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Diabetic ketoacidosis Symptoms & causes

If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized. Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. DKA, HHS, and severe hypoglycemia are all serious life-threatening complications of diabetes that require prompt diagnosis, treatment, and close monitoring. The diagnosis of hyperglycemic emergencies, DKA and HHS, is made based on the presence of hyperglycemia, an assessment of acid–base status, and the presence or absence of ketonemia. Treatment for both DKA and HHS include fluid resuscitation, insulin, and close monitoring of electrolytes along with treatment of any underlying precipitating factors.

Ethanol metabolism

The evaluation consists of 11 yes or no questions that are intended to be used as an informational tool to assess the severity and probability of an alcohol use disorder. The test is free, confidential, and no personal information is needed to receive the result. It can be helpful to understand the basic guidelines for alcohol consumption so you can determine whether you are drinking above recommended levels and engaging in potentially harmful alcohol use. Your prognosis will be impacted by the severity of your alcohol use and whether or not you have liver disease.

Symptoms

• Your doctor and other medical professionals will watch you for symptoms of withdrawal.
• If you develop any of these symptoms, seek emergency medical attention.
• An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury.
• DKA is a rapidly evolving condition with symptoms typically presenting within a 24-hour period.

The hyperglycemia then leads to a direct and indirect increase in serum osmolality. Serum osmolality is determined by the formula 2serum sodium + serum glucose/ 18 + BUN (i.e., blood urea nitrogen); therefore as the serum glucose levels rise, there will be a direct increase in the serum osmolality. After correcting the intravascular depletion, the remaining goal of fluid management is to replace half of the estimated fluid deficit over the course of 12 to 24 hours. If the corrected serum sodium remains low, the normal saline infusion can be continued but in general decreased to 250 to 500 mL/hour.

• All chronic alcohol misusers attending the ED should receive intravenous B vitamins as recommended by The Royal College of Physicians.23 Strenuous efforts must be made to exclude concomitant pathology.
• On physical examination, patients may appear dehydrated with dry mucous membranes, decreased skin turgor, tachycardia, and hypotension.
• It is important for there to be a period of overlap during the transition to avoid iatrogenically causing an insulin-deficient state and the possibility of the patient re-developing DKA.
• A detailed list of antihyperglycemic medications, recent additions, and any dose adjustments should be reviewed.
• This paradox is due to the normal action of insulin to drive potassium intracellularly and out of the serum.
• In addition, patient-specific factors such as impaired renal function and liver dysfunction, which can affect the metabolism of medications, may prolong the duration of monitoring and treatment of hypoglycemia.

Diabetic ketoacidosis

In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), blood urea nitrogen (BUN) and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurements. Alcoholic ketoacidosis is usually triggered by an episode of heavy drinking. If you alcoholic ketoacidosis smell can’t eat for a day or more, your liver will use up its stored-up glucose, which is a type of sugar. When your liver uses up its stored glucose and you aren’t eating anything to provide more, your blood sugar levels will drop.

What to Know About Alcoholic Ketoacidosis

• Seeking help as soon as symptoms arise reduces your chances of serious complications.
• Abdominal distension, decreased bowel sounds, ascites, or rebound tenderness occurred rarely and only in the presence of other demonstrable intra‐abdominal pathology such as pancreatitis, severe hepatitis, and sepsis or pneumonia.
• Patients should also be provided with the necessary diabetes medications and supplies on discharge.
• Injury and surgery can lead to stress, which has been shown to trigger hyperglycemia.

To avoid this, the basal insulin dose should be administered and the intravenous insulin infusion can be discontinued 2 hours after the dose is given. Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. The pathophysiology of HHS is similar to that of DKA with some specific intricacies. However, in HHS, the insulin deficiency is only relative, as the pancreas continues to make insulin but is unable to keep up with the demand needed to overcome peripheral tissue insulin resistance. In the setting of a relative insulin deficiency, the cells in the periphery enter a perceived “starvation” state leading to the release of the counterregulatory hormones glucagon, cortisol, growth hormone, and catecholamines. The counterregulatory hormones work to promote glycogenolysis and gluconeogenesis, leading to worsening hyperglycemia.

However, most patients will have normal or increased levels of phosphate at initial presentation. The initial hyperphosphatemia is likely secondary to the concentrated levels in the setting of intravascular volume depletion and acute renal impairment. Studies have not shown any benefit of phosphate replacement in the management of DKA, but replacement is indicated in those with severe hypophosphatemia with serum phosphate levels less than 1 mg/dL. In the event of severe hypophosphatemia, 20 to 30 mEq of potassium phosphate can be added to the fluids to prevent complications, which include cardiac arrhythmias and respiratory compromise. Talk to a healthcare provider about ways to reduce moderately high ketone levels.

• The hyperglycemia-induced osmotic diuresis also promotes the loss of other electrolytes in the urine including potassium, calcium, phosphorous, and magnesium.
• Alcoholic ketoacidosis is a problem caused by drinking a lot of alcohol without eating food.
• A healthcare provider may order a breath test if they need to rapidly check for elevated levels of ketones.
• If not treated quickly, alcoholic ketoacidosis may be life-threatening.