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DKA was 1st described in 1886 untill introduction of insulin therapy in 1920,it was fatal. Now mortalitiy rate is <5%. Definition: : Definition: BSL > 250mg/dl(13.9mmol/L) Blood pH < 7.3 / serum bicarb < 15meq/l Ketonuria +++ / ketones in serum > 5meq/l In 2006 ADA,categorised DKA into 3 stages of severity: : In 2006 ADA,categorised DKA into 3 stages of severity: Causes: : Causes: Slide 8: DKA also occurs in TYPE 2 DM,more common in african-american. This condition is called ketosis-prone type 2 diabetes Mechanism: : Mechanism: DKA absolute lack of insulin Inc glucagon Inc glucagon Dec insulin ratio Gluconeogenesis (dec conc, of F2-6-bisphosphate) Inc glucose levels Osmotic diuresis Inc liberation of FFA due to loss of inhibitory action of insulin on lipase In liver converted into ketone bodies Dec pH Metabolic acidosis Ketosis-prone ketogenesis: : Ketosis-prone ketogenesis: Exact mechanism is unknown. Occurs in type-2 diabetics. Dec insulin release due to end organ insulin resistance Increase level of glucose ketogenesis Slide 11: Dehydration occurs as a result of 2 parallel processes: Inc glucose Inc ketones acidosis Hyperglycemia glycosuria Osmotic diuresis vomiting Fluid & electrolyte depletion (Renal hypoperfusion) Clinical features:symptoms : Clinical features:symptoms predominant symptoms severe DKA Nausea -confusion Vomiting -stupor Intense thirst -5% coma Polyuria Abdominal pain hyperventilation Signs : Signs Signs of dehydration(dry mouth,skin turgor dec) Tachycardia Hypotension abd tenderness Kussmoul sign Acetone breath hypothermia Slide 14: How to approach a pt with DKA? Slide 15: History: can develpe over several days, symptoms mostly occur within 24hr. Ask abt symptoms of hyperglycemia e.g. -polyuria,polydipsia,nocturia,wt loss,muscle pains & cramps Symptoms of acidosis & dehydration: -abd pain,SOB,confusion,coma Other symptoms -vomiting,signs of inf(UTI,RTI), weakness,nonspecific malaise Physical examination: : Physical examination: Dehydration: reported in 3-5 % pts Slide 17: BP is usually normal untill last stage Tachycardia Capillary refill is maintained Pt have a smell of acetone Impaired consciousness 20% level of consciousness depends on serum osmolality ¬ on acidosis >320mosm/l s/osmolality=2(Na)+K+glucose/18 Coma 10% pts Abd tenderness Investigations: : Investigations: BSL Electrolytes Urine complete CBC ABGs RFTs X-ray chest ECG Treatment goals: : Treatment goals: Fluid replacement Dec serum glucose Electrolyte replacement Antibiotics if infection Slide 20: Management: Typical deficits: : Typical deficits: Fluid replacement: : Fluid replacement: Average fluid deficit is abt 6L -3L from ECC(0.9%NaCl) -3L from ICC (0.5%DW) However 6L is not required by every pt,it depends upon degree of dehydration. fluid deficit in L=(0.6*wt in kg)[(Na/140)-1] Scheme: isotonic saline 1L in 1/2hr 1L in 1hr then 1L in 2hr i.e 500ml/hr Slide 23: Plasma osmolality can be used to measure severity of dehydration 2(Na)+glucose/18+BUN/2.8 Subsequent fluid replacement: -hypotonic saline 0.45% at 200-1000ml/hr (because in DKA H2O loss>NaCl,both compartments will gradually be replaced) -5%DW added if BSL <250mg/dl Slide 24: Advantage of early rehydration: -restores circulatory volume -dec conc. Of catecholamines,glucagon Monitoring: -by CVP,JVP -urine output -basal crepts Complication: -ARDS -cerebral edema -hyperchloremic acidosis Insulin therapy: : Insulin therapy: Bolus dose 0.1unit/kg IV then 0.1 unit/kg/hr in a continuous infusion or bolus dose 10unit IV then 5-10units/hr If infusion not possible then 10units IM stat then 4-6units/hr IM BSL should dec by 100mg/dl/hr If BSL does not dec by 10 %,repeat loading dose,double the infusion rate every 2 hour untill BSL dec by 10% When BSL<250mg/dl,dec insulin to 1-4units/hr Slide 26: Electrolyte replacement: Potassium: : Potassium: At presentation K level is normal or high (K is shifted to ECC in exchange for hydrogen ions that accumulate in acidosis) so K is not added in 1st drip. Dec K level occurs because -osmotic diuresis -insulin shifts K insie the cells -sec hyperaldosteronism Total K loss equals 3-5meq/kg body wt k 4.0-5.0 20mmol KCl/L k3.0-4.0 30mmol KCL/L k <3.5 40mmol KCL/L Do not exceed >40meq/l. the goal is to maintain the s/K concentration in the range of 4 to 5 mEq per L Slide 28: ECG changes in hypokalemia: Inverted T wave Prominent U wave Long PR ST segment depression Sodium: : Sodium: Initial plasma Na conc are low or normal despite of H2O loss due to osmotic shift of H2O Hyponatremia occurs due to osmolar compensation for hyperglycemia Add 1.6 meq to plasma Na for every 100 mg of glucose Corrected Na= [(plasma glucose-100)1.6/100]+ measured Na Or =Na+2.4[(glucose-5.5)/5.5] Bicarbonate: : Bicarbonate: Its use is controversial because there is no diff in reduction of glucose or ketoanion May aggravate hypokalemia Can be used in pts with pH<7.0 -pH 6.9-7.0---- 44meq of bicarb in 0.45%Nacl over 30 min to 1hour -pH <6.9------88meq of bicarb Phosphate: : Phosphate: At presentation,serum PO4 may be normal or inc Total body PO4 is dec by 1mmol/kg Dec PO4 occurs because it re-enters the cell after administration of insulin & Osmotic diuresis leads to inc urinary PO4 losses. so while correcting hypokalemia give 2/3 Kcl & 1/3 KPO4.( reduces the chloride load that might contribute to hyperchloremic acidosis) Slide 32: Complications of hypophosphatemia: Respiratory depression Skeletal muscle weakness Hemolytic anemia Cardiac dysfunction Studies unable to prove that replacement of PO4 is beneficial in DKA But may be helpful in pts with Anemia CCF Pneumonia hypoxia Slide 33: Antibiotics: broad-spectrum antibiotics are given for infections,while waiting for C/S Special measures: : Special measures: Bladder cathetrization NG tubes CVP line in shocked pts For DVT prophylaxis,S/C heparin in comatose, elderly or obese pts. Subsequent monitoring: : Subsequent monitoring: Monitoring is done by making a flow sheet: Pts name age/sex Complications: : Complications: Hypotension: -can lead to renal failure -plasma expanders or whole blood is given if sys BP< 80 & not responding to NaCl Cerebral edema: -caused by rapid reduction of BSL or hypotonic fluids ARDS: -hypoxemia on ABGs or pulse oximetry Resolution: : Resolution: Resolution of DKA is defined as general improvement in symptoms e.g ability to tolerate oral nutrition &fluids, blood(pH>7.3),ketones in blood (<1 mmol/l) or none in urine. Once this has been achieved, insulin may be switched to the usual S/C regimen, one hour after which the IV administration can be discontinued. Slide 39: In pts with suspected ketosis-prone type 2 diabetes, determination of antibodies against glutamic acid decarboxylase and islet cells may aid in the decision whether to continue insulin administration long-term (if antibodies are detected), or whether to attempt treatment with oral medication. Follow up: : Follow up: Once pt is able to drink & anion gap dec & ketonuria cleared S/C insulin is started Pt is discharged on S/C insulin Dietry plan BSL charting Weekly follow up initially Prevention: : Prevention: Attacks of DKA can be prevented in known diabetics to an extent by adherence to "sick day rules"; these are clear-cut instructions to patients on how to treat themselves when unwell. Instructions include advice on how much extra insulin to take when sugar levels appear uncontrolled, an easily digestible diet rich in salt and carbohydrates, means to suppress fever and treat infection, and recommendations when to call for medical help. 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