Diabetic acidosis

Because alcohol intoxication may be simulated by many pathologic conditions, including diabetic acidosis, the postconvulsive depression of epilepsy, uremia, head injuries, and poisonings by any other central nervous depressant and some stimulants (280), a diagnosis of acute alcoholism should not be made casually chemical testing of blood, urine, or expired air is always desirable. 

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. 

If the body is unable to neutralize acids due to a disease or other problem, a condition called acidosis can result. Acidosis occurs when the bloods pH goes below its normal level of 7.35. One disease that can cause acidosis is diabetes. Diabetic acidosis is caused by a lack of insulin. This condition most often occurs when a Type I diabetic misses his or her scheduled dose of insulin. 

Because ketones are passed out of the body in the urine, a doctor can detect the onset of diabetic acidosis by doing a urine test. If ketones are present in the urine, it is a signal to the doctor that the patients diabetes is out of control. Without treatment, the patient could get very sick. On rare occasions, even Type I or Type II diabetics who take their medication can develop acidosis, usually as a result of some other serious health issue such as an infection or a heart attack. 

Diabetic acidosis can develop in a matter of hours. Therefore, under certain circumstances, doctors may ask a diabetic patient to test for ketones at home using special test strips that can detect ketones in urine. For example, doctors recommend that diabetic patients test their urine every 4 to 6 hours if their blood sugar levels are very high. Patients should also test for ketones if they are sick with a cold or the flu, or if they experience any of the symptoms of acidosis. These symptoms include a very dry mouth, frequent urination, shortness of breath, and fruity smelling breath. Diabetic acidosis can be life-threatening, leading to a diabetic coma or death. It needs immediate medical care. Diabetic acidosis is also called ketoacidosis. 

Neurons are very sensitive to changes in the pH of the interstitial fluid surrounding them. Normally, the pH of arterial blood is 7.4. Under conditions of alkalosis, in which pH increases, the excitability of neurons also increases, rendering them more likely to generate action potentials. This inappropriate stimulation of the nervous system may lead to seizures, particularly in epileptics predisposed to them. Under conditions of acidosis, in which pH decreases, the excitability of neurons is depressed, rendering them less likely to generate action potentials. This lack of nervous system stimulation may lead to a comatose state. Severe diabetic acidosis or acidosis associated with end-stage renal failure will often lead to coma. 

Salicylate or aspirin overdose is characterized by tinnitus, confusion, rapid pulse rate, and increased respiration. The decreased partial pressure of arterial C02 (Pco2) plus increased fixed acids first cause alkalosis, which is followed by metabolic acidosis, dehydration, and loss of fixed bases. The picture may resemble diabetic acidosis, but the history of salicylate ingestion and blood salicylate levels above. 540 mg/100 mL clinch the diagnosis. 

Faich GA, Fishbein HA, Ellis SE. The epidemiology of diabetic acidosis a population based study. Am ] Epidemiol 1983 117 551. 

Oral Treatment of hypokalemia in the following conditions With or without metabolic alkalosis digitalis intoxication familial periodic paralysis diabetic acidosis diarrhea and vomiting surgical conditions accompanied by nitrogen loss, vomiting, suction drainage, diarrhea, and increased urinary excretion of potassium certain cases of uremia hyperadrenalism starvation and debilitation corticosteroid or diuretic therapy. 

Takaike H, Uchigata Y, Iwasaki N, Iwamoto Y. Transient elevation of liver transaminase after starting insulin therapy for diabetic acidosis or ketoacidosis in newly diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract 2004 64 27-32. 

Values less than approximately 10 mmo /L or greater than about 20 mmol/L may indicate error. Elevated values may be found in patients with renal failure, diabetic acidosis, cardiac failure, anoxia, and other conditions (see Chapter 46). Low values occur in hypoproteinemia and with intravenous hydration. The capabilities of AG control procedures have been studied by Cembrowski and co-workers,who recommend that the average AG of groups of eight or more patients be used to provide a more sensitive statistical control. 

The total protein concentration of serum obtained from a healthy ambulatory adult is 6.3 to 8.3 g/dL and 6.0 to 7.8 g/dL from an adult at rest. The two general causes of alterations of serum total protein are a change in the volume of plasma water and a change in the concentration of one or more of the specific proteins in the plasma. Decrease in the volume of plasma water (hemoconcentration) is reflected as relative hyperproteinemia concentrations of all the individual plasma proteins are increased. Hyperproteinemia is noted in dehydration caused by inadequate water intake or excessive water loss as in severe vomiting, diarrhea, Addison s disease, or diabetic acidosis. Hemodilution (increase in plasma water volume) is reflected as relative hypoproteinemia concentrations of aU the individual plasma proteins are decreased. Hemodilution occurs with water intoxication or salt retention syndromes, during massive intravenous infusions, and physiologically when a recumbent position is assumed. A recumbent position decreases total protein concentration by 0.3 to 0.5 g/dL and many individual proteins including albumin by up to 10%. 

Production of organic acids that exceeds the rate of elimination (e.g., the production of acetoacetic acid and p-hydroxybutyric acid in diabetic acidosis and of lactic acid in lactic acidosis). 

Hyperkalemia may occur in renal disease and adrenal insufficiency owing to impairment of normal secretory mechanisms. Metabolic acidosis, in particular diabetic acidosis, and catabolism of cellular protein in starvation or fever cause K+ release from cells. Treatment consists of correction of the acidosis and promotion of cellular uptake of K+ by administration of insulin, which enhances glucose intake. In severe cases, ion exchange resins given orally bind K+ in intestinal secretions. 

Bronstein, H. D., Kantrowitz, P. A., and Schaffner, F., Marked enlargement of the liver and transient ascites associated with the treatment of diabetic acidosis. New Engl. J. Med. 261, 1314-1318 (1959). 

We shall not discuss here either the classic increase in the blood and urine levels of ketone bodies during diabetic acidosis or the metabolic origin of such an increase data about these subjects have been treated in recent reviews (F2). 

Ketoacidosis Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU]... 

Furthermore, a large-scale of intraabdominal or extraabdominal disorders can cause acute abdominal pain. Intraabdominal causes may have a genitourinary (urinary tract infection, ovarian torsion) or biliopancreatic origin (colecistitis, pancreatitis, etc.). Extraabdominal causes include abdominal pain referred from non-abdominal organs (pneumonia, discitis) and abdominal pain related to a systemic disease, such as diabetic acidosis, hypothyroidism, lead metals poisoning, sickle cell anemia, and porphyria. Fortunately, these different causes... 

Other conditions where increased fat mobilization has been implicated in fatty liver are fasting (Dole, 1956), diabetic acidosis (Bierman et al., 1957), thyrotoxicosis (Rich et dl., 1958), excessive growth hormone (Raben and Hollenberg, 1959), or catecholamine production (Feigelson et al., 1961). 

At present, the important clinical indication areas for therapy with thiamine are the beriberi of alcoholics and Wernicke s encephalopathy (Korner and Vollm 1976). In both cases, therapy is started with daily doses of at least 50-100 mg (in severe cases up to 200 mg) thiamine administered parenterally. Therapy is then continued with oral doses of 100-300 mg daily. Neuritis accompanying pregnancy responds particularly well to vitamin therapy. In some severe disorders of the intermediate metabolism (e.g., diabetic acidosis, severe hepatic malfunction), the necessary phosphorylation of thiamine in the organism is no longer ensured. Thiamine has, therefore, to be administered directly in its active form, thiamine pyrophosphate (TPP, cocarboxylase). Instances of toxicity of thiamine have been reported, primarily showing effects on the cardiovascular and nervous systems (Un-NA 1972 DiPalma and Ritchie 1977). 

Kennan, A. L. 1962. Glutamine synthesis in rats with diabetic acidosis. Endocrinology. 71 203. 

Incorporation of Radioactivity into Lipids by Human Blood. I. Pattern of Incorporation of Radioactivity into Fatty Acids by Blood from Normal Subjects and Patients in Diabetic Acidosis... 

These changes in GSH level, observed in both human and experimental diabetes, could be the result of (a) a diminished rate of GSH synthesis (b) the interaction of acetone bodies and GSH or (c) the secondary conse-cjuence of the electrolyte abnormalities associated with diabetic acidosis. 

This phenomenon was first observed in a case of diabetic acidosis by Heyl (1880) and quite certainly only reflects the degree of plasma turbidity resulting from increase in VLDLP and/or chylomicrons. The fundus in lipemia retinalis is characteristic and can only be imitated to some degree by leukemias. The retinal vessels appear flattened and show increased light reflexes arteries and veins are difficult to distinguish on a salmon colored background. Vision is usually not impaired, and the case of de Rosa (1952) with blindness of the left eye was due to other changes (atrophy of the left optic nerve with massive lipid deposits lateral to the optic disc.)... 

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