DIABETES KETOACIDOSIS

1. DIABETIC KETOACIDOSIS

2. • DKA, a potentially fatal complication of diabetes, occurs in up to 5% of
patients with T1DM annually and can occur in insulin-deficient patients
with T2DM.
• Diagnostic Testing
• Laboratories
• Labs will show an anion gap metabolic acidosis and positive serum b-
hydroxybutyrate or ketones (a semiquantitative measurement of acetone,
acetoacetate, and b-hydroxybutyrate).
• Plasma glucose level usually is elevated, but the degree of hyperglycemia
may be moderate (<300 mg/dL) in 10% to 15% of patients with DKA.
• Pregnancy and alcohol ingestion are associated with “euglycemic DKA.”

3. • Urine ketones are generally present in DKA.
• Hyponatremia, hyperkalemia, azotemia, and hyperosmolality are
other findings.
• Serum amylase, transaminase, and/or triglyceride levels may be
elevated.
• A focused search for a precipitating infection is recommended if
clinically indicated.
• An electrocardiogram (ECG) should be obtained to evaluate
electrolyte abnormalities and for unsuspected myocardial ischemia.

6. TREATMENT
• IV access and supportive measures should be instituted without
delay.
• Fluid deficits- The average degree of dehydration for most patients
is approximately 7% to 9% of body weight. Hypotension indicates a
loss of >10% of body fluids.
• Restoration of circulating volume- first 2-3 hrs @ 0.5-1 L/
hr.[Harrison- 0.9% NS @10-20 ml/kg /hr]
• Replenish total body water deficits; -0.45% or 0.90% NaCl saline
infusion at 150 to 500 mL/hr depending on the appropriate
corrected serum sodium level .
• [Harrison- 0.45% NS @250-500 ml/hr ---f/b---- 150-250ml/hr ]

7. JOSLIN’s GUIDELINES FOR
DKA

8. • Do not exceed a change in osmolality >3 mOsm/kg/hr.
• The success of the fluid replacement is judged by
improvement in blood pressure, urine output, and clinical
examination.
• Maintenance fluid replacement is continued until the fluid
intake/output records indicate an overall positive balance
similar to the estimated fluid deficit.
• Complete fluid replacement in a typical DKA patient may
require 12 to 24 hours to accomplish.

10. A decrease in BG levels of 50 to 75 mg/dL/hr is an appropriate response; lesser
decrements suggest
•insulin resistance,
•inadequate volume repletion, or
•Inadequate insulin dose or delivery. If insulin resistance is suspected, the hourly
dose of regular insulin should be increased progressively by 50% to 100% until an
appropriate glycemic response is observed.
WASHINGTON MANUAL
Excessively rapid correction of hyperglycemia at rates >100
mg/dL/hr should be avoided to reduce the risk of osmotic
encephalopathy.
Maintenance insulin infusion rates of 1 to 2 U/hr can be
continued (indefinitely) until the patient is clinically improved,
the serum bicarbonate level rises to >/= 15 mEq/L, and the anion
gap has closed.

11. WASHINGTON MANUAL
• An IV bolus of regular insulin, 10 to 15 U (0.15
U/kg), should be administered immediately.
• This should be followed by a continuous infusion
of regular insulin at an initial rate of 5 to 10 U/hr
(or 0.1 U/kg/hr).
• A solution of regular insulin, 100 U in 100 mL of
0.9% saline, infused at a rate of 10 mL/hr delivers
10 U/hr of insulin.

12. • In mild episodes of DKA, short-acting insulin can be used
SC.
• Insulin infusion is continued until the acidosis resolves and
the patient is metabolically stable.
• As the acidosis and insulin resistance associated with DKA
resolve, the insulin infusion rate can be decreased to 0.05–
0.1 units/kg per hour

13. • It is crucial to continue the insulin infusion until
adequate insulin levels are achieved by administering
long-acting insulin by the SC route.
• Even relatively brief periods of inadequate insulin
administration in this transition phase may result in
DKA relapse.
• The improvement in acidosis and anion gap, a result of
bicarbonate regeneration and decline in ketone bodies,
is reflected by a rise in the serum bicarbonate level and
the arterial pH.

14. • Dextrose (5%) in 0.45% saline should be infused
once plasma glucose level decreases to 250
mg/dL and the insulin infusion rate should be
decreased to 0.05 U/kg/hr to prevent dangerous
hypoglycemia.
• start a separate dextrose-containing infusion of
50 to 100 mL/hr and adjusting the fluid
replacement accordingly.

15. Potassium stores are depleted in DKA (estimated deficit 3–5 mmol/kg [3–5 meq/kg]).

16. BICARBONATE INFUSION (harrison’s)
The results of most clinical trials do not support the routine use of bicarbonate
replacement, and one study in children found that bicarbonate use was associated
with an increased risk of cerebral edema.
However, in the presence of severe acidosis (arterial pH <7.0), the ADA advises bicarbonate
(50 mmol/L [meq/L] of sodium bicarbonate in 200 mL of sterile water with 10 meq/L KCl
per hour for 2 h until the pH is >7.0).

17. PHOSPHATE & MAGNESIUM
• Hypophosphatemia may result from increased glucose usage, but
randomized clinical trials have not demonstrated that phosphate
replacement is beneficial in DKA.
• If the serum phosphate is <0.32 mmol/L (1 mg/dL), then phosphate
supplement should be considered and the serum calcium monitored.
• Hypomagnesemia may develop during DKA therapy and may also require
supplementation.
• Magnesium therapy is indicated in patients with ventricular arrhythmia
and can be administered as magnesium sulfate (50%) in doses of 2.5 to 5.0
mL (10 to 20 mEq of magnesium) IV.
• IV antimicrobial therapy

19. Monitoring of therapy
• BG levels should be monitored hourly, serum electrolyte
levels every 1 to 2 hours,
• arterial blood gas values as often as necessary for a
severely acidotic or hypoxic patient.
• Serum sodium tends to rise as hyperglycemia is corrected;
failure to observe this trend suggests that the patient is
being overhydrated with free water.
• Serial serum ketone measurements are not necessary
because ketonemia may persist after clinical recovery and
because the most commonly used assays measure all
ketones, not just b-hydroxybutyrate.
WASHINGTON MANUAL

20. • Restoration of renal buffering capacity by
normalization of the serum bicarbonate level and
closure of the anion gap are more reliable indices of
metabolic recovery.
• Use of a flowchart is an efficient method of tracking
clinical data (e.g., weight, fluid balance, mental status)
and laboratory results during the management of DKA.
• Continuous ECG monitoring may be required for
proper management of potassium in patients with
oliguria or renal failure.

21. HYPER OSMOLAR HYPERGLYCEMIC
STATE
Compared to DKA, patients with NKHS may require as much as 10 to 12 L of positive
fluid balance over 24 to 72 hours to restore total deficits.

22. (WASHINGTON MANUAL)
• In patients with marked hyperglycemia (>600
mg/dL), regular insulin, 5 to 10 U IV,
immediately------followed by continuous
infusion of 0.10 to 0.15 U/kg/hr.
• Once plasma glucose decreases to 250 to 300
mg/dL, insulin infusion can be decreased to 1
to 2 U/hr and 5% dextrose should be added
to the IV fluids.

23. HYPERGLYCEMIC HYPEROSMOLAR
STATE (HARRISON)
• TREATMENT-
• Volume depletion and hyperglycemia are prominent features of
both HHS and DKA.
• Fluid replacement should initially stabilize the hemodynamic status
of the patient (1–3 L of 0.9% normal saline over the first 2–3 h).
• If the serum sodium is >150 mmol/L (150 meq/L), 0.45% saline
should be used.
• hemodynamic stability achieved
• IV fluid administration is directed at reversing the free water deficit
using hypotonic fluids (0.45% saline initially, then 5% dextrose in
water [D5W]).

24. • reasonable regimen for HHS begins with an IV insulin bolus
of 0.1 unit/kg followed by IV insulin at a constant infusion
rate of 0.1 unit/kg per hr
serum glucose does not fall
• increase the insulin infusion rate by two fold.
• glucose should be added to IV fluid when the plasma
glucose falls to 13.9 mmol/L (250 mg/dL), and the insulin
infusion rate should be decreased to 0.05–0.1 unit/kg per
hour

25. TREATMENT OF HYPOGLYCEMIA

26. IV dextrose ----initial bolus, 20 to 50 mL of 50% (WASHINGTON MANUAL)
dextrose, should be given immediately, followed by infusion of D5W (or D10W) to maintain BG
levels above 100 mg/dL.
Glucagon, 1 mg IM (or SC), is an effective initial therapy for severe hypoglycemia in patients
unable to receive oral intake or in whom an IV access cannot be secured immediately.
Vomiting is a frequent side effect and therefore care should be taken to prevent the risk of
aspiration.

28. DIFFERENCE OF VENOUS , ARTERIAL
AND CAPILLARY BLOOD GLUCOSE
• There is a 3–5 mg/mL difference between arterial and
venous levels, with higher differences in the postprandial
state.
• Levels are higher in the arterial blood because some of the
glucose diffuses from the plasma to interstitial fluid (IF) as
blood circulates through the capillary system.
• Arterial blood glucose and capillary blood glucose have
been shown to be almost identical in concentration,even
though the distribution of the glucose to the systemic
capillaries does not occur instantaneously.

29. • Glucose concentrations measured by glucose meters are
whole blood levels, which can differ from plasma glucose
levels by up to 11% (plasma higher).
• Abnormal hematocrit concentrations can result in falsely
low (hematocrit >50%) or high (hematocrit <40%) glucose
levels mainly found in glucometer because glucometer
generally measure the plasma glucose. Increase in
hematocrit cause decrease in plasma volume------falsely
low BG levels
• Any delay in processing or transportation of samples can
decrease glucose levels by 5–7%/h
• The blood sampled from the skin prick comes from the
capillaries of dermis with a small amount of blood from cut
arterioles and venules providing a mix concentration.

30. • Blood flow to the skin is controlled by many factors,
including autonomic nervous system, temperature,
hormonal changes during menstrual cycle for females,
and chemical inputs.
• Capillary blood glucose levels at the fingertip have
been shown to correlate well with systemic arterial
blood glucose levels.
• Plasma glucose values are about 11% higher than
those of whole blood when the hematocrit is normal.
• Postprandial capillary blood glucose levels are higher
than venous blood glucose levels by up to 20%,
probably due to glucose consumption in tissues

31. PLASMA v/s SERUM GLUCOSE
• With regards to the differences in blood glucose
level between plasma and serum, some studies
reported that plasma glucose is higher than
serum glucose whereas other studies found no
difference.
• Nonetheless, measurement of glucose in serum is
not recommended for the diagnosis of diabetes
• while plasma allows samples to be centrifuged
promptly without waiting for the blood to clot.