Patient information zAge:27 y/o zgender:female zID:U zadmission date:94/1/1 zchief complaint:sudden dizziness and vomiting
Present illness zThis 27 y/o woman is a patient of IDDM diagnosed in 92/01 and recieved insulin control since then (currently Norvomix 34 IU QDAC + 20 IU QNAC). She is also a patient of Grave`s disease s/p subtotal thyroidectomy in 87/11.She was in usual health status until last night, sudden dizziness and nausea, vomiting awoke her.She was sent to our ER. At ER, her vital sign was stable, no fever.
Present illness zBlood sugar level was 550mg/dL. ABG revealed metabolic acidosis (pH 7.256, PCO2 25.6mmHg, HCO3 11.5mmol/L). U/A revealed glucose 3+ and ketobody 3+. According to her self,she did not take insulin for one dose.Under the impression of DKA, she was admitted for further treatments.
Physical examination zGeneral appearance : acute ill-looking. zConsciousness : alert. zMentality and cognition : good. zT/P/R : 37.7/137/22, BP: 152/68 mmHg. zHEENT : OP scar over low neck. zBreath sound : clear. zHeart sound : RHB, no murmur. zBowel sound : normoactive. zAbdomen : soft, flat, no tenderness, no palpable mass. zExtremities : freely movable, no edema.
Clinical course zAdmitted on 94/1/1 and RI pump use zchange to SC insulin on 94/1/2 zdischarge on 94/1/7 z 出院帶藥 -Humulin N 10 QNAC 10 IU -Humulin R 10 QNAC 12 IU -NovoRapid Pe QDAC 16 u -NovoRapid Pe QLAC 16 u
Introduction-DKA zepidemiology:DKA accounts for 14% of hospital admissions for diabetes in America. zDiagnosis criteria:hyperglycemia (serum glucose greater than 300 mg/dL) and metabolic acidosis (pH less than 7.30 and HCO3 less than 15 mEq/L) accompanied by ketonemia, ketonuria (acetone, s- hydroxybutyrate, and acetoacetate)
pathophysiology zDKA is always caused by insulin deficiency, either relative or absolute zInsulin deficiency results in decreased glucose uptake with tissue starvation resulting in proteolysis and lipolysis providing amino acids and glycerol for gluconeogenesis;in the liver, insulin deficiency results in glycogenolysis,enhanced gluconeogenesis and ketogenesis.
Clinical presentation-symptom and sign zAbdominal pain,usually diffuse zaltered mental status zkussmaul respiration:rapid and deep breath znausea,vomiting zpolydipsia,polyuria zconsider DKA in any ill-looking children.
Clinical presentation-lab zSerum glucose:usually >300 mg/dl zserum ketosis and ketonuria zhigh anion gap metabolic acidosis zelevated amylase or even lipase zelevated lipase is not diagnostic of pancreatitis.Many conditions result in elevated lipase and amylase without evidence of pancreatits. zKetonuria:positive in dehydration,starvation,diabetic ketoacidosis (DKA),alcoholic ketoacidosis
Management zFluid zelectrolyte zinsulin zmonitor zdeal with precipitating factor zr/o possible complications
Management-fluid zFluid deficit:usually 100 ml/kg zinfusion rate:give the first liter immediately,and then 150ml ~500ml/hr according to clinical judgement(including osmolarity,absence or presence of pulmonary edema and so on).Fluid replacement is usually completed in about 24 hrs. zfluid selection:use N/S until serum sugar is lower than 250 mg/dl.Use D5W or suntose after serum sugar is lower than 250 mg/dl.If initial serum sodium> 155meg/l,give half N/S. zfluid could be discontinued if oral intake is well tolerated.
Management-insulin zRI pump:100 u in 100 ml fluid.The serum sugar should decreased at a rate of 75 mg/dl in the first hour. zAfter serum sugar reached 250 mg/dl,change fluid to D5W or suntose. zKeep serum sugar in 150mg/dl~250 mg/dl for one or two days to close anion gap and make condition stable. zChange to SC insulin after anion gap was closed and condition was stable.It usually takes one or two days from RI pump to SC insulin and seems there is no clear point to guide when to change to SC insulin. zThe dose of SC insulin could be:A.M.—2/3 total insulin dose (2/3 intermediate-acting, 1/3 short-acting) and P.M.—1/3 total insulin dose (1/2 intermediate, 1/2 short-acting) zothers:1)since insulin binds to the IV tubing, run off about 50 to 100 mL to saturate all the binding sites in the system before connecting the tubing to the patient.2) the insulin drip and dextrose infusion are discontinued 30 to 60 minutes after the first dose of SC insulin.3)hold insulin if initial serum potassium was lower than 2.5 mmol/l.
Management-electrolyte zSodium—6 mEq/kg (range 5 to 13 mEq/kg) zPotassium—5 mEq/kg (range 4 to 6 mEq/kg) zChloride—4 mEq/kg (range 3 to 9 mEq/kg) zPhosphate—3 mEq/kg (range 2 to 5 mEq/kg)
Management-electrolyte zReplacement potassium may be given half as potassium acetate (KAc) and half as potassium phosphate (KPO4). Acetate is converted to bicarbonate in the liver and can help correct metabolic acidosis. Using potassium chloride in fluid replacement is not recommended because it causes hyperchloremic metabolic acidosis, which may be associated with a lower rate of recovery from DKA, although studies have not confirmed this.
Management-electrolyte zPotassium:usually mEq/hr,and adjust according to serum potassium level. zHold insulin if serum potassium is lower than 2.5 mEq/l zconsider phosphate replacement only if serum phosphate is lower than 1 mg/dl.
Deal with precipitating factor zFailing to take insulin, the most common cause of recurrent DKA, particularly in adolescents(insulin should be injected,even the patient is NPO for some reasons.) zinfection,the second most common factor zother physical or emotional stress condition.
R/o possible complication-cerebral edema zincidence is estimated to be 0.7 to 1.0 per 100 episodes of DKA and is inversely related to age. It occurs rarely in patients over 20 years of age.Mortality is about 70%, and only 7% to 14% of patients recover fully. zCerebral edema usually occurs about six to 12 hours after initiation of therapy.Cerebral edema is rare before 3.5 hours and after 22 hours.
R/o possible complication-cerebral edema zS/s:persistent headache,altered mental status, pupillary changes, seizures, and abnormal vital signs—tachycardia, bradycardia, hypotension, hypertension, or irregular respirations. zTreatment:elevate the head of the bed to 30°,Infuse mannitol 1 g/kg immediately,intubate the patient using rapid sequence induction and hyperventilate to PaCO2 25 to 30 torr,restrict IV fluids,obtain an urgent head CT scan
R/o possible complication-cerebral edema zRisk factor:1)higher BUN concentrations and 2)more severe hypocapnia.3)Smaller increases in the serum sodium concentration during therapy.4)treatment with bicarbonate. Neither the initial serum glucose concentration nor the rate of change in the serum glucose concentration during therapy was associated with the development of cerebral edema, after adjustment for other covariates; the same was true of the rates of fluid, sodium, and insulin administration.
R/o possible complication-cerebral edema zPathophysiology 1.old hypothesis:caused by the accumulation of osmolytes in brain cells exposed to hyperosmolar conditions. A rapid decrease in extracellular osmolality during treatment would then result in osmotically mediated swelling of the brain 2.new hypothesis:cerebral edema in children with diabetic ketoacidosis is related to brain ischemia-based on the fact that cerebral edema is not necessarily caused by therapeutic intervention and hypocapnia-,age-,treatment with bicarbonate-,BUN concentration-related.