium as the associated shifts in fluid affect the brain (iRocket, 2005).
A finger prick to measure one's plasma glucose level will reveal the presence of extreme hyperglycemia. (This should be confirmed with serum glucose.) An electrolyte panel will reveal an elevated anion gap metabolic acidosis, and the actual blood pH can be determined by an arterial blood gas.
Infection is a common precipitant of DKA; its presence is usually investigated with a complete blood count (to look for elevated white blood cells), urinalysis, and chest radiograph. In older patients, an ECG should be obtained since the medical stress from a myocardial infarction can precipitate DKA.
Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis (Delbridge et a!., 2006).
Acidity results from the dissociation of the H+ ion at physiological pH of metabolic ketone bodies such as acetoacetate, and p-hydroxybutyrate. Acetone has no easily liberated proton, and is thus non-acidic in human biochemical environments. In diabetic patients, ketoacidosis is usually accompanied by insulin deficiency, hyperglycemia, and
dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents glucose absorption and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood.
Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine (Osmotic diuresis), exacerbating the acidosis.