diabetic acidosis treatment diabetic ketoacidosis and hyperglycemic syndrome protocol
Juan Carlos Segura, Angel Fernández-Fúnez, Antonio Hernández.
diabetic acidosis treatment
diabetic acidosis treatment Diabetic ketoacidosis and nonketotic hyperosmolar hyperglycemic syndrome are the most important acute complications of diabetes mellitus, both due to their frequency and associated mortality. Although discussed separately, they represent the extreme points of emergencies caused by poor diabetes control, both are characterized by insulinopenia, and differ only in the degree of dehydration and the severity of metabolic acidosis. Three mechanisms have been proposed that would explain the higher degree of dehydration and the lack of ketogenesis in SHHNC: a higher level of pancreatic insulin reserve, a lower level of counterregulatory hormones, and the inhibition of lipolysis by the same hyperosmolar situation.
1. Concept.
CAD is an acute and serious complication in which an absolute or relative insulin deficiency, together with an increase in glucagon and other counterregulatory hormones, leads to the appearance of hyperglycemia (producing osmotic diuresis, dehydration and hypovolemia) and ketosis causing metabolic acidosis . Its mortality is estimated at less than 5%.
2. Triggers.
The triggers of CAD in order of frequency are: infections (30-35%) incorrect insulin dosage (15-30%), onset of diabetes mellitus (20-25%), intercurrent illnesses (10-20%, especially alcohol abuse, AMI, stroke, severe trauma, acute abdomen, major surgery, endocrine diseases, drugs -especially glucocorticoids and thiazides-) and without apparent cause (2-10%).
3. Clinic.
Symptoms are: polyuria, polydipsia, asthenia, anorexia, vomiting, abdominal pain, decreased consciousness (coma <10%). Among the signs we find: cutaneous-mucosal dehydration, hypotension, tachycardia, hot skin, Kussmaul respiration and ketotic breath. The examination should be directed not only at the diagnosis of CAD but also at the triggering cause.
“The diagnosis of CAD should be considered in all patients with decreased level of consciousness or hyperventilation.”
4. The diagnosis
The diagnosis is based on the following criteria: Glucose> 250 mg / dl, pH <7.3; HCO3 <15 mmol / L and positive ketonemia (> 5 mmol / L), or failing that, positive ketonuria> 3+. In addition, it is accompanied by a GAP anion almost always high and glycosuria> 3+.
5. Laboratory tests.
diabetic acidosis treatment
The laboratory tests to perform immediately are blood glucose, glycosuria and ketonuria with test strips that suggest the diagnosis.
They will be carried out on a delayed basis to confirm the diagnosis and investigate the triggering cause: blood glucose, arterial blood gas, plasma urea and creatinine, ions (Na, K, CI), complete blood count, plasma osmolality, GAP anion, abnormal urine and sediment, ECG , Chest X-ray, Simple abdominal X-ray (if appropriate).
6. General treatment measures.
- Two venous accesses are preferable for the infusion of fluid therapy and insulin separately.
- Find the cause you triggered and carry out an appropriate treatment. Antibiotherapy after taking cultures if infection is suspected.
- Prophylactic heparinization if coma or very hyperosmolar state.
- Control of PVC in situations where strict control of water balances is necessary (unstable heart disease, advanced age or poor peripheral perfusion).
- Nasogastric tube if altered level of consciousness, severe vomiting or paralytic ileus.
- Urinary catheterization if difficulty of exact collection is anticipated (urinary retention, decreased level of consciousness) or diuresis <20 ml in the first hour.
- Consider admission to the ICU if pH <6.9 or K <2 or there is a complication that justifies it (eg: AMI, sepsis).
7. Controls
The controls to be carried out during the treatment are the following:
- Schedules: capillary blood glucose, BP, heart and respiratory rate, PVC (if necessary), diuresis.
- Every 2, 4, 6, 12 and 24 hours: water balances, basic serum biochemistry checks (urea, creatinine, sodium, potassium and glucose) and venous blood gas.
8. Fluid therapy to be used in CAD patients.
The type of fluid to be used, in principle, will always be physiological (NaCl 0.9%). It is used hypotonic (0.45% NaCl) in severe hypernatremia (Na> 150 mEq / L) and temporarily until the natraemia drops to <145 mEq / L. If blood glucose falls below 250 mg / dl, 5% glucose should be added at a rate of 100 ml / h.
Regarding the infusion rate of the fluid, it will be the following: in the first hour 1000 ml, 500 ml / hour in the following three hours, 250 ml / hour from the 5th to the 8th hour and then 500 ml every 4 hours. It is recommended not to exceed 5-6 liters a day.
9. Insulin therapy stops ketogenesis and lowers blood glucose.
The type of insulin to be administered is regular. The administration route of choice is intravenous with a continuous infusion pump.
diabetic acidosis treatment
The dose to be administered is 10 U bolus I.V. followed by 0.1 U / Kg / hour in IV infusion. continuous (50 U in 500 cc of 0.9% S F. Ex. 60 kg x 0.1 = 6 U / h at 60 ml / h). If blood glucose does not decrease> 100 mg / dl in the first 2-3 hours, double the dose, after evaluating the rate of hydration. When blood glucose is less than 250 mg / dl, and acidosis bloodsugar persists, associate 5% glucose at 100 ml / h and adjust the dose to 1-4 IU / hour of regular insulin to maintain blood glucose between 150-200 mg / dl. If an infusion system is not available, the intramuscular route in hourly boluses is recommended.
10. Potassium supplements
They will be administered in the form of potassium chloride depending on their plasma levels: if it is> 5.5 mEq / l do not administer but measure at the hour, between 4.5-5.5 mEq / l 20 mEq / l, between 3, 5-4.5 mEq / l 30 mEq / l and <3.5 mEq / l 40 mEq / l.
Hypokalemia is the leading preventable metabolic cause of death in DKA. Do not exceed 30 mEq / 500 ml if via peripheral or 60 mEq / hour. In case of anuria, do not administer K. If the K is less than 3, comment with ICU.
11. Baking soda
It will be administered in the case of manifest Kussmaul respiration and if the pH is less than 7.0 and / or the bicarbonate is less than 5 mmol / l.
The doses to be administered depend on the pH levels: if it is between 6.9 and 7.0, 41 mmol of sodium bicarbonate (250 ml of 1/6 M bicarbonate) to pass in one hour (1/6 M = 0.1666 mEq / ml ) together with an additional 10 mEq of CLK; if the pH is <6.9: 83 mmol of sodium bicarbonate (500 ml of 1/6 M sodium bicarbonate) to pass in two hours and 20 mEq of CIK. Do not add CLK to the bicarbonate solution, especially if it is 1 Molar, due to the risk of precipitation. Stop the infusion when the pH is greater than 7.2.
12. Suspension of insulin infusion.
The suspension of the insulin infusion can be considered when the pH> 7.3 and the bicarbonate> 15, although it is essential to administer the first subcutaneous insulin dose 60 minutes before suspending the insulin infusion.
If the patient can eat, a diet is prescribed with calories adjusted to the weight and divided into 6 intakes, provision of fluids according to the state of hydration and electrolytes, pre- and postprandial controls of capillary glycemia and insulin regimen:
If CAD in onset DM: Insulin 0.5-0.7 IU / kg / day divided into three doses: Breakfast 25% rapid insulin s.c., lunch 35% rapid insulin s.c. and dinner 10% rapid insulin s.c. and 30% insulin NPH s.c.
If CAD in known DM: previous insulin dose. Glycemic profile.
If oral tolerance is inadequate, it is preferable to maintain a regular intravenous insulin infusion (1-4 IU / hour) together with 5% glucose at an approximate rate of 100 ml / hour, adjusting the insulin dose to maintain a blood glucose level between 100 -200 mgr / dl, or what is equivalent, use a GIP infusion: 5% glucose 500ml / 6 hours with 10 mEq of KCl and 5 IU of regular insulin if the blood glucose remains between 100-150, with blood glucose controls capillary every 6 hours increasing 2-3 IU / 6 hours of regular insulin units for each fraction of 50 mgr / dl above 150 mgr.
