Diabetic Ketoacidosis: Glucose remains in the bloodstream (Range:300-800)
Usually type 1 (insulin deficit) but can occur in type 2’s
CAUSES:
#1 – Infection (UTI, pneumonia, etc.); missed or inadequate insulin; Newly Diagnosed
If untreated can lead to:
Hyperglycemia: 3 P’s: Polyphagia = hunger; Polyuria = urination; polydipsia = thirst
Increases plasma osmolality
Cellular dehydration (body attempts to return plasma osmolality to normal)
Major diuresis = loss of Na; K; Phosphorous
Ketosis:
Gluconeogenesis is the conversion of non carbs (fats) into glucose. The breakdown of fats produces ketones which
go into the blood stream and produce ketonemia and ketonuria.
Acidemia:
Acid ketones dissociate and hydrogen ions are released which pH and acid goes into the blood
Na and HCO3 are usually there to buffer the H+ ions but they are lost in the urine and are missing.
ASSESSMENT FINDINGS:
HA, Malaise, Polyuria, Polydipsia, Polyphagia
Later: N/V, Anorexia, dehydration LATE: LOC, Coma
PHYSICAL EXAM:
Fluid Volume Deficit or IVVD S/S: Flushed dry skin, Facial rubor, Dry mucous membranes, skin tugor, tenting >
3 seconds, sunken eyes
Tachycardia; hypotension
Fruity breath; Kussmauls (Deep rapid respirations) = Body compensating by trying to “breath” off the excess
acid.
LAB:
Serum Na (If elevated could indicate dehydration)
*****Initally Serum K = H+ ions go into the cell “pushing” the K out causing excess K in the blood (When
acidosis is fixed K goes back in)
Serum C02 (on renal panel) otherwise known as HCO3 is less than <15 = METABLOIC ACIDOSIS
Anion Gap = Normal 8-14 Formula: Na-Chloride+CO2
High Anion Gap > 14 metabolic acidosis: ketoacidosis, lactic acidosis, toxic ingestion, renal failure
Normal or non-anion gap metabolic acidosis: GI or Renal r/t loss of bicarbonate
TREATMENT:
Hydration Therapy: Fluid deficit may be 4-10L
Lowers the hyperglycemia by: Dilution; GFR
Type: N/S; ½ N/S
o Acute phase: NS 500/Hr; ½ NS 250/Hr (FAST)
o Phase 2: (Maintenance) ½ NS 100-250/Hr
o Phase 3: (Stable) Convert to Sub Q insulin…and D5W or D5 ½ NS to lower the glucose slowly
Insulin:
Regular insulin IV Bolus 0.1-0.4 U/Kg
CI Regular = b/c of low perfusion r/t IVVD ; 1:1 ratio (100U insulin: 100mL NS); Math Question: 10U insulin
= ___ mL/Hr? ANS:10
(If you give sub Q with IVVD, insulin won’t be used properly and when the IVVD is fixed they will get hit with all
the insulin at once)
Usually 5-10 U/Hr initially; then 3-6 U/Hr (May need to double the dose Q1-2 Hr if the glucose isn’t responding
properly and going down)
Goal is to serum Glucose by 75-100 Mg/DL PER HOUR!
Ketosis and Acidemia take longer to correct than the glucose…So even when glucose is approaching normal…
Still continue Insulin.
Blood Glucose is 250 mg/dl CHANGE IVF from NS to D5 ½ NS to prevent hypoglycemis and cerebral edema.
*Cerebral Edema occurs when the glucose is reduced too quickly
, S/S HYPOglycemia: confusion, slurred speech; anxiety; weakness; jitteriness; hunger; sweating; nervousness;
dizzy
TX HYPOglycemia: AAO – candy, juice, milk, fruit, icing Unconscious – IV D50
Potassium Supplement: Regardless of initial Serum K HYPOkalemia causes Ventricular Dysrythmias!!!!!
Hydration decreases the serum K
Correction of acidosis decreases the serum K when the H+ ions go out and the K goes back into the cell
Insulin carries the K back into the cell which decreases the serum K
Start the K supplement as long as there isn’t a marked elevation in K, no EKG changes, & GOOD RENAL
FUNCTION!
********SO if you see this pt. with ½ NS and 40 KCL Piggy back at 175mL/Hr this is why
LABS frequently Q 1-2 Hr until WNL the Q 6-8 Hr
May see split K replacement with Phosphate (PO4) in form of KPO4 if they are low on phosphate
Bicarbonate:
Not necessary when pH > 7.1 (No clear guideline between 6.9-7.1)
pH< 6.9 add NaHCO3 to IVF NEVER GIVE IVP Add to D5W or ½ NS to make IVF isotonic
DANGER if corrected too quickly…osmotic disequilibrium…..cerebral edema
Hyperglycemic Hyperosmolar NON-Ketotic Syndrome (HHNS)
******Hyperglycemia and hyperosmolarity are biggest problem….but NO ketosis or metabolic acidosis.
Main difference is DKA has no insulin; HHNS has a low level of insulin that will not prevent the hyperglycemia
but enough to prevent breakdown of fats, which prevents ketoacidosis.
Occurs most often in 50-70 YO with Hx of diabetes or mild Type 2
Precipitating event: Acute illness; Meds that increase insulin dependency like Thiazides
Signs & Symptoms:
Osmotic diuresis from hyperglycemia
Serum Glucose 600-1200 mg/dl; Serum osmolality > 350
PROFOUND dehydration (IVVD)
Hypotension; HYPERnatremia
Mental status changes with focal neuro deficits and hallucinations secondary to cerebral edema and
dehydration r/t hyperosmolality
Medical Management:
Fluid Replacement N/S or ½ NS…Watch for CHF
Correct electrolytes
Insulin administration…Glucose will drop as hydration increases so less insulin b/c no ketoacidosis
BUT may still see CI Regular insulin and addition of Dextrose as serum glucose approaches 250
(ATN) Acute Tubular Necrosis/ACUTE KIDNEY INJURY
AKI-sudden dec. in renal function manifested by accumulation of waste metabolites
-kidney cannot form and excrete urine
* recovery depends on health status
CAUSES: hypoTN, hypoVOLemia, nephrotoxic agent exposure
CATEGORIES OF ARF
-pre-renal: involves external pbl from kidney
reduce bld flow leading to dec GFR
low urine NA
CAUSES: HYPOVOLEMIA, DEC. co, DEC SVR
-intrarenal: direct dmg in kidney
-Acute Tubular necrosis: dmg to kidney caused from surg with hypoTN/hypoVOL....ischemia and sepsis #1
NSG: look at VS during surg
-Post Renal: mechanical obstruction to outflow
Usually type 1 (insulin deficit) but can occur in type 2’s
CAUSES:
#1 – Infection (UTI, pneumonia, etc.); missed or inadequate insulin; Newly Diagnosed
If untreated can lead to:
Hyperglycemia: 3 P’s: Polyphagia = hunger; Polyuria = urination; polydipsia = thirst
Increases plasma osmolality
Cellular dehydration (body attempts to return plasma osmolality to normal)
Major diuresis = loss of Na; K; Phosphorous
Ketosis:
Gluconeogenesis is the conversion of non carbs (fats) into glucose. The breakdown of fats produces ketones which
go into the blood stream and produce ketonemia and ketonuria.
Acidemia:
Acid ketones dissociate and hydrogen ions are released which pH and acid goes into the blood
Na and HCO3 are usually there to buffer the H+ ions but they are lost in the urine and are missing.
ASSESSMENT FINDINGS:
HA, Malaise, Polyuria, Polydipsia, Polyphagia
Later: N/V, Anorexia, dehydration LATE: LOC, Coma
PHYSICAL EXAM:
Fluid Volume Deficit or IVVD S/S: Flushed dry skin, Facial rubor, Dry mucous membranes, skin tugor, tenting >
3 seconds, sunken eyes
Tachycardia; hypotension
Fruity breath; Kussmauls (Deep rapid respirations) = Body compensating by trying to “breath” off the excess
acid.
LAB:
Serum Na (If elevated could indicate dehydration)
*****Initally Serum K = H+ ions go into the cell “pushing” the K out causing excess K in the blood (When
acidosis is fixed K goes back in)
Serum C02 (on renal panel) otherwise known as HCO3 is less than <15 = METABLOIC ACIDOSIS
Anion Gap = Normal 8-14 Formula: Na-Chloride+CO2
High Anion Gap > 14 metabolic acidosis: ketoacidosis, lactic acidosis, toxic ingestion, renal failure
Normal or non-anion gap metabolic acidosis: GI or Renal r/t loss of bicarbonate
TREATMENT:
Hydration Therapy: Fluid deficit may be 4-10L
Lowers the hyperglycemia by: Dilution; GFR
Type: N/S; ½ N/S
o Acute phase: NS 500/Hr; ½ NS 250/Hr (FAST)
o Phase 2: (Maintenance) ½ NS 100-250/Hr
o Phase 3: (Stable) Convert to Sub Q insulin…and D5W or D5 ½ NS to lower the glucose slowly
Insulin:
Regular insulin IV Bolus 0.1-0.4 U/Kg
CI Regular = b/c of low perfusion r/t IVVD ; 1:1 ratio (100U insulin: 100mL NS); Math Question: 10U insulin
= ___ mL/Hr? ANS:10
(If you give sub Q with IVVD, insulin won’t be used properly and when the IVVD is fixed they will get hit with all
the insulin at once)
Usually 5-10 U/Hr initially; then 3-6 U/Hr (May need to double the dose Q1-2 Hr if the glucose isn’t responding
properly and going down)
Goal is to serum Glucose by 75-100 Mg/DL PER HOUR!
Ketosis and Acidemia take longer to correct than the glucose…So even when glucose is approaching normal…
Still continue Insulin.
Blood Glucose is 250 mg/dl CHANGE IVF from NS to D5 ½ NS to prevent hypoglycemis and cerebral edema.
*Cerebral Edema occurs when the glucose is reduced too quickly
, S/S HYPOglycemia: confusion, slurred speech; anxiety; weakness; jitteriness; hunger; sweating; nervousness;
dizzy
TX HYPOglycemia: AAO – candy, juice, milk, fruit, icing Unconscious – IV D50
Potassium Supplement: Regardless of initial Serum K HYPOkalemia causes Ventricular Dysrythmias!!!!!
Hydration decreases the serum K
Correction of acidosis decreases the serum K when the H+ ions go out and the K goes back into the cell
Insulin carries the K back into the cell which decreases the serum K
Start the K supplement as long as there isn’t a marked elevation in K, no EKG changes, & GOOD RENAL
FUNCTION!
********SO if you see this pt. with ½ NS and 40 KCL Piggy back at 175mL/Hr this is why
LABS frequently Q 1-2 Hr until WNL the Q 6-8 Hr
May see split K replacement with Phosphate (PO4) in form of KPO4 if they are low on phosphate
Bicarbonate:
Not necessary when pH > 7.1 (No clear guideline between 6.9-7.1)
pH< 6.9 add NaHCO3 to IVF NEVER GIVE IVP Add to D5W or ½ NS to make IVF isotonic
DANGER if corrected too quickly…osmotic disequilibrium…..cerebral edema
Hyperglycemic Hyperosmolar NON-Ketotic Syndrome (HHNS)
******Hyperglycemia and hyperosmolarity are biggest problem….but NO ketosis or metabolic acidosis.
Main difference is DKA has no insulin; HHNS has a low level of insulin that will not prevent the hyperglycemia
but enough to prevent breakdown of fats, which prevents ketoacidosis.
Occurs most often in 50-70 YO with Hx of diabetes or mild Type 2
Precipitating event: Acute illness; Meds that increase insulin dependency like Thiazides
Signs & Symptoms:
Osmotic diuresis from hyperglycemia
Serum Glucose 600-1200 mg/dl; Serum osmolality > 350
PROFOUND dehydration (IVVD)
Hypotension; HYPERnatremia
Mental status changes with focal neuro deficits and hallucinations secondary to cerebral edema and
dehydration r/t hyperosmolality
Medical Management:
Fluid Replacement N/S or ½ NS…Watch for CHF
Correct electrolytes
Insulin administration…Glucose will drop as hydration increases so less insulin b/c no ketoacidosis
BUT may still see CI Regular insulin and addition of Dextrose as serum glucose approaches 250
(ATN) Acute Tubular Necrosis/ACUTE KIDNEY INJURY
AKI-sudden dec. in renal function manifested by accumulation of waste metabolites
-kidney cannot form and excrete urine
* recovery depends on health status
CAUSES: hypoTN, hypoVOLemia, nephrotoxic agent exposure
CATEGORIES OF ARF
-pre-renal: involves external pbl from kidney
reduce bld flow leading to dec GFR
low urine NA
CAUSES: HYPOVOLEMIA, DEC. co, DEC SVR
-intrarenal: direct dmg in kidney
-Acute Tubular necrosis: dmg to kidney caused from surg with hypoTN/hypoVOL....ischemia and sepsis #1
NSG: look at VS during surg
-Post Renal: mechanical obstruction to outflow
