NURSING CARE OF PATIENTS WITH

DKA

Desi Natalia Trijayanti Idris

STIKES RS Baptis Kediri
DKA
PRECIPITATING FACTORS
 Failure to take insulin  Medical Stress
 Failure to increase insulin  Counterregulatory
hormones
 Illness/Infection
 Oppose insulin
 Pneumonia
 Stimulate glucagon release
 MI

 Stroke  Hypovolmemia
 Acute stress  Increases glucagon and
 Trauma catecholamines
 Emotional  Decreased renal blood flow
 Decreases glucagon

degradation by the kidney

 Insulin Deficiency
Glucose uptake Lipolysis
Proteolysis

Glycerol Free Fatty Acids

Amino Acids

Gluconeogenesis
Hyperglycemia Glycogenolysis Ketogenesis

Osmotic diuresis Dehydration Acidosis

DIABETIC KETOACIDOSIS
Due to:
Severe insulin deficiency
Excess counterregulatory hormones
Glucagon
Epinephrine
Cortisol
Growth hormone
 ROLE OF INSULIN
 Required for transport of glucose into
 Muscle
 Adipose
 Liver
 Inhibits
lipolysis
 Absence of insulin
 Glucose accumulates in the blood
 Liver
 Uses amino acids for gluconeogenesis
 Converts fatty acids into ketone bodies
 Acetone, Acetoacetate, β-hydroxybutyrate
 Increased counterregulatory hormones
 COUNTERREGULATORY HORMONES -
DKA
Increases Activates Activates Inhibits insulin
insulin glycogenolysis lipolysis secretion
resistance and
gluconeogenesis
Epinephrine
X X X X
Glucagon
X
Cortisol
X X
Growth
Hormone X X X
 SIGNS AND SYMPTOMS OF DKA
 Polyuria, polydipsia  Fruity breath
 Enuresis  Acetone
 Dehydration  Kussmaul breathing
 Tachycardia
 Mental status changes
 Orthostasis
 Combative
 Abdominal pain  Drunk
 Nausea  Coma
 Vomiting
LAB FINDINGS
 Hyperglycemia

 Anion gap acidosis

 (Na + K) – (Cl + Bicarb) >12
 Bicarbonate <15 mEq/L
 pH <7.3
 Urine ketones and serum
ketones
 Hyperosmolarity
DIFFERENTIAL DIAGNOSIS
ANION GAP ACIDOSIS
 Alcoholic ketoacidosis
 Lactic acidosis

 Renal failure

 Ethylene glycol or methyl alcohol poisoning

 Starvation in late pregnancy or lactation (rare)

ATYPICAL PRESENTATIONS
 DKA can be present with BS <300
 Impaired gluconeogenesis
 Liver disease
 Acute alcohol ingestion

 Prolonged fasting

 Insulin-independent glucose is high (pregnancy)

 Chronic poor control but taking insulin

 Bedside urine ketones false negatives
 Measure acetoacetate not β-hydroxybutyrate
 Send blood to lab
TREATMENT OF DKA
 Initial hospital management
 Replace fluid and electrolytes
 IV Insulin therapy
 Glucose administration
 Watch for complications
 Disconnect insulin pump

 Once resolved
 Convert to home insulin
regimen
 Prevent recurrence
TREATMENT OF DKA
FLUIDS AND ELECTROLYTES
 Fluid replacement
 Restores perfusion of the tissues
 Lowers counterregulatory hormones
 Average fluid deficit 3-5 liters
 Initial resuscitation
 1-2liters of normal saline over the first 2 hours
 Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours
 When fluid overload is a concern
 If hypernatremia develops ½ NS can be used
TREATMENT OF DKA
FLUIDS AND ELECTROLYTES

 Hyperkalemia initially present

 Resolves quickly with insulin drip
 Once urine output is present and K<5.0, add 20-40 meq KCL
per liter.
 Phosphate deficit
 May want to use Kphos
 Bicarbonate not given unless pH <7 or bicarbonate <5
mmol/L
TREATMENT OF DKA
INSULIN THERAPY
 IV bolus of 0.1-0.2 units/kg (~ 10 units) regular insulin
 Follow with hourly regular insulin infusion

 Glucose levels
 Decrease75-100 mg/dl hour
 Minimize rapid fluid shifts

 Continue IV insulin until urine is free of ketones

TREATMENT OF DKA
GLUCOSE ADMINISTRATION
 Supplemental glucose
 Hypoglycemia occurs
 Insulin has restored glucose uptake
 Suppressed glucagon

 Prevents rapid decline in plasma osmolality

 Rapid decrease in insulin could lead to cerebral edema
 Glucose decreases before ketone levels decrease
 Start glucose when plasma glucose <300 mg/dl
INSULIN-GLUCOSE INFUSION FOR DKA
Blood glucose Insulin Infusion D5W Infusion
<70 0.5 units/hr 150 cc/hr
70-100 1.0 125
101-150 2.0 100
151-200 3.0 100
201-250 4.0 75
251-300 6.0 50
301-350 8.0 0
351-400 10.0 0
401-450 12.0 0
451-500 15.0 0
>500 20.0 0
COMPLICATIONS OF DKA
 Infection  Cerebral Edema
 Precipitates DKA  First 24 hours
 Fever  Mental status changes
 Leukocytosis can be secondary to  Tx: Mannitol
acidosis  May require intubation with
 Shock hyperventilation
 If not improving with fluids r/o
MI
 Vascular thrombosis
 Severe dehydration
 Cerebral vessels
 Occurs hours to days after DKA
 Pulmonary Edema
 Result of aggressive fluid
resuscitation
ONCE DKA RESOLVED
TREATMENT
 Most patients require 0.5-0.6 units/kg/day
 Pubertal or highly insulin resistant patients
 0.8-1.0 units/kg/day
 Long acting insulin
 1/2-2/3
daily requirement
 NPH, Lente, Ultralente or Lantus
 Short acting insulin
 1/3-1/2given at meals
 Regular, Humalog, Novolog
 Give insulin at least 2 hours prior to weaning
insulin infusion.
PREVENTION OF DKA
SICK DAY RULES
 Never omit insulin
 Cut long acting in half
 Prevent dehydration and
hypoglycemia
 Monitor blood sugars
frequently
 Monitor for ketosis
 Provide supplemental fast
acting insulin
 Treat underlying triggers
 Maintain contact with
medical team
GOALS OF DISCUSSION
 Pathophysiology of DKA
 Biochemical criteria for DKA

 Treatment of DKA

 Prevention of DKA

 Hyperosmolar Nonketoic Syndrome

HYPEROSMOLAR NONKETOTIC
SYNDROME
 Extreme hyperglycemia and dehydration
 Unable to excrete glucose as quickly as it enters the
extracellular space
 Maximum hepatic glucose output results in a plateau of
plasma glucose no higher than 300-500 mg/dl
 When sum of glucose excretion plus metabolism is less than
the rate which glucose enters extracellular space.
HYPEROSMOLAR NONKETOTIC
SYNDROME
 Extreme hyperglycemia and hyperosmolarity
 High mortality (12-46%)
 At risk
 Older patients with intercurrent illness
 Impaired ability to ingest fluids
 Urine volume falls
 Decreased glucose excretion
 Elevated glucose causes CNS dysfunction and fluid
intake impaired
 No ketones
 Some insulin may be present
 Extreme hyperglycemia inhibits lipolysis
HYPEROSMOLAR NONKETOTIC
SYNDROME PRESENTATION
 Extreme dehydration
 Supine or orthostatic hypotension

 Confusion coma
 Neurological findings
 Seizures
 Transienthemiparesis
 Hyperreflexia
 Generalized areflexia
HYPEROSMOLAR NONKETOTIC
SYNDROME PRESENTATION
 Glucose >600 mg/dl
 Sodium
 Normal, elevated or low
 Potassium
 Normal or elevated
 Bicarbonate >15 mEq/L
 Osmolality >320 mOsm/L
HYPEROSMOLAR NONKETOTIC
SYNDROME TREATMENT
 Fluid repletion
 NS 2-3 liters rapidly
 Total deficit = 10 liters
 Replete ½ in first 6 hours
 Insulin
 Make sure perfusion is adequate
 Insulin drip 0.1U/kg/hr

 Treat underlying precipitating illness

CLINICAL ERRORS
 Fluid shift and shock
 Giving insulin without sufficient fluids
 Using hypertonic glucose solutions
 Hyperkalemia
 Premature potassium administration before insulin has begun to act
 Hypokalemia
 Failure to administer potassium once levels falling
 Recurrent ketoacidosis
 Premature discontinuation of insulin and fluids when
ketones still present
 Hypoglycemia
 Insufficient glucose administration
CONCLUSION
 Successful management requires
 Judicious use of fluids
 Establish good perfusion
 Insulin drip
 Steady decline
 Complete resolution of ketosis

 Electrolyte replacement
 Frequent neurological evaluations
 High suspicion for complications
 Determine etiology to avoid
recurrent episodes