Wrenn et al found altered mental status in 15% of patients, attributable in all but one case to hypoglycaemia, severe alcohol intoxication, or infection. Fever was seen in only two patients, both with other likely underlying causes. Following resuscitation, our patient had plasma electrolyte levels corrected, nutritional supplementation provided and completed an alcohol detoxification regimen. Given the early recognition of AKA and concurrent management, our patient had a good outcome. Diabetic ketoacidosis can be treated and you can get better from it, especially if you get medical help right away.
Differential diagnosis
In patients with ketoacidosis, however, the liver metabolizes the incoming free fatty acids in an additional, unusual way. Under the influence of excess glucagon, some of the free fatty acids are converted to ketone bodies and secreted into the blood, causing severe health consequences. Examination should reveal a clear level of consciousness, generalised abdominal tenderness (without peritoneal signs), and tachypnoea. There may be concomitant features of dehydration or early acute alcohol withdrawal. Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent.
- The major cause of morbidity and mortality in patients diagnosed with AKA is under-recognition of concomitant diseases (that may have precipitated the AKA, to begin with).
- It’s important to note that AKA treatment also includes addressing any underlying issues, such as alcohol use disorder, and may involve a multidisciplinary approach including medical, nutritional, and psychological support.
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People with type 2 continue to produce insulin in early disease stages; however, their bodies do not respond adequately to the hormone (i.e., the patients are resistant to insulin’s effects). Thus, insulin does not lower blood sugar levels to the extent that it does in people without diabetes. For example, obesity, inactivity, and cigarette smoking may worsen genetically determined insulin resistance. Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase (CAT) transports free fatty acids into the mitochondria and therefore regulates their entry into the oxidative pathway. The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation.
- Glycogen is a large molecule that consists of numerous glucose molecules and serves as a storage form of glucose in the tissues, particularly the liver.
- Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis.
- Good blood sugar and blood pressure control as well as regular eye examinations are essential for the prevention of retinopathy.
- Numerous studies have investigated alcohol’s effects on the control of blood sugar levels in diabetics.
- Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent.
Differential Diagnosis
They attributed this to the administration of therapy (intravenous dextrose) rather than the withdrawal of the toxin, ethanol. Management and prevention of Alcoholic Ketoacidosis (AKA) strongly rely on making significant lifestyle changes, particularly in relation to alcohol consumption and nutritional intake. Since AKA often develops in the context of heavy alcohol use combined with poor dietary habits, addressing these areas is crucial for both recovery and prevention of recurrence. Treatment for Alcoholic Ketoacidosis (AKA) primarily focuses on correcting the dehydration, electrolyte imbalances, and acidosis that characterize this condition.
Metabolism of ethanol
Diabetes and alcohol consumption are the two most common underlying causes of peripheral neuropathy. Among diabetics, the prevalence of neuropathy with obvious symptoms (i.e., alcoholic ketoacidosis symptomatic neuropathy) increases with increasing disease duration. That increase in prevalence was most apparent in patients with a disease duration of less than 4 years.
Possible Complications
- Diabetic eye disease (i.e., retinopathy) is another troublesome tissue complication of diabetes and one of the leading causes of blindness in the United States today.
- For example, long-term alcohol use in well-nourished diabetics can result in excessive blood sugar levels.
- Ultimately, insulin secretion declines even further, to levels below those seen in nondiabetics (although generally still higher than those seen in type 1 diabetics).
- Those researchers also reported that diabetics who consumed more than eight standard drinks per week developed peripheral neuropathy faster than did diabetics who consumed eight or fewer drinks per week.
