A) Pathology: Occurs in the setting of absolute insulin deficiency or relative insulin defiicency with counter-regulatory hormone excess --> Hyperglycemia --> inc Ketone Bodies (B-Hydroxybutyrate and Acetoacetate) --> inc Anion Gap.
   B) Clinical Findings
      1) Precipitating factors: Infection, insulin and/or dietary noncompliance, pregnancy, cardiovascular event (MI), trauma
       2) Manifestations: Polyuria, polydypsia, anorexia, nausea, vomiting, abdominal pain, ileus, dehydration, Kussmaul's respirations, acetone halitosis, delta MS
       3) Diagnosis: Requires an anion-gap metabolic acidosis with hyperketonemia in a hyperglycemic patient. Hyperketonemia established by the nitroprusside reaction which documents only inc AcAc and not inc BOHB.
   C) Management (Identify and treat precipitating event)
       1) Volume resuscitation for an initial fluid defecit of 10 --> 15% of IBW with normal saline. Avoid initial use of hypotonic saline which can cause cerebral edema \n
       2) K+ losses are usually increased unless renal insufficiency is present. Seial serum K+ measurements are essential for titrating K+ replacement during initial therapy \n
       3) Acidosis therapy with sodium bicarbonate is controversial. Bicarbonate therapy may be appropriate for patients with pH <= 7.0 and its use continues to be controversial. Potential harmful effects of bicarbonate therapy include dec K+, paradoxical CNS acidosis, systemic metabolic alkalosis, tissue anoxia, and dec ketone metabolism \n
       4) Insulin replacement with initial IV bolus of 5-10 units regular insuline followed by 0.1 u/kg/hr of either IM or IV bolus or continuous drip. Continue with intensive insulin therapy until anion gap normalizes and then swith to subcutaneous regular insulin q 4-6 hr. D5 should be started when glucose <= 250 mg%. Intermediate or long acting insulin should be restarted once anion gap normalizes with acute regular insulin therapy after 48 - 72 hours. Avoid hypoglycemia due to aggressive insulin administration or lack of adequate glucose administration
       5) Correct hypophosphatemia and hypomagnesemia
       6) Avoid ARDS with volume overload, and hyperchloremic acidosis with excessive chloride administration.