HHNS	DKA
Replacement of fluid losses	· Resuscitate with isotonic saline (NS) initially followed by hypotonic saline (1/2NS). In HHNS water losses usually exceed sodium losses resulting in hypertonic dehydration. · If severely hyperosmolar (>330) begin with hypotonic fluids (1/2 NS). · Replace at a rate of 1 – 2 L/hr for first 1 to 2 hours followed by 1 L/hr for 3 to 4 hour. · Goal is to replace half of TBW deficit over first 12 hours and remainder in the next 24 hours.	· Initial goal is to correct intravascular volume beginning with isotonic saline (NS), then correct total body water deficit in the following 24 to 48 hours with hypotonic saline (1/2NS or D5-1/2NS). · If initial corrected serum sodium is > 150 or when calculated serum Osm >320 may begin with hypotonic saline. · Begin initial replacement with NS at 1-2 L/hr for first 1-2 hours followed by 250/hr. Over-aggressive fluid replacement can lead to symptomatic brain swelling and pulmonary edema.
Correction of hyperglycemia (and acidosis in DKA)	· Begin with hydration alone – glucose concentration may fall by 80 to 200 per hour with hydration alone. Manage HHNS using drip or SQ insulin. Because the primary problem is one of dehydration, mainstay of therapy should be rehydration. · Insulin drip may be used but remember that hydration comes first in HHNS. Subcutaneous insulin is usually sufficient and is not accompanied by the risks of hypoglycemia that one has with insulin drips. Frequent assessment of the patients’ clinical status and labs followed by judicious use of insulin is preferable to simply using an insulin sliding scale.	· The next challenge is to correct the acidosis by addressing insulin deficiency. · LOADING DOSE OF INSULIN: 0.1 to 0.2 U/kg IV · INITIATE INSULIN DRIP (5-10 U/hr) to restore euglycemia and correct acidosis while limiting rapid changes in serum osmolality. o Follow blood glucose hourly x 4 – 8 hours. o Goal of decrease of 75 – 100 of serum glucose/hr. o CHANGE IVF TO D5-1/2NS when plasma glucose reaches 250 (to avoid hypoglycemia and excessive decline in Sosm that might precipitate cerebral edema) with the goal of continuing the insulin infusion and resolving the acidosis (close anion gap). o Decrease insulin drip to Regular Insulin 1u per hour for every 100cc hr of D5-1/2NS in IVFs. · Bicarbonate controversial; avoid it in general but consider it if pH <7.0.
Electrolyte repletion	· Potassium: regardless of measured K, there is always total body K depletion (3 to 5 in DKA and 5 to 10 in HHNS). If initial measured K is normal or low there is severe K deficit. Hypertonicity, insulin deficiency, and acidosis can cause shift of K out of the intracellular space which in the setting of diuresis causes significant urinary loss of K. As rehydration and correction of hyperglycemia occurs, K reenters the cell causing further decrease of serum K. If patient has normal renal function, for the first 3 to 4 hours, add K to IVFs as follows: K < 3.5 give >40meq/L, K 3.5-4.0 give 40/L, K=4.0-4.5 give at 30/L, K=4.5-5.0 give at 20/L, K=5.0-5.3 give at 10/L. Follow K closely! · Phosphate: Like K, there is often total body phosphate deficit in both DKA and HHNS. Actual repletion of phosphate is rarely required unless it is severe (i.e., less than 1.0). Always follow serum calcium because rapid phosphate repletion can cause hypocalcemia. · Magnesium: Caution in renal failure, replace only if severe (<1.6) or in refractory hypokalemia.
Detection of Precipitants and Complications	· Infection: Associated with development of DKA or develops as a complication of DKA in 35%. Look for potential sources of infection and consider empiric antibiotics. · MI: serial troponins and ECGs should be considered even in the absence of cardiac symptoms · Cerebral edema: suspect if persistent altered mental status despite improvement of the above or if hyperglycemia reversed too aggressively. Stat head CT and mannitol IV if indicated. · Shock · Hypoglycemia or Hypokalemia · Secondary acute renal failure: May develop due to subclinical rhabdomyolysis (if suspected can follow CPK since clinical myoglobinuria is rare), thrombosis causing prerenal ARF (hyperosmolality and hypernatremia shown to alter factor VIII and cause hypercoagulable state)