Keto Acidosis or Diabetic Keto Acidosis and Intensive Care Unit

Nursing Care for Diabetic Keto Acidosis in Intensive Care Unit  

Keto Acidosis or Diabetic Keto Acidosis related Problem and Intensive Care Unit Management by Nurses.

Endocrine problems in the intensive care unit

Diabetic Keto Acidosis

    Diabetic keto acidosis is a life-threatening emergency in patients with diabetes mellitus, particularly those with type 1 diabetes mellitus. It results from a lack of insulin when the body begins to metabolize fat for energy, producing ketone bodies in the process.

    The clinical presentation is polyuria, polydipsia, abdominal pain, vomiting, fatigue, lethargy, and coma. There is marked dehydration, tachycardia, hypotension, tachypnea from acidosis, and a fruity breath odor. This can be triggered by infections, missed insulin dose, heart attack or angina pectoris, medications, pancreatitis, and other stressors. A lack of insulin and/or an excess of glucagon leads to the breakdown of glycogen to glucose, leading to hyperglycemia. This in turn leads to glycosuria and osmotic diuresis. Because of this, exaggerated symptoms of diabetes are seen with polydipsia, polyuria, and dehydration. The lack of insulin in the peripheral tissues leads to the breakdown of fat into fatty acids to form ketone bodies (acetoacetate and beta-hydroxybutyrate), leading to acidosis and its effects.

Diagnosis

    Hyperglycemia, blood or urine ketones, and acidosis are classic findings in diabetic ketoacidosis (DKA). Arterial blood gas analysis shows acidosis with compensatory respiratory alkalosis. Electrolytes and renal function tests (urea nitrogen and creatinine) should be measured in conjunction with investigations into the cause of the precipitation of DKA.

It can be divided into:

Mild: pH between 7.25-7.30 Moderate: pH between 7.00-7.25

Heavy: pH < 7.00.

Management

    Because of the severe dehydration associated with DK, fluid replacement remains the mainstay of treatment. Normal saline (0.9% NaCl) remains the fluid of choice. Insulin is an essential tool to stop peripheral ketosis and fat metabolism and reduce the formation of keto acids. Sometimes a bolus dose of 0.1 units per kg is given, followed by an infusion of 0.1 units/kg/h. Once blood sugar starts to drop, you can slow down or add glucose drip.

    Electrolyte levels must be monitored when adding insulin, as insulin drives potassium into cells and causes dangerous hypokalemia. Therefore, potassium should be regularly measured and replaced in intravenous fluids. With regular blood sugar and electrolyte levels, close monitoring is essential. Caution should be exercised with concomitant cardiac and renal dysfunction. Treatment of the initiating cause should be done in conjunction with CHD. If neurological function deteriorates during treatment, ICU admission is warranted and fluid intake should be carefully monitored. This can mean cerebral edema, which can be fatal if not treated properly.

Nonketotic Hyperosmolar Diabetic Coma

    Hyperosmolar nonketotic coma (HONK), or hyperosmolar hyperglycemic state (HHS), occurs when blood glucose levels rise to dangerously high levels, leading to increases in osmolarity and dehydration. This is most commonly seen in type 2 diabetics with low or undetectable ketone bodies. It is associated with higher morbidity and mortality than diabetic ketoacidosis (DKA). This is usually associated with an altered mental state and can be triggered by infection, stroke, angina or myocardial infarction, or other acute condition. There is a relative insulin deficiency leading to polyuria, dehydration, and hemoconcentration. Some insulin is still present and prevents the ketosis seen in DKA.

Diagnosis

The American Diabetes Association has published guidelines for diagnosing HONK:

1. Plasma glucose >600 mg/dl

 2. Serum osmolality > 320 mOsm/kg

3. Severe dehydration requiring up to 9 liters of fluid replacement

4. serum pH > 7.30

5. Bicarbonate > 15 mEq/L

6. Little or no ketonuria/ketonemia

7. Altered consciousness.

This is more commonly seen in the elderly, reduced intake, sepsis, and obese patients.

Management

    Aggressive fluid resuscitation with isotonic solutions is required. The preferred IV fluid is normal saline. Caution is advised as most patients are elderly with underlying cardiac and renal dysfunction. Fluids should be replaced within 24-48 hours. A small amount of insulin is needed, but be careful because blood sugar levels drop quickly with fluid replacement. Electrolyte replacement and careful monitoring are required to avoid cerebral edema. Identification of the cause of the deterioration and treatment of the cause should be done in conjunction with the HONK treatment.

Hypoglycemia

    Hypoglycemia is a life-threatening medical emergency involving dangerously low blood sugar levels. This can manifest as seizures, confusion, dysphoria, coma, and, rarely, permanent brain damage or death. This is commonly seen in patients with diabetes mellitus who are being treated. It is rarely seen in other groups of patients, including those with insulinomas, alcoholics, adrenal insufficiency, prolonged starvation, inborn metabolic disorders, severe infections, liver failure, and poisoning. In addition to effects on the brain, autonomic effects such as sweating, palpitations, anxiety, nausea, hunger, visual disturbances, and weakness can also be seen.

Diagnosis

    Whipple's triad is generally used for diagnosis. These include: 

1. Symptoms of hypoglycemia

2. Low blood sugar

3. Resolution of symptoms by glucose treatment.

    Blood sugar usually stays between 72 and 144 mg/dL. Symptoms of hypoglycemia generally appear below 50-55 mg/dL. levels Distinguish myxedema from coma, delirium, sepsis, pheochromocytoma, accidental overdose, suicide attempts, hepatic failure, and neurosis. Significant episodes of hypoglycemia can increase the risk of cardiac events.

Management

    If the patient is awake, glucose-containing fluids can be given orally. Other foods such as crackers, oranges, apples, or juices can also be given orally. Onset of action is within 5 minutes and complete resolution of symptoms should be expected within 10-20 minutes. if patients are combative or comatose, the intravenous route can be used. IV dextrose can then be infused and the patient needs to be fairly fast. IM glucagon can be used in cases where intravenous access is difficult or impossible.