1 / 69

I am sharing 'ketoacidosis

Diagnosis and treatment of diabetic ketoacidosis

30947
Download Presentation

I am sharing 'ketoacidosis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Professor /Doctor ,Mohammed Bamashmos (MD)

  2. Defination What is DKA? ■ Diabetic ketoacidosis (DKA) is an extreme metabolic state caused by insulin deficiency. The breakdown of fatty acids (lipolysis) produces ketone bodies (ketogenesis), which are acidic. Acidosis occurs when ketone levels exceed the body’s buffering capacity ■

  3. What you should know ■ ■ Diabetic ketoacidosis (DKA) is a common, serious, and preventable complication of type 1 diabetes, with a mortality of 3-5%. It can also occur in patients with other types of diabetes ■ It can be the first presentation of diabetes. This accounts for about 6% of cases ■ The diagnosis is not always apparent and should be considered in anyone with diabetes who is unwell ■ Diagnosis is based on biochemical criteria. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA ■ Immediate treatment consists of intravenous fluids, insulin, and potassium, with careful monitoring of blood glucose and potassium levels to avoid hypoglycaemia and hypokalaemia

  4. Pathogenesis

  5. Causes

  6. Symptoms

  7. Diagnosis

  8. • Laboratory Findings ■ Although the diagnoses of DKA and HHS can be suspected on clinical grounds, confirmation is based on laboratory tests. The syndrome of DKA consists of the triad of hyperglycemia, hyperketonemia, and metabolic acidosis. ■ In the past, the most widely used diagnostic criteria for DKA included a blood glucose level >250 mg/dl, a moderate degree of ketonemia, serum bicarbonate <15 mEq/l, arterial pH <7.3, and an increased anion gap metabolic acidosis. Although these criteria served well for research purposes, they have significant limitations in clinical practice because the majority of patients with DKA present with mild metabolic acidosis despite elevated serum glucose and β-hydroxybutyrate concentrations. Thus, the biochemical criteria for diagnosis were recently modified ■

  9. ■The diagnostic criteria for HHS include a plasma glucose concentration >600 mg/dl, a serum osmolality >320 mOsm/kg of water, and the absence of significant ketoacidosis. Although by definition patients with HHS have a serum pH >7.3, a serum bicarbonate >18 mEq/l, and negative ketone bodies in urine and plasma, mild ketonemia may be present. Approximately 50% of patients with HHS have an increased anion gap metabolic acidosis as the result of concomitant ketoacidosis and/or an increase in serum lactate levels.2

  10. ■ Common Laboratory Pitfalls – Presence of leukocytosis ;Patients with DKA frequently present with leukocytosis in the absence of infection. However, a leukocyte count >25,000 mm3 or the presence of >10% neutrophil bands is seldom seen in the absence of bacterial infection – False low serum NA; ( pseudohyponatremia ) The admission serum sodium is usually low because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia. To assess the severity of sodium and water deficit, serum sodium may be corrected by adding 1.6 mg/dl to the measured serum sodium for each 100 mg/dl of glucose above 100 mg/dl. An increase in serum sodium concentration in the presence of hyperglycemia indicates a rather profound degree of water loss. – Pseudonormoglycemia ;Extreme hypertriglyceridemia, which may be present during DKA due to impaired lipoprotein lipase activity, may cause lipemic serum with spurious lowering of serum glucose (pseudonormoglycemia) and serum sodium (pseudohyponatremia) in laboratories still using volumetric testing or dilution of samples with ion-specific electrodes. – The admission serum potassium concentration is usually elevated in patients with DKA. In a recent series,3 the mean serum potassium in patients with DKA and those with HHS was 5.6 and 5.7 mEq/l, respectively. These high levels occur because of a shift of potassium from the intracellular to the extracellular space due to acidemia, insulin deficiency, and hypertonicity. – serum phosphate level may be normal or elevated because of metabolic acidosis. Dehydration also can lead to increases in total serum protein, albumin, amylase, and creatine phospho-kinase concentration in patients with acute diabetic decompensation. – serum creatinine, which is measured by a colorimetric method, may be falsely elevated as a result of interference by blood acetoacetate levels. – Plasma bicarbonate level may be misleading higher than expected or normal if patients has chronic respiratory acidosis due to pulmonary diseases – Blood PH may be misleading higher than expected or mormal if there concurrent metabolic alkalosis due to diuretic ingestion , excessive mineralocorticoid action , or excessive gastric fluid loss – Plasma glucose may be less than 250 mg if patients ingested large 8amount of alcohol , or starved

  11. ■TREATMENT; 1. General measure ; Admission to ICU ; ∙ ■Indication ; a. b. c. d. e. f. g. h. i. If HCO3 less than 10 PH less than 7.2 K ≥6 Hypotension despite rapid volume repletion Renal failure or oliguria CNS dysfunction HF Age ≥65 Concurrent cormorbid condition as sepsis Monitor the following Weight at admission and every 6-12h Fluid intake and output every 1-2h BP,puse , respiration , mental state every 1-2h Laboratory test including ; BS every 1-2 h , K every 1-2h , Na, CL. Ketone every 4h Blood PH, PCO2, PO2 at admission then as needed Urine ketone ECG ∙ a. b. c. d. e. f. g.

  12. 1. Specific therapy ; Fluid TherapyTotal body water deficit 100 mL/kg, and sodium deficit 7-10 mmol/kg. ∙ ∙ ■Types ; Normal saline Ringer lactate Colloid volume expander as plasma in shock Half strength NS ∙ ∙ ∙ ∙ ∙ ∙ ∙ ∙ ■Indication for use ;This choice is guided by the plasma sodium level, which should rise as plasma glucose falls, and by the patient’s cardiac status. Measured or even corrected plasma sodium levels reaching 150 meq/l or a history of congestive heart failure indicate the need for more hypotonic fluids. The optimal rate of fluid replacement after circulatory volume has been initially stabilized cannot be stated categorically because it will vary with the original degree of dehydration, with renal or cardiac function, and with time into treatment.

  13. ■Rate ; 2–3 L of 0.9% saline over first 1–3 h ? (15–20 mL/kg per hour); or 1litre of NS in first hour then 500ml per hour for 3-4 h or 15-20 ml |kg |h in children 10-20 ■Who to calculate fluid deficiet ; ■Water deficiet in littres = .6×weight in Kg [(sodium |140)-1} ■ subsequently, ■Check the corrected Na ; ■Who to check corrected Na ; add 1.6 meq of NCL to each 100 mg increase in plasma glucose above 100 ■Or measured sodium +0.016×(glucose -100) ■If ≤130meq continue in NS at rate of 250-500ml |h ■If ≥136 give 0.45% saline at 250–500 mL/h; ■Check BS every hour ■If ≥250 mg continoues in NS

  14. ■Who to monitor ; ■. It is vital to document that a cumulative positive balance is occurring by comparing ■fluid intake with output every 1–2 h. Urine flow can remain 100–200 ml/h until plasma glucose has declined to 250 mg/dl (14 mmol/l). In addition, there may be continuing gastrointestinal fluid losses or excessive ventilatory fluid losses due to fever. Plasma sodium should be checked to ensur e that it is gradually increasing as plasma glucose falls. If this is not happening, there may be excessive administration of free water, which may increase the risk of clinically significant wcerebral edema. ■ ■

  15. ■NSULIN THERAP ■Benefit ; ■Insulin increases peripheral glucose utilization and decreases hepatic glucose production, thereby lowering blood glucose concentration. In addition, insulin therapy inhibits the release of FFAs from adipose tissue and decreases ketogenesis, both of which lead to the reversal of ketogenesis. ■Types of insulin ; Regular insulin ∙ ∙ ■Dose ; Give bolus dose of 0.15 iu per kg or 10 iu ∙ ∙

  16. Then give continuous IV infusion at rate of 5-6 iu |h or 0.1iu|kg|h ■When to delay insulin therapy ; in severe hypokalemia ; if serum K is less than 3.3 ■Method ; ∙ ∙ Intravenous ∙ Intramuscular and SC ; A conscious patient with mild DKA could be admitted to a general hospital ward. In such patients, the administration of regular insulin every 1–2 h by subcutaneous or intramuscular route has been shown to be as effective in lowering blood glucose and ketone bodies concentration as giving the entire insulin dose by intravenous infusion.32,33 Furthermore, it has been shown that the addition of albumin in the infusate was not necessary to prevent adsorption of insulin to the IV tubing or bag.33 Such patients should receive the recommended hydrating solution and an initial “priming” dose of regular insulin of 0.4 unit/kg of body weight, given half as intravenous bolus and half as a subcutaneous or intramuscular injection). The effectiveness of intramuscular or subcutaneous administration has been shown to be similar; however, subcutaneous injections are easier and less painful ∙

  17. ■Monitoring ; Check blood glucose every 1-2 h Expected result is fall in the plasma glucose by 75mg |dl|h if no response increase dose of insulin by two to three fold every 2-3h ∙ ∙ In the rare instances in which the glucose level does not decrease by at least 10% or 50 mg/dL in 1 hour, the insulin infusion rate should be increased by 50% to 100% and a second bolus of intravenous insulin should be administered. As the glucose level decreases, it is usually necessary to decrease the rate of infusion. After the glucose reaches approximately 250 mg/dL, it is prudent to decrease the insulin infusion rate and administer dextrose. It usually takes an additional 12 to 24 hours to clear ketones from the circulation after hyperglycemia is controlled. With resolution of ketosis, the rate of infusion approaches the physiologic range of 0.3 to 0.5 U/kg per day. ∙

  18. ■Who to monitor the effectiveness of insulin 1. By measurinhg plasma glucose level ■Expected result is fall in BS by 50 mg |h . if no effect after 4-8h you have to double the dose 1. The effectiveness of insulin therapy should also be demonstrated within 4–8 h by an increase in plasma bicarbonate, and/or a decrease in the plasma anion gap, and a decrease in plasma ketones or _-hydroxybutyrate level (if available). It is not necessary to monitor arterial pHroutinely, but it should be rechecked if there is evidence of an 2. inadequate response to insulin, if sodium bicarbonate has been administered (see below), or if coexisting pulmonary disease complicates the acid-base picture. Consultation with a diabetologist is strongly recommended if there is insulin unresponsiveness, insulin allergy, an admission pH <7.0, or coma. ■

  19. ■When plasma glucose levels reach 250 mg/dl in DKA or 300 mg/dl in HHS, the insulin infusion rate is reduced to 0.05 unit/kg/h (3–5 units/h), and dextrose (5–10%) should be added to intravenous fluids. Thereafter, the rate of insulin administration may need to be adjusted to maintain the above glucose values until ketoacidosis or mental obtundation and hyperosmolality are resolved. During therapy, capillary blood glucose should be determined every 1–2 hours at the bedside using a glucose oxidase reagent strip. Blood should be drawn every 2–4 h for determination of serum electrolytes, glucose, blood urea nitrogen, creatinine, magnesium, phosphorus, and venous pH.

  20. ■When to decrease insulin dose ■ The insulin dose may be reduced when 1. plasma bicarbonate has risen to 18 meq/l, 2. the anion gap has decreased to 15 meq/l, 3. plasma ketones and urine ketones have virtually disappeared, ■4- arterial pH has risen to 7.30, or _- hydroxybutyrate has decreased to 1.0 mmol/l. Plasma ketones may persist because some _-hydroxybutyrate is converted to acetoacetate during the recovery phase. ■ Two units per hour intravenously is usually a satisfactory insulin dosage— along with 5% glucose at 100–150 ml/h (5–7.5 g glucose/h)—with which to maintain BS at 150-250 mg to prevent recurrent KA ■When to delay insulin therapyIn some hyperglycemic patients with severe potassium deficiency, insulin administration may precipitate profound hypokalemia,34 which can induce life-threatening arrhythmias and respiratory muscle weakness. Thus, if the initial serum potassium is lower than 3.3 mEq/L, potassium replacement should begin immediately by an infusion of KCl at a rate of 40 mEq/h, and insulin therapy should be delayed until serum potassium is ≥3.3 mEq/L

  21. ■RANSITIONTO SUBCUTANEOUS INSULIN ■Patients with moderate to severe DKA should be treated with continuous intravenous insulin until ketoacidosis is resolved. ■ Criteria for resolution of ketoacidosis include a 1. blood glucose <200 mg/dl, 2. a serum bicarbonate level ≥18 mEq/L, 3. a venous pH >7.3, 4. and a calculated anion gap ≤12 mEq/L.

  22. ■The criteria for resolution of HHS include 1. improvement of mental status, 2. blood glucose <300 mg/dL, 3. and a serum osmolality of <320 mOsm/kg. ■When these levels are reached, subcutaneous insulin therapy can be started. If patients are able to eat, split-dose therapy with both regular (short-acting) and intermediate-acting insulin may be given. It is easier to make this transition in the morning before breakfast or at dinnertime. ■Patients with known diabetes may be given insulin at the dosage they were receiving before the onset of DKA. In patients with newly diagnosed diabetes, an initial insulin dose of 0.6 unit/kg/day is usually sufficient to achieve and maintain metabolic control. Two-thirds of this total daily dose should be given in the morning and one-third in the evening as a split-mixed dose. ■If patients are not able to eat, intravenous insulin should be continued while an infusion of 5% dextrose in half-normal saline is given at a rate of 100–200 mL/h. ■A critical element to avoid recurrence of hyperglycemia or ketoacidosis during the transition period to subcutaneous insulin is to allow a 1- or 2-h overlap of intravenous insulin infusion during the initiation of subcutaneous regular insulin to ensure adequate plasma insulin levels.

  23. ■Potassium ■When to start K - Serum K is less than 5 meq - No oliguria ; urine flow more than 50ml \ H - Normal ECG ■When to stop K - Serum K more than 5.5 - Oliguria except if serum K less than 4 , or ECG changes of hypokalemia ( u wave ) - ECG changes of hyperkalemia (peaked T wave, QRS widening) ■Causes of hypokalemia ; Despite a total body potassium deficit of ∼3–5 mEq/kg of body weight, most patients with DKA have a serum potassium level at or above the upper limits of normal. These high levels occur because of a shift of potassium from the intracellular to the extracellular space due to acidemia, insulin deficiency, and hypertonicity. Both insulin therapy and correction of acidosis decrease serum potassium levels by stimulating cellular potassium uptake in peripheral tissues. Therefore, to prevent hypokalemia, most patients require intravenous potassium during the course of DKA therapy. ■Method and types ; Replace-ment with intravenous potassium (two-thirds as potassium chloride [KCl] and one-third as potassium phosphate [KPO4]) should be initiated as soon as the serum potassium concentration is below 5.0 mEq/L. ■The treatment goal is to maintain serum potassium levels within the normal range of 4–5 mEq/L.

  24. ■Dose ; - usually replace potassium at 10 to 20 mEq/hour (half as potassium chloride and half as potassium phosphate), if serum K ≤5.5 , normal ECG, normal urine flow ; monitor serum levels at least every 2 hours initially, and monitor ECG morphology. - Occasionally, patients with DKA who have had protracted courses that include vomiting, hypokalemia ≤3.3 , and acidosis if bicarbonate is given require 40 to 60 mEq/hour by central line to prevent further decreases in the serum potassium concentration - Or according to serum K –level a. ≥ 5 no K is given b. + 4.0–5.0, 20 meq/l c. K+ 3.0–4.0, 30–40 meq/l d. K+ <3.0, 40–60

  25. ■Bicarbonate; ■Adverse effect of metabolic acidosis ; ■Severe metabolic acidosis can lead to - impaired myocardial contractility, - cerebral vasodilatation and coma, and - several gastrointestinal complications. ■ Side effect of rapid alkalinization ■ - hypokalemia, paradoxical central nervous system acidosis, and worsened intracellular acidosis (as a result of increased carbon dioxide production) with resultant alkalosis. Controlled studies have failed to show any benefit from bicarbonate therapy in patients with DKA with an arterial pH between 6.9 and 7.1.35 However, most experts in the field recommend bicarbonate replacement in patients with a pH <7.0. In patients with DKA with arterial pH ≥7.0, or in patients with HHS, bicarbonate therapy is not recommended. for dosing guidelines.

  26. ■Serum bicarbonate is always low in DKA, but a true deficit is not present because the ketoacids and lactate anions are metabolized to bicarbonate during therapy. The use of bicarbonate in the treatment of DKA is highly controversial. No benefit of bicarbonate therapy has been demonstrated in clinical trials. In fact, in two trials, hypokalemia was more common in bicarbonate-treated patients. There are theoretical considerations against the use of bicarbonate. Cellular levels of 2,3-diphosphoglycerate are depleted in DKA, causing a shift in the oxyhemoglobin dissociation curve to the left and thus impairing tissue oxygen delivery. Acidemia has the opposite effect, and therefore acute reversal of acidosis could decrease tissue oxygen delivery. In addition, in vitro data suggest that pH is a regulator of cellular lactate metabolism, and correction of acidosis could increase lactate production. These observations are of questionable clinical relevance, however.

  27. ■We reserve bicarbonate therapy for patients with severe acidosis (pH <6.9), patients with hemodynamic instability if the pH is less than 7.1, and patients with hyperkalemia with ECG findings. When bicarbonate is used, it should be used sparingly and considered a temporizing measure while definitive therapy with insulin and fluids is under way. ■Indications for Considering Bicarbonate Therapy ■_ pH <7.0 or HCO3 – <5.0 meq/l ■_ Hyperkalemia (K+ >6.5 meq/l) ■_ Hypotension unresponsive to fluidreplacement ■_ Severe left ventricular failure ■_ Respiratory depression ■_ Late hyperchloremic acidosis ■ ■DOSE ; 100meq Nabicar in 4ooml water at rate of 200ml |h ■ 1ampule = 50meq

  28. ■Repeat as needed every 2h till PH more than 7 ■Approximately 1 mEq/kg of bicarbonate is administered as a rapid infusion over 10 to 15 minutes, and further therapy is based on repeated arterial blood gas sampling every 30 to 120 minutes. Potassium therapy should be considered before treatment with bicarbonate is undertaken, because transient hypokalemia is not an uncommon complication of the administration of alkali. ■

  29. ■Phosphate ■Total body phosphate deficiency is universally present in patients with DKA, but its clinical relevance and benefits of replacement therapy remain uncertain. Several studies have failed to show any beneficial effect of phosphate replacement on clinical outcome.36 Furthermore, aggressive phosphate therapy is potentially hazardous, as indicated in case reports of children with DKA who developed hypocalcemia and tetany secondary to intravenous phosphate administration.37 Theoretical advantages of phosphate therapy include prevention of respiratory depression and generation of erythrocyte 2,3-diphosphoglycerate. ■Because of these potential benefits, careful phosphate replacement may be indicated in patients with cardiac dysfunction, anemia, respiratory depression, and in those with serum phosphate concentration lower than 1.0–1.5 mg/dl. If phosphate replacement is needed, it should be administered as a potassium salt, by giving half as KPO4 and half as KCl. In such patients, because of the risk of hypocalcemia, serum calcium and phosphate levels must be monitored during phosphate infusion.

More Related