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• DKA - acidosis accompanied by the accumulation of ketone bodies in diabetes patient. (1) • Consist of the biochemical triad of ketonemia, hyperglycemia, and acidemia. (2) • Most patients with DKA have autoimmune type 1 diabetes , however patients with type 2 diabetes are also at risk during catabolic stress of acute illness. (3)
• Absolute or relative insulin deficiency accompanied by an increase in counter-regulatory hormones which enhances hepatic gluconeogenesis , glycogenolysis , and lipolysis. (3,4)
• Absolute insulin deficiency may occur in certain condition such as undiagnosed type 1 diabetes and patient who miss their insulin doses. (5) • Relative insulin deficiency may occur when concentrations of counterregulatory hormones increase in response to stress conditions. (5)
(3) • Lipolysis increase serum fatty acids which will undergo oxidation as an alternative energy source to produce ketone bodies resulting ketonemia and metabolic acidosis. (2) .• Gluconeogenesis and glycogenolysis will increase the blood glucose level and causing hyperglycemia. (3) • Fluid depletion can occur due to hyperglycemia induce osmotic diuresis. vomiting due to ketoacidosis and inability to take in fluid due to diminished level of consciousness.
or abdominal pain Tachypnea Hypotension Tachycardia Hypothermia Polyuria. polydipsia.Sign and symptoms • • • • • • • • Dry skin Characteristic acetone (ketotic) breath odor Nausea. and nocturia . vomiting.
NUMBER 7. VOLUME 32. JULY 2009 .Diagnostic criteria (3) DIABETES CARE.
Goals of therapy • Expansion of the intravascular volume. • Initiation of intravenous insulin infusion therapy. electrolyte & acid base status. • Treatment of concurrent infection if present. • Correction of deficit in fluids. • Assessment and monitoring of therapy. .
clearance of ketones and correction of electrolytes imbalance.General management issues… 1. Typical deficits in DKA: Water (ml/kg) Sodium (mmol/kg) Chloride (mmol/kg) Potassium (mmol/kg) 100 7-10 3-5 3-5 . Fluid administration and deficits the most important initial therapeutic intervention to restore circulatory volume.
1 units/kg is recommended Priming dose of insulin is not necessary provided if the insulin infusion is started promptly at a dose of at least 0.1 unit/kg/hr . (Kitabchi 2008)(2) . reduction of blood glucose and correction of electrolyte imbalance Administration of intravenous insulin infusion at a fixed rate of 0. Insulin therapy Insulin has the effects of suppression of ketogenesis.2.
.3.5 mmol/L/hr Increase in venous bicarbonate by 3 mmol/L/hr Reduce capillary blood glucose by 3 mmol/L/hr Serum potassium level should be maintain between 4-5 mmol/L If these rates are not achieved then the fixed rate of intravenous insulin infusion should be increased. Metabolic treatment targets The recommended targets are Reduction of blood ketone concentration by 0.
4. . Intravenous glucose concentration Administration of intravenous infusion of 10% glucose is necessary in order to avoid hypoglycemia and to allow the continuation of a fixed rate IVII to suppress ketogenesis. Introduction of 10 % glucose is recommended when the blood glucose falls below 14mmol/L IVII should not be discontinued until the patient is eating and drinking normally.
Management pathway Joint British Diabetes Societies Inpatient Care Group. The Management of Diabetic Ketoacidosis in Adults (March 2010). .
9% sodium chloride solution Start a fixed rate IVII after starting fluid therapy Established monitoring regime – hourly blood glucose. Immediate management upon diagnosis at the first hour Aims Start IV 0. ketone measurement and at least 2 hourly serum potassium for the 1st 6 hours Clinical and biochemical assessment of the patient .1.
9% Nacl over 10-15 minutes.Intravenous access and initial investigation ABC. 2. Once SBP above 90 mmHg follow fluid replacement as in table 1 .Restoration of circulating volume SBP below 90 mmHg give 500ml of 0. clinical assessment.Actions 1. lab investigation. IV fluid replacement. and consider precipitating causes and treat appropriately.
Table 1 .
5 mmol/L – add 2 g KCl each liter 3 – 3.• Fluid replacement (Sarawak handbook 3rd ed) ▫ ▫ ▫ ▫ ▫ 1 liter NS in 1 hour Then 1 liter in 2 hour Then 1 liter in 4 hour Then 1 liter in 6 hour Then 1 liter in 8 hour • • • • • • Potassium replacement More than 5 mmol/L – no need add KCl 4.0 mmol/L – add 1 g KCl each liter 3.5 – 5.5 – 4.5 mmol/L – add 3 g KCl each liter Less than 3 add 4 g KCl each liter .
To maintain K level at 4-5 mmol/L with 20-40 mmol/L K. . Potassium replacement Serum K is often high on admission (although total body potassium is low) but falls precipitously upon treatment with insulin.3. 4.1 unit/kg/hr Only give stat dose of insulin if there is a delay in setting up a fixed rate of IVII. Starting a fixed rate intravenous insulin infusion 50 units of insulin made up to 50 ml of NS and infused at a fixed rate of 0.
2. 60 minutes to 6 hours Aims Clear the ketones from blood and suppress ketogenesis Achieve a rate of fall of ketones of at least 0.5 mmol/L/hr Or bicarbonate should rise by 3 mmol/L/hr and blood glucose should fall by 3 mmol/L/hr Maintain serum K and avoid hypoglycemia .
bicarbonate rise at least 3 mmol/L/hr or glucose falling at least 3 mmol/L/hr .Reassess patient and monitor vital signs Consider urinary catheterisation isfincontinent or anuric Accurate fluid balance chart.Actions 1.5ml/kg/hr 2.Review metabolic parameters Assess the resolution of ketoacidosis Calculate the rate of change of ketone level fall or glucose or rise in bicarbonate Ketone falling at least 0.5mmol/L/hr. minimum urine output 0.
Increase the rate of intravenous insulin infusion if the ketone or glucocose level did not fall or bicarbonate level did not increase as above. . Continue the IVII until ketones less than 0.3 mmol/L.9% Nacl solution. 10% glucose should be given at 125ml/hr with 0.3 and/or venous bicarbonate over 18 mmol/L If glucose falls below 14 mmol/L. venous pH over 7.
6 to 12 hours Aims Ensure that clinical and biochemical parameters are improving Continue IV fluid replacement and IVII Assess for complications of treatment example fluid overload or cerebral edema Avoid hypoglycemia Actions 1.3 mmol/L. and venous pH over 7. Reassess and monitor patient vital sign 2.3 . Review of biochemical and metabolic parameters Resolution of DKA is defined as ketones less than 0.
Continue iv fluids if not eating or drinking Reassess for complications of treatment Transfer to subcutaneous insulin if patient eating and drinking normally . Aims Ensure all parameters are improving or have normalised.12 to 24 hours By 24 hours the ketonemia and acidosis should have resolved.
Reassess and monitor patient vital sign 2.Actions 1. Ideally give subcutaneous fast acting insulin and a meal and discontinue IV insulin one hour later.3 mmol/L.3 3. Review of biochemical and metabolic parameters Resolution is defined as ketones < 0. Subcutaneous insulin is started before IV insulin is discontinued. venous pH > 7. .
.5 mmol/L and patient is passing urine. Joint British Diabetes Societies Inpatient Care Group.9% Nacl solution with potassium 40 mmol/L is given as long K level below 5.Complication of DKA treatment Hypokalemia and hyperkalemia Potentially life threatening Risk of acute renal failure associated with severe dehydration and therefore recommend that no potassium should be given with initial fluid resuscitation K will always falls as the DKA is treated with insulin and recommended that 0. The Management of Diabetic Ketoacidosis in Adults (March 2010).
Hypoglycemia Blood glucose may fall very rapidly as ketoacidosis is corrected and is a common mistake to allow the blood glucose drop to hypoglycemic levels This may result a rebound ketosis by counter regulatory hormones. Once blood glucose drops to 14 mmol/L intravenous glucose 10% should be given to patient Joint British Diabetes Societies Inpatient Care Group. Severe hypoglycemia can associate with cardiac arrhythmias brain injury and death. The Management of Diabetic Ketoacidosis in Adults (March 2010). .
Pulmonary edema Rapid infusion of crystalloids over a short period of time increase the risk of complication Elderly and impaired cardiac function patient also at the risk of developing pulmonary edema Joint British Diabetes Societies Inpatient Care Group.Cerebral edema More common in children Exact cause is unknown but recent studies suggest that cerebral hypoperfusion with subsequent reperfusion may be the mechanism operating. . The Management of Diabetic Ketoacidosis in Adults (March 2010).
020. The Management of Diabetic Ketoacidosis in Adults (March 2010).Recommendation and discussion 1. Arterial vs venous measurement? • Difference btw arterial and venous pH is 0.15 units and bicarbonate is 1.88mmol/L • Not really affect the diagnosis or management of DKA • Venous blood are easily obtained Measure venous rather than arterial bicarbonate and pH Joint British Diabetes Societies Inpatient Care Group. .
9% sodium chloride solution should be the fluid of choice for resuscitation in all clinical areas as it supports safe practice and is available ready to use. • However hypotension results from a loss of electrolyte solution and it is more physiological to replace with crystalloid fluid. Colloid vs crystalloid • Many guideline suggest that in hypotensive patients initial fluid resuscitation should use colloid.2. The Management of Diabetic Ketoacidosis in Adults (March 2010). • It is recommended that 0. Joint British Diabetes Societies Inpatient Care Group. .
The Management of Diabetic Ketoacidosis in Adults (March 2010).9% Nacl vs compound sodium Joint British Diabetes Societies Inpatient Care Group. .0.
Intravenous phosphate? • No evidence of benefit of phosphate replacement • However. The Management of Diabetic Ketoacidosis in Adults (March 2010). .3.1 unit/kg/hr 4. in the presence of respiratory and skeletal muscle weakness. phosphate replacement should be considered. Initiating treatment with a priming dose of insulin? • Is not really necessary if the insulin infusion is started promptly at a dose of at least 0. Joint British Diabetes Societies Inpatient Care Group.
5. Intravenous bicarbonate? • Is not indicated • Adequate fluid and insulin therapy will resolve the acidosis • Acidosis is an adaptive response to improve oxygen delivery to the tissue causing a right shift to the oxygen dissociation curve . . • Excessive bicarbonate may cause a rise in CO2 partial pressure in CSF and may lead to a CSF acidosis. The Management of Diabetic Ketoacidosis in Adults (March 2010). • Use of bicarbonate may increase the risk of cerebral edema in children and young adults Joint British Diabetes Societies Inpatient Care Group.
•Thank you .
Hyperglycemic crises in adult patients with diabetes. 4. 2013 Abdelghaffar. Umpierrez. The Management of Diabetic Ketoacidosis in Adults (March 2010). Kitabchi. http://emedicine. Joseph n. Guillermo e.medscape.thefreedictionary. Abbas E.com/keto acidosis 2. licensee InTech . http://medicaldictionary. John m. Miles. 3. july 2009. Fisher. Joint British Diabetes Societies Inpatient Care Group. number 7. Diabetic Ketoacidosis: Clinical Practice Guidelines. Diabetes care. Shereen Abdelghaffar.References 1.com/article/118361overview#aw2aab6b2b3aa 5. volume 32.
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