DKA

Definition:

Hyperglycemia >120mg/dL (generally 300 mg/dL) and ketoacidosis 2ry to  insulin insufficiency.  This can be simplified as following:
¯ insulin ®­ gluconeogenesis in liver (then  protein breakdown)
® glyconeolysis + lipolysis (­ in FFA) ® hyperglycemia ® osmotic diuresis

Etiology:

1. Wrong dosage
    
2. UTI
    
3. MI
    
4. Infection
    
5. Thyroid pathology
    
6. Pregnancy
    
7. Pancreatic CA or 90% pancreatic removal 2ry to Whipple
    
8. No cause found

1. N/V, Abdominal pain
    
2. Hypotension / Tachycardia / Poor skin turgor / Dry muocsa 2ry to hypovolemia
    
3. Tachypnea (to compensate for acidosis) = Kussmaul
    
4. ¯MS. This is important since it is directly influenced by  Osmolality.
    
5. Hypothermia can occur.

Labs / DX:

1. ­ glucose >300mg/dL, pH <7.3, Ketonemia & AG acidosis. Note that markedly elevated  ketonemia may not be evident on lab    result since only acetoacetate is measured. If ketoacidosis is 2ry to b-hydroxybutyric acid, one may miss the presence of mild ketosis in acidotic pt.  Ketosis may not be evident if pt is well hydrated and has good UO. By spilling ketones in the urine, kidney retains Chloride. The  retention of Chloride is balanced with HCO3 excretion and AG remains near normal, masking both ketosis and lactic acidosis. If this pt is given 0.9% NS as IVF, Chloride retention will continue to increase while HCO3 will continue to fall and pt will develop  Hyperchloremic Metabolic Acidosis. In this case 1/2NS would be a better choice.  The above mechanism also explains why HCO3 on SMA shouldn't be used as a guideline to the treatment. One must follow the AG, not the HCO3, when treating DKA.
    
2. CBC to R/O infection. Also will show hemoconcentration.
    
3. SMA will estimate glucose, AG acidosis = Na-(Cl+HCO3), prerenal azotemia, hyponatremia. To avoid errors  the real Na+ decreases by 1.6mEq/L for every 100mg/dL glucose above l00 mg/dl of glucose.
    
4. Frequent K+ monitoring. May be high initially, but drops precipitously  with use of insulin. EKG may be helpful to detect K+ levels ( peaked T if   ­ K or  ST¯ and U waves  if ¯ K ).
    
5. Ca++ ( can be ¯ 2ry to hyperventilation. EKG will show >QT), Mg++ , PO4, serum Ketones.
    
6. R/O infection ( CXray, UA, blood culture, skin ulcers/cellulitis),  R/O MI (EKG, CPK).
    
7. ABG does not add any information. pH can be measured with VBG (difference between VBG pH and ABG pH is 0.05). It is also of notice that the pH, if compensated, does not tell us about metabolic acidosis state - i.e. AG . There is no need to estimate pCO2 since there is no retention. There is no need to  know pO2 since oxygenation is not affected. The HCO3 value is more accurate from SMA.
    
8. Osmolality calculated as follows: 2(Na) + (glucose/18) + (BUN/2.8).

Treatment:

1. Correct fluid deficit in pt presenting in DKA. The deficit can be as high as 5-10L and Na+ deficit can be 400mEq/L. Thus IVF in form of NS over ½- 1hr is most important initial modality of treatment. In people susceptible to fluid overload, CVP monitor is advised. NS IVF is then given @ a rate of 200-250ml/hr until serum glucose is 250 mg/dL and then is switched to D5NS or D51/2NS
    
2. Insulin 10 Units  IV push then  0.1 U/kg/hr (7 U/hr) and do FS q2hr. The goal is to decrease  glucose by 50mg/dL/hr and not lower than 250mg/dL, then  titrate downward.
    
3. K+ should be added when this is <5.5mEq/L in form of KCl ( or K2PO4 if PO4 is < 1.0 mmol/kg)
    
4. The need of  HCO3 is guided by serum pH (not by bicarb level) and is given when this is 7.1 or lower. Bicarb administration may cause unnecessary OxyHgb curve shift to Left preventing O2 unloading. It also can create paradoxical cerebral acidosis since CO2 generated by HCO3, crosses the BBB while HCO3 does not.
    
5. HypoPO4 is corrected if this is <1.0 mmol/kg and given in the form of K2PO4 ( if K is low) or NaPO4. There is no evidence that PO4 repletion offers significant improvement in outcome except perhaps pts  at risk for low phosphate such as angina or pregnancy in order to ­ 2,3 DPG.
    
6. As pt is treated he/she may develop a rise in ketones, because as the ketosis improves betahydrobutiric acid converts to  acetoacetate, which is measured by serum ketone assay, and indicates improvement. Thus,  one may  erroneously interpret this as deterioration in pt's state rather  than improvement. Thus, ketones can not be used as treatment guideline. Follow AG instead. When checking ketones, always check for serum ketones, not urine ketones.

1. Admit to ICU if hemodynamically  unstable.
    
2. Pt in mild DKA that improves in  the ER with IVF and insulin and ketonemia resolves, as long as infection and other precipitating factors such as MI are ruled out, pt can go to floor or even dc home  if no more IVF needed.

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