Transcript Diabetic Ketoacidosis Case Presentation

DIABETIC KETOACIDOSIS (DKA)
Hannah Allegretto
University of Pittsburgh School of Pharmacy
PharmD Candidate 2013
THE CASE
JJ is a 59yo male admitted into the ER on
8/01/2012 with severe hyperglycemia and
confusion
 Patient did not know how he arrived at the
hospital, and states, “I don’t feel like myself.”
 Diagnosis: Diabetic Ketoacidosis
 PMH: DM2 x 13 years, hypercholesterolemia x 12
years, cardiac catheterization (2009),
cholecystectomy (2010), laminectomy at L4-5
(unknown date)

THE CASE (CONTINUED)

Labs upon arrival:
Glucose: 461 mg/dL
 K: 4.7 mmol/L
 Bicarbonate: 9 mEq/L
 Scr: 1.75 mg/dL
 pH: 7.26
 Ketones: >80mg/dL


Anion Gap: 31.7 mmol/L
Vitals:

BP: 137/79, Pulse: 94 beats/min, RR: 20, Temp: 36.7C
Weight: 105.7kg
 Medications:


Lantus 40u SQ daily, Lipitor 10mg daily, ASA 81mg
daily, Glucovance 5/500mg QID
OBJECTIVES
Describe the epidemiology and pathophysiology
of DKA
 Identify the diagnostic lab parameters for DKA
 Recognize the signs and symptoms of DKA
 Identify patient specific precipitating causes to
developing DKA
 Select appropriate treatment regimens and
monitoring parameters for managing DKA
 Describe how to prevent future DKA episodes

EPIDEMIOLOGY OF DKA

Estimated Incidence: 4-8 cases per 1,000 persons
with diabetes per year
More common in type 1 diabetics
 Accounts for 1-2% of all diabetes related admissions


50% of diabetes-related admissions in young people
Hospital costs may exceed $1 billion annually
 Death occurs in ~2% of patients if not treated
promptly

http://emedicine.medscape.com/article/118361-overview#a0156
PATHOPHYSIOLOGY OF DKA

Characterized by:
Hyperglycemia
 Ketosis
 Acidosis


Occurs due to a relative or absolute insulin
deficiency which causes an increase of counterregulatory hormones


Glucagon, cortisol, growth hormone, epinephrine
This imbalance promotes:
Hepatic gluconeogenesis
 Glycogenolysis
 Lipolysis

http://emedicine.medscape.com/article/118361-overview#a0104
PATHOPHYSIOLOGY, CONTINUED
Increased hepatic gluconeogenesis and
glycogenolysis leads to severe hyperglycemia
 Lipolysis leads to an increase of free fatty acids
in the serum


Metabolism of free fatty acids produces ketones
In early stages, the body can buffer the effects of
excess ketones, resulting in a normal arterial pH,
but having a base deficit and mild anion gap
 As ketones continue to accumulate in the body,
they eventually flow into urine.
 If left untreated, pH and bicarbonate levels will
drop

http://emedicine.medscape.com/article/118361-overview#a0104
ELECTROLYTE DISTURBANCES

When glucose in the body rises above 220mg/dL,
it will begin to spill into the urine


Glucose will draw H20 into the renal tubules,
producing excess urine osmotic diuresis
Osmotic diuresis leads to:
Dehydration
 Volume depletion
 Net loss of Na+, K+, Ca2+, Mg2+, Cl-, and PO42

Ketones also spill into the urine, but are buffered
before excreted

Na+ used as the buffer water follows Na+further
volume depletion and dehydration
Mistovich J. Understanding the presentation of diabetic ketoacidosis.
DIAGNOSTIC CRITERIA
Mild
Moderate
Severe
>250
>250
>250
Arterial pH
7.25-7.30
7.00-<7.24
<7.00
Serum
Bicarbonate
(mEq/L)
15-18
10-<15
<10
Urine ketones
Positive
Positive
Positive
Serum ketones
Positive
Positive
Positive
>10
>12
>12
Alert
Alert/drowsy
Stupor/coma
Plasma glucose
(mg/dL)
Anion Gap
Alteration in
sensoria or
mental
obtundation
.
Diabetes Care. 2009; 32:1335-43
SIGNS AND SYMPTOMS

Early signs:
Tired/fatigued
 Excessive thirst
 Excessive urination
 Dry mouth


Later signs:






Nausea/vomiting
Abdominal pain
Confusion
Kussmaul’s respirations
“Fruity” smelling breath
Fever
Treat Endocrinol. 2003; 2: 95-108
PRECIPITATING CAUSES

Infection
UTI
 Pneumonia

Psychological stress
 Noncompliance with DM medications
 Trauma
 Stroke
 Alcohol abuse
 Pulmonary embolism
 Medications

Treat Endocrinol. 2003; 2: 95-108
PRECIPITATING CAUSES, CONTINUED

Infection
On admission, JJ’s WBC count: 12.9 x 103
 Uroscreen (08/01/12): negative


Possible blood infection
Tx: Levaquin 500mg PO QAM
 08/06/2012: WBC 5.6 x 103


Noncompliance
JJ was very confused upon admission
 Did not know what medications he should be taking
and when he should be taking them

TREATMENT

Therapeutic Goals:





Improve circulatory volume and tissue perfusion
Decrease serum glucose and plasma osmolality
Clearing serum and urine of ketones at a steady rate
Correcting electrolyte imbalances
Identifying and treating precipitating events
Diabetes Care. 2001; 24: 131-53.
TREATMENT, CONTINUED

Start IV fluids
1L of 0.9% NaCl in the first hour, followed by:
 If corrected serum sodium normal or elevated:



If corrected serum sodium low:


0.45% NaCl at 250-500mL/hr
0.9% NaCl at 250-500mL/hr
Successful fluid replacement evidenced by:
Increase in BP
 Measurement of fluid input/output


Deficits should be corrected within the first 24
hours
Diabetes Care. 2001; 24: 131-53.
TREATMENT, CONTINUED

Fluids, continued


5% dextrose with 0.45% NaCl at 150-250mL/hr
initiated when serum glucose reaches 200mg/dL
Insulin Therapy: Regular
0.1u/kg IV bolus dose, then
 0.1u/kg/hr IV continuous infusion
 Goal:

Reduce plasma glucose concentration at a rate of 5075mg/dL per hour.
 If serum glucose does not fall by at least 10% in the first
hour, give 0.14u/kg IV bolus, then resume previous therapy

Diabetes Care. 2001; 24: 131-53.
TREATMENT, CONTINUED

Insulin therapy

Plasma glucose reaches 200mg/dL
Decrease insulin infusion rate to 0.02-0.05u/kg per hour
 Add 5% dextrose with 0.45% NaCl at 150-250mL/hr to IV
fluids
 Keep serum glucose between 150 and 200 mg/dL until
resolution
 REMEMBER: hyperglycemia corrects faster than
ketoacidosis


After resolution:

Initiate SC multidose regimen
 Continue IV infusion for 1-2 hours after SC insulin begun
 Insulin naïve: 0.5-0.8u/kg daily and adjust insulin as
needed
 Known diabetes: resume previous insulin dosing, so long
as it is sufficient
Diabetes Care. 2001; 24: 131-53.
TREATMENT, CONTINUED

Potassium therapy

Potassium depleted by:
Insulin therapy
 Correction of acidosis
 Volume expansion


K+ > 5.2 mEq/L


K+ < 3.3 mEq/L


Do not give K+ but check level every 2 hours
Hold insulin and give 20-30 mEq/hr until K+ > 3.3 mEq/L
K+ 3.3-5.2 mEq/L

Give 20-30 mEq K+ in each liter of IV fluid to keep serum
K+ between 4-5 mEq/L
Diabetes Care. 2009; 32:1335-43.
TREATMENT, CONTINUED

Bicarbonate therapy

pH > 6.9


No HCO3- administered
pH < 6.9
100mmol in 400mL H2O + 20 mEq KCl infused over 2 hours
 Repeat every 2 hours until pH > 7


Risks:
Increased risk of hypokalemia
 Decreased tissue oxygen uptake
 Cerebral edema
 Development of paradoxical CNS acidosis

Diabetes Care. 2001; 24: 131-53.
MONITORING
Monitoring is KEY!
 Check electrolytes, BUN, venous pH, creatinine,
and glucose every 2 hours until stable


Resolution of DKA Criteria:
Blood glucose < 200 mg/dL
 Serum bicarbonate >18 mEq/L
 Venous pH > 7.3
 Anion gap < 12 mEq/L

Diabetes Care. 2001; 24: 131-53.
PREVENTION
Intensive patient education
 Effective communication with health care
providers during acute illness
 Patient compliance
 Increased access to heath care

Diabetes Care. 2001; 24: 131-53.
THE CASE

Labs upon arrival:






Glucose: 461 mg/dL
K: 4.7 mmol/L
Bicarbonate: 9 mEq/L
Scr: 1.75 mg/dL
pH: 7.26
Ketones: >80mg/dL
Anion Gap: 31.7 mmol/L
TREATMENT FOR JJ

IV Fluids
1L of 0.9% NaCl in the first hour, followed by
 0.45% NaCl at 500mL/hr


Insulin: Regular
11u IV bolus dose, then
 11u/hr IV continuous infusion
 Goal: Reduce plasma glucose concentration at a rate
of 50-75mg/dL per hour.


Potassium:

Give 25 mEq K+ in each liter of IV fluid to keep
serum K+ between 4-5 mEq/L
TREATMENT FOR JJ, CONTINUED

Bicarbonate:


None, JJ’s pH > 6.9
When plasma glucose reaches 200mg/dL:
Decrease insulin infusion rate to 4 units per hour
 Add 5% dextrose with 0.45% NaCl at 250mL/hr to IV fluids
 SQ Insulin: resume Lantus 40 units SQ. Continue IV
infusion for 1-2 hours after Lantus restarted
 Assess efficacy of Lantus dosing, consider short acting
insulin before meals if needed


Monitoring:

Check electrolytes, BUN, venous pH, creatinine, and
glucose every 2 hours until stable
ENDPOINT GOALS
Blood glucose < 200 mg/dL
 Serum bicarbonate >18 mEq/L
 Venous pH > 7.3
 Anion gap < 12 mEq/L


Education/Counseling:





Taking medications as prescribed
Contacting health care provider immediately in acute
illness
Warning signs/symptoms of emergency
Discount programs if financially unstable
Diabetic testing logs
REFERENCES





Medscape Reference. Drugs, Diseases, and Procedures. Diabetic
Ketoacidosis. http://emedicine.medscape.com/article/118361-overview
(accessed 2012 Aug 6).
Mistovich J. Understanding the presentation of diabetic ketoacidosis.
http://www.ems1.com/ems-products/education/articles/385223Understanding-the-Presentation-of-Diabetic-Ketoacidosis (accessed
2012 Aug 6).
Kitabchi AE, Umpierrez GE, Miles JM et al. Hyperglycemic crises in
adult patients with diabetes. Diabetes Care. 2009; 32:1335-43.
Kitabchi AE, Umpierrez GE, Murphy MB et al. Management of
hyperglycemic crises in patients with diabetes. Diabetes Care. 2001;
24: 131-53.
Umpierrez GE, Kitabchi AE. Diabetic ketoacidosis: risk factors and
management strategies. Treat Endocrinol. 2003; 2: 95-108.
Questions??