1_Diabetic keoacidosis must be such as uremia, gastroenteritis with metabolic acidosis, lactic acidosis, aspirin poisoning, hypoglycemic coma, encephalitis and encephalopathy. Diabetic ketoacidosis exists when there is hyperglycemia(blood sugar>300mg/dl), ketonaemia, acidosis(ph<7.3), serum NAHCO3 <15meq/l, glucosuria and ketonuria. Precipitating factors are trauma, infection, vomiting and psychological disturbances.
differentiated from acidosis and coma due to other causes : Depending on initial presentation it may divided into 3 phases:
Treatment 1_Ketoacidosis 2_post ketotic or transitional period. 3_continuing phase.
Ketoacidosis: the immediate goal of treatment is expansion of intravascular compartment by correction of water and electrolytes depletion. The total fluid requirement = deficit + maintenance. The initial phase which is regarded as life saving measure is by giving normal saline 20_30ml/kg/hour and shift to 1/2 normal saline 0.45% NACL for the subsequent replacement therapy. Because of the hyperosmolarity of the blood the quick and rapid replacement therapy leads to shift of water into the intracellular compartment which has been implicated in development of cerebral edema which is one of the major complication of diabetic therapy in children. For the same reason 1/2 normal saline must be given after the first hour of hydration, also administration of 5% of glucose in 0.2 normal saline must be initiated when the blood sugar approaching 250mg/dl in order to limit rapid decline in serum osmolarity and reduce the risk of cerebral edema.
KCL therapy: during the second hour of hydration KCL should be given provided the patient has good urine output, the early administration of KCL is due to shift of K+ from extracellular to intracellular compartment because of correction of acidosis and use of insulin. 10_20 meq/500cc of 1/2 normal saline should be given during the second hour of hydration. ECG record and serum K level must be done initially and periodicaly to adjust K therapy.phosphate: should be replace KCL after 3 rd hour of fluid therapy for the following
Potassium causes: 1-it decreases acidosis which is almost inevitable because of excess amount of chloride. 2-it is important for formation of 2,3DPG whish is essential for utilization of O2 to the peripheral tissue, decease in 2,3DPG leads to shift of oxygen dissociating curve to the left which leads to lactic acidosis. 3-hypophosphatemia leads to resistance to insulin action.
Alkali therapy: in most of the cases, acidosis is corrected by proper fluid and electrolytes replacement and insulin therapy. However when ph <7.15 alkali therapy should be instructed because acidosis leads to 1-depression of respiratory center 2-peripheral vasodilatation and hypotension 3-myocardial dysfunction 4-resistance of insulin action 5-electrolytes 2 over 2hours then
disturbance. For ph>7.2 5 no therapy. If ph 7.15_7.25 or HCO3 40meq/m
revaluation If ph<7.15 and NAHCO3 80meq/m 2 over 2hours, then revaluation. If ph<7 then the child should be managed in ICU. Excess alkali therapy may lead to : 1-hpokalaemia by shifting of K from extra to intracellular compartments. 2-alkalosis by shifting of O2 dissociation curve to the left leading to decreased O2 to tissue leading to lactic acidosis. 3hypocalcaemia by decreasing ionized Ca. 4-paradoxical cerebral acidosis because HCO3 passes through blood brain barriers slowly while CO2 passes freely.   arrange and explain without deleting 
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