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1、Diabetic ketoacidosis(DKA),emergency department of shengjing hospital zhang hong lei,case,Mr wang，M，52 years oldchief complaint：polydipsia,polyuria,weakness for1week，vomiting for 10 hourphysical exam:tachypnea,BP 150/90mmHg,HR:120bpm,SaO2:99%ABG:PH:7.06,PaCO2:12mmHg,PaO2:117mmmHg,HCO3-:3.4mmol/L,Lac
2、tate:3.1mmol/L,BE:-24.7mmol/L，AG:34.6mmol/LBUN:15.9mmol/L,Cr:147mmol/LK+:8mmol/L,Na+:118mmol/L,Cl-:80mmol/L,Glu:33mmol/Lurinalysis:ketone:3+,gravity:1.024,glu:4+,problem,what is the diagnosiswhat is the reason of hyperkalemia and hyponatremiawhat is the reason of Metabolic acidosishow to dispose the
3、 disease if you are the ER doctor on call,Introduction,DKA is a syndrome in which insulin deficiency and glucagonexcess combine to produce a hyperglycemic,dehydrated,acidotic patient with profound electrolyte imbalance,Pathophysiology,Pathophysiology,Pathophysiology,Insulin deficiency and glucagon e
4、levation results in hyperglycemia,which in turn cause glycosuria Glucose in the renal tubules draws water,sodium,potassium,magnesium,calcium,phosphorus,and other ions from the circulation into the urine This osmotic diuresis combined with poor intake and vomiting produces the profound dehydration an
5、d electrolyte imbalance associated with DKA As a result of acidosis and dehydration,however,the initial reported values for these electrolytes may be higher than actual body stores.,Pathophysiology,Insulin deficiency results in activation of lipase that increases circulating free fatty acid(FFA)leve
6、ls.Long-chain FFAs,now circulating in abundance as a result of insulin deficiency,are partially oxidized and converted in the liver to acetoacetate and-hydroxybutyrate.This alteration of liver metabolism to oxidize FFAs to ketones rather than the normal process of re-esterification to triglycerides
7、appears to correlate directly with the altered glucagon/insulin ratio in the portal blood.,Pathophysiology,Glucagon is elevated fourfold to fivefold in DKA and is the most influential ketogenic hormone.Despite the increased pathologic glucagon-mediated production of ketones,the body acts as it does
8、in any form of starvation,to decrease the peripheral tissues use of ketones as fuel.The combination of increased ketone production with decreased ketone use leads to ketoacidosis.The acidosis cause the body to increase lung ventilation and rid the body of excess acid with Kussmauls respiration,Etiol
9、ogy,DKA may be caused by cessation of insulin intake or by physical or emotional stress despite continued insulin therapy.Most often,DKA occurs in patients with type 1 diabetes and is associated with inadequate administration of insulin,infection,or myocardial infarction(MI).DKA can also occur in ty
10、pe 2 patients and may be associated with any type of stress,such as sepsis or gastrointestinal(GI)bleeding,Diagnostic Strategies,History Clinically,most patients with DKA complain of a recent history of polydipsia,polyuria,polyphagia,visual blurring,weakness,weight loss,nausea,vomiting,and abdominal
11、 pain.,Diagnostic Strategies,Physical Examination Typical findings include tachypnea with Kussmauls respiration,tachycardia,frank hypotension,the odor of acetone on the breath,and signs of dehydration,Diagnostic Strategies,Laboratory Tests On the patients arrival to the ED,serum and urine glucose an
12、d ketones,electrolytes,and arterial blood gases(ABGs)should be checked.Glucose is usually elevated above 350 mg/dL;however,euglycemic DKA(blood glucose 300 mg/dL)has been reported in up to 18%of patients.ABGs demonstrate a low pH.Metabolic acidosis with an anion gap is primarily the result of elevat
13、ed plasma levels of acetoacetate and-hydroxybutyrate,although lactate also contribute to this condition,Diagnostic Strategies,Laboratory Tests A complete urinalysis helps in the determination of urine ketone.Elevations of urine specific gravity,BUN,and hematocrit suggest dehydration,Diagnostic Strat
14、egies,Laboratory Tests Sodium is often low in the presence of significant dehydration because it is strongly affected by hyperglycemia;hypertriglyceridemia;salt-poor fluid intake;and increased GI,renal,and insensible losses When hyperglycemia is marked,water flows from the cells into the vessels to
15、decrease the osmolar gradient,thereby creating dilutional hyponatremia.Lipids also dilute the blood,thereby further lowering the value of sodium,Diagnostic Strategies,Laboratory Tests Acidosis and the hyperosmolarity induced by hyperglycemia shift potassium,from the intracellular to the extracellula
16、r space.Dehydration produces hemoconcentration,which contributes to normal or high initial serum potassium readings in DKA,even with profound total body deficits While insulin is administered and the hydrogen ion concentration decreases,the patient needs considerable potassium replacement.,Diagnosti
17、c Strategies,Laboratory Tests All laboratory determinations must be interpreted with caution.The diagnosis of pancreatitis is confounded by the usually elevated urine and serum amylase levels in DKA.Typically,this is salivary amylase,but most laboratories are not equipped to make this distinction.A
18、serum lipase determination helps to distinguish pancreatitis from elevated salivary amylase levels.,Differential Considerations,Alcoholics,especially those who have recently abstained fromdrinking,with Kussmauls respiration,and acidemic ABG values may have alcoholic ketoacidosis.These patients may b
19、e euglycemic or hypoglycemic,Alcoholic ketoacidosis accounts for approximately 20%of all cases of ketoacidosis.Ketoacidosis can also develop with fasting in the third trimester of pregnancy and in nursing mothers who do not eat,Differential Considerations,Other entities that may manifest with variou
20、s combinations of altered mental status,acidosis,and abdominal pain include hypoglycemia,cerebrovascular accident(stroke),trauma,sepsis,hyperglycemic hyperosmolar nonketotic coma,postictal states,lactic acidosis,uremic acidosis,and abdominal emergencies.Intoxications by ethanol,salicylates,methanol
21、all share some features of DKA.,Management,General Measures The comatose patient,especially if vomiting,requires intubation.The patient in hypovolemic shock requires aggressive fluid resuscitation with 0.9%saline solution.When hyperglycemia,ketosis,and acidosis have been established,fluid,electrolyt
22、e,and insulin therapy should begin,Management,Dehydration The severely dehydrated patient is likely to have a fluid deficit of 3 to 5 L.Fluid rate should be adjusted according to age,cardiac status,and degree of dehydration to achieve a urine output of 1 to 2 mL/kg/hr.Fluid resuscitation alone may h
23、elp to lower hyperglycemia.,Management,Insulin DKA cannot be reversed without insulin,and insulin therapy should be initiated as soon as the diagnosis is certain.In the past,very high dosages of insulin were administered to diabetic patients in DKA because they were thought to be extremely insulin-r
24、esistant.However,low-dosage insulin therapy has proved as effective as high-dosage therapy High dosages of insulin have potentially harmful effects,including a greaterincidence of iatrogenic hypoglycemia and hypokalemia.The current therapy of choice is regular insulin infused at 0.1 U/kg/hr upto 5 t
25、o 10 U/kg/hr,mixed with the IV fluids.,Management,Insulin Because the half-life of regular insulin is 3 to 10 minutes,IV insulin should be administered by constant infusion rather than by repeated bolus.When the blood glucose has dropped to 250 to 300 mg/dL,dextrose should be added to the IV fluids
26、to prevent iatrogenic hypoglycemia and cerebral edema.In patients with euglycemic DKA,dextrose should be added to the IV fluids at the start of insulin therapy,Management,Potassium Potassium replacement is invariably needed in DKA.The initial potassium level is often normal or high despite a large d
27、eficit because of severe acidosis.Potassium levels often plummet with correction of acidosis and administration of insulin.Potassium should be administered with the fluids while the laboratory value is in the upper half of the normal range.Renal function should be monitored.In patients with low seru
28、m potassium at presentation,hypokalemia may become life-threatening when insulin therapy is administered.IV potassium should be vigorously administered in concentrations of 20 to 40 mEq/L as required.,Management,Magnesium Magnesium deficiency is a common problem in patients with DKA without renal di
29、sease.Both the initial pathophysiology and the therapy for DKA induce profound magnesium diuresis.Magnesium deficiency may exacerbate vomiting and mental changes,promote hypokalemia and hypocalcemia,or induce fatal cardiac dysrhythmia.it is reasonable to include 0.35 mEq/kg of magnesium in the fluid
30、s of the first 3 to 4 hours,with further replacement dependent on blood levels and the clinical picture.,Management,Acidosis Acidosis also decreases after fluid infusion alone.Increased perfusion improves tissue oxygenation,thus diminishing the formation of lactate.Increased renal perfusion promotes
31、 renal hydrogen ion loss,the improved action of insulin in the better-hydrated patient inhibits ketogenesis.Bicarbonate therapy may be indicated in severely acidemic patients(pH 7.0).The use of bicarbonate is not warranted in less ill patients When bicarbonate therapy is deemed necessary,the pH shou
32、ld not be corrected above 7.1.,Prognosis,The precipitating causes of DKA may have associated morbidityand mortality rates equal to or worse than those for DKA itself.These include iatrogenic causes as well as infection and MI.Morbidity in DKA is largely iatrogenic:(1)hypokalemia from inadequate pota
33、ssium replacement,(2)hypoglycemia from inadequate glucose monitoring and failure to replenishglucose in IV solutions when serum glucose drops below 250 to 300 mg/dL(3)alkalosis from overaggressive bicarbonate replacement,(4)congestive heart failure from overaggressive hydration,(5)cerebral edema pro
34、bably caused by too rapid osmolal shifts.Poor prognostic signs include hypotension,azotemia,coma,and underlying illness,Summary,Diabetic Ketoacidosis（DKA）manifests clinically as a triad:hyperglycemia(usually200 mg/dL),ketonemia,acidemia(pH 7.3).DKA can be caused by any condition that reduces insulin
35、 availability or activity or that increases glucagon.Precipitating events usually include infections,surgery,and emotional orphysical stressors.Treatment is aimed at fluid replacement over the first 24 to 48 hours,insulin replacement,and potassium replacement.,key,what is the diagnosis DKAwhat is th
36、e reason of hyperkalemia and hyponatremia As a result of acidosis and dehydration,however,the initial reported values for potassium may be higher than actual body stores.Sodium is often low in the presence of significant dehydration because it is strongly affected by hyperglycemia;hypertriglyceridem
37、ia;salt-poor fluid intake;and increased GI,renal,and insensible losseswhat is the reason of Metabolic acidosis Metabolic acidosis with an anion gap is primarily the result of elevated plasma levels of acetoacetate and-hydroxybutyrate,how to dispose the disease if you are the ER doctor on call Treatment is aimed at fluid replacement over the first 24 to 48 hours,insulin replacement,and potassium replacement,thanks for attention,
