Presentation on theme: "Diabetic Ketoacidosis in Children"— Presentation transcript:
1Diabetic Ketoacidosis in Children Jim Tsung, MDBellevue Hospital Center
2DKAIs the most common cause of hospitalization of children with diabetesIs the most common cause of death in children with diabetesIs fatal in <1% (from 1-2% of children in the 1970’s)Most DKA deaths are attributable to cerebral edema (62-87%), which occurs in 0.4-1% of kids with DKACiordano B, Rosenbloom AL, Heller DR, et al: Regional services for children and youth with diabetes.Pediatrics. 1977;60:Rosenbloom AL. Intracerebral crises during treatment of diabetic ketoacidosis. Diabetes Care 1990;13:22-33.Edge J, Ford-Adams M, Dunger D. Causes of death in children with insulin-dependent diabetesArch Dis Child. 1999;81:
3BackgroundThough it varies depending on the population, 20-40% of newly diagnosed T1DM patients are in DKA.Therefore, a major goal of outpatient diabetes management is to prevent DKAwith a high index of suspicion with early DKA symptoms in new or established T1DM patientswith close supervision of established patientsPinkney J et al. Presentation and progress of childhood diabetes mellitus: a prospective population-based study.Diabetologia. 1994;37:70-74.G, Fishbein H, Ellis E. The epidemiology of diabetic acidosis: a population-based study.Am J Epidemiol. 1983;117:551
4Etiology of DKA--New Onset DM Always due to insulin deficiency--absolute or relativeMany previously undiagnosed patients have been seen in pediatric offices or ERs where a detailed history and lab studies could make the diagnosis before DKA ensuesA simple urine dip could be life-saving!High index of suspicion is especially important in infants and young children
5Etiology of DKA--Established Patients ***Failure to take insulin, especially in adolescents--most common cause of recurrent DKAAcute stress--trauma, febrile illness, psychological turmoil with elevated counterregulatory hormones (glucagon, epi, GH, cortisol)
6Etiology of DKA--Established Patients (continued) Poor sick day managementnot giving insulin because the child is not eatingfailing to increase insulin for the illness, as dictated by fingerstick blood sugarsfailure to monitor ketones
7Definition Definitions vary, but in general: Hyperglycemia > 200 mg/dlKetonemia/ketonuria--large serum or urine ketonesAcidosis with venous pH <7.3Serum bicarb <18Mild 16-22Moderate 10-15Severe <10*Sometimes DKA can occur with normoglycemia when there is continued insulin therapy, vomiting, and/or reduced intake of carbohydrates
9Presentation Hyperglycemia insulin deficiency causes decrease glucose uptake with tissue starvation, glycogenolysis, and gluconeogenesis from protein and lipid breakdown.Thirst/Dehydration 20 Osmotic Diuresis/Vomitingdehydration is usually hyperosmolar, so may be underestimated by clinical examAcidosisfrom breakdown of lipids to ketone bodies to ketoacidsFruity Odor from Acetone (ketone body, not a ketoacid)from tissue hypoperfusion/dehydration
10Presentation (continued) Kussmaul (rapid deep) respirationcompensatory response to the metabolic acidosis, contributing to dehydrationComa- due to hyperosmolarity, not acidosisCalculated osm >320 is associated with comaHyperosmolarity- largely due to glucose, calculated as:2(Na) + Glucose/ BUN/2.8Other: Na, K, BUN, Cr, WBC
11Management--GeneralResuscitation (ABC’s, O2) if in shock/poor perfusion with NS or albumin cc/kg over min, may repeat as needed, NGT if vomiting and impaired LOC.The cause of cerebral edema remains unclear.Too rapid reduction of intravascular osmolality thought to aggravate the process. Recommended to rehydrate children with DKA more slowly than in other causes of dehydration.However, newer evidence seems to question this.Start, maintain, and utilize your flowsheet!
12Management--FluidsInitial fluid bolus with NS will depend on assessment of severity of dehydrationmost kids in DKA are 10% dehydrated, unless there is hypotension, poor peripheral perfusion, etc.e.g If 10% dehydrated, should get 10 cc/kg NS over 1 hour
13FluidsIVF needed =Maintenance + Deficit + Ongoing LossesCaution: Fluids should not exceed L/m2/day, as this has been associated with cerebral edema and poor outcome (?)
14Fluids Maintenance-as per usual, amount based on weight (4/2/1 rule) Deficit replacement usually over 48 hours5% dehydration = 0.05 L/kg10% dehydration = 0.1 L/kgConsider deficit replacement over 72 hours if marked hyperosmolality (Gluc >1000 or serum osm >320) or if corrected Na is >150 mEq/Le.g. 30 kg kid with 10% dehydration has a fluid deficit of (30)(0.1)=3 Liters, 300 cc of which have already been replaced with the 10 cc/kg NS bolus, leaving a 2700 cc fluid deficit
15Fluids Ongoing losses-usually do not need to replaced If very polyuric or vomiting excessively, can replace urine/vomitus output 0.5 cc/ccReassessment of I/O’s at least every 4 hrs for first 24 hrs
16Sodium Maintenance = 3-5 mEq/kg/day Deficit = 6 mEq/kg Serum Na may be high, normal, or low depending on fluid statusMany find calculation cumbersome, so can usually use 1/2 NS as replacement fluid and NS as deficit fluid (running piggyback)
17SodiumUse NS if the corrected sodium is <140 and/or if serum osm >310*To correct Na: Add 1.6 mEq/L to the measured Na for every 100 mg/dl of glucose over 100 mg/dlMonitor electrolytes every 2 hours at first, and then every 4 hours when trend is normalizing
18PotassiumDKA is associated with total body K depletion, while correction of acidosis causes hypokalemia due to an intracellular K shift, so add K sooner rather than laterAdd K once the patient has documented urine output and no peaked T’s on ECG or K 6Hypokalemia on presentation is an ominous sign; beware of arrhythmias
19Potassium Usually add 20 mEq KCl and 20 mEq of KPhos per liter to IVFs Some centers prefer Kacetate instead of Kphos for theoretical improvement of acidosisIf even mildly hypokalemic, add 40 mEq KCl and 20 mEq of Kphos per liter. Consider K run(s) if hypokalemic.If serum K <3, hold insulin until K has been added to IVFs
20Phosphate Body Phosphate is depleted in DKA Need for replacement is controversialPhosphate should be given if there has been prolonged illness or if a prolonged period without food is anticipateCan give half of K requirement as KPhosIf Phos <3, give half of K requirement as KphosIf hypocalcemia develops, stop Phos and adjust total K as KCl
21Bicarbonate: Don’t Do It! May be given if pH < considering that severe acidosis can be life-threatening, but…Sudden correction of serum pH can paradoxically lower CSF pH, it should be given by slow IV infusion over several hoursEndogenous production of HCO3 occurs as ketones are metabolizedThe usual calculations for correction of acidosis greatly overestimate bicarbonate needed in DKAMay increase the risk of hypokalemiaBicarb use has been associated with increased risk of cerebral edema**Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:
22InsulinGoal is to decrease blood sugar by mg/dl/hr, after initial drop from rehydration, avoiding rapid dropsUsual starting dose is 0.1 u/kg/hr (100 units in 500 cc NS, 0.1 u/kg/hr=0.5ml/kg/hr)Consider starting at 0.05 u/kg/hr if new diabetic, age < 2 yrs, marked hyperglycemia (>1200), or recent large SQ insulin dose in known diabetic
23Insulin (continued)If poor response on 0.1 u/kg/hr (e.g. insulin resistance, ongoing infection), may need to increase drip to u/kg/hr, but first make sure IV is infusing properly.Continue insulin infusion until ketonemia is cleared/clearing. Adjust rate of drip to maintain blood glucose Do not decrease drip below 0.03 u/kg/hr. If pt is becoming hypoglycemic at this rate, increase dextrose concentration.
24GlucoseAdd D5W to IVF when glucose drops below mg/dl. If necessary, may further increase dextrose concentration to D7.5 - D10.Consider “2 Bag System” *: One bag NS/0.45NS & 2nd bag D10 NS/0.45NS given simultaneously to vary dextrose concentration while maintaining constant fluid and electrolyte adminstration.More cost-effective than single bag systemMonitor glucose hourly either by fingerstick (if within range of the meter) or by grey top glucose.*Grimberg A, Cerri R, Satin-Smith M, et al. The "two bag system" for variable intravenous dextrose and fluid administration: benefits in diabetic ketoacidosis management. J Pediatr. 1999;134:376-3
25OtherIf patient is not improving, reevaluate IVF calculation, insulin delivery system and dose, change insulin bag, consider sepsis and antibiotics.
27Risks Factors for Cerebral Edema New Onset DKA (OR-2.9) and YoungerHigher blood urea nitrogen concentrationsPresenting with greater hypocapnia (↓PCO2)A lesser rise in the measured serum sodium concentration during treatment (as the serum glucose concentration falls)Bicarbonate administrationNo association found for rate of infusion, volume, rate of change of glucose or sodium concentrationsEdge JA, Hawkins MM, Winter DL, Dunger DB. The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child. 2001;85:16-22.Glaser N et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. N Engl J Med. 2001;344:Mahoney C, Vlcek B, DelAguila M. Risk factors for developing brain herniation during diabetic ketoacidosis. Pediatr Neurol. 1999;21:
28Signs & Symptoms of Cerebral Edema during DKA Treatment Most commonly occurs in the first 24 hrs (5-15 hrs) after starting rehydration therapy when the child may seem to be improvingDoes occur prior to treatment in 5% of cerebral edemaHeadache-most often sudden, severeAltered Mental Status--agitation, combativeness, disorientation, increased drowsiness, incontinenceFocal Neurologic Signs-cranial nerve palsies, opthalmoplegia, posturingPapilledema, seizures, resp arrest are late signs with a very poor prognosis
29Signs & Symptoms of Cerebral Edema during DKA Treatment pupillary changes (asymmetry, sluggish to fixed)change in VS: hypertension or hypotension, tachycardia, bradycardia, or arrhythmia, apnea, gasping, decr 02 satfalling corrected Namust exclude hypoglycemia as a cause of the symptoms before instituting therapy
31Cerebral Edema Treatment Mannitol should be immediately available during DKA treatmentExclude hypoglycemiaMannitol 1 g/kg IV over 20 minutesCut IVF rate in half until situation improvesNGT in vomiting child with impaired LOCElevate headConsider intubation/hyperventilationBut, has been associated with poorer outcome*Consider continuous mannitol infusionHead imaging (CT/Eyeball US) after stabilized as hemorrhage, thrombus, or infarct may also occur*Marcin J, Glaser N, Barnett P, et al. Clinical and therapeutic factors associated with adverse outcomes in children with DKA-related cerebral edema. J Pediatr. 2003;141:
32Other Complications to Watch For: Pulmonary EdemaCNS hemorrhage or thrombosisOther large vessel thrombosis (femoral catheter)Pancreatitis (salivary amylase elevated; check lipase)Renal FailureIntestinal necrosisRhinocerebral Mucormycosis
33Transport IssuesOn call for Established T1 Diabetic may consider Sliding Scale:Calculate the present total daily dose (TDD) of insulin (fast plus slow acting).Blood glucose mg% and urine ketones negative - give 10% TDDBlood glucose mg% and urine ketones positive - give 20% TDDBlood glucose >400mg% - give 20% TDDAvoid use of sedatives or anti-emetics during transport to avoid masking symptoms associated with cerebral edemaMake sure the transport glucometer is working!
34Primum Non Nocere Do not give bolus insulin Do not give boluses of sodium bicarbonateDo not start insulin until a fluid bolus has been given and maintenance fluids begun. This may wait until admission to the hospital if this occurs within 2 hours of admission to the ED.Do not give more than 20cc/kg as a single fluid bolus. (?)Do not give more than a total of 30cc/kg of bolus fluids unless the patient is in shock. (?)Do not give more than 3750cc of maintenance fluids in 24 hours (2500cc/m2/24hrs). (?)