CREATED BY :

Nur Intan Hayati Husnul Khotimah S.Kep.,Ners.,M.Kep

Disampaikan Pada Perkuliahan Keperawatan Gawat Darurat (KGD)
DIABETIC KETOASIDOSIS ??????
 Hyperglycemia BG > 200 mg/dl (11 mmol/l)
(young or partially treated children, pregnant adolescents may present
with “euglycemic ketoacidosis”)

 Venous pH <7.3 and/or bicarbonate <15 mmol/L

 mild DKA pH <7.3 bicarbonate <15
 moderate pH <7.2 bicarbonate <10
 severe pH <7.1 bicarbonate < 5

 Glucosuria and ketonuria/ketonemia (β-HOB)

 Wide geographic variation in DKA rates at diabetes
onset: 15 -70%

 A state of absolute or relative insulin deficiency

aggravated by ensuing hyperglycemia, dehydration,
and acidosis-producing derangements in intermediary
metabolism, including production of serum acetone.

 Can occur in both Type I Diabetes and Type II Diabetes

 In type II diabetics with insulin deficiency/dependence

 The presenting symptom for ~ 25% of Type I Diabetics.

 An acute metabolic complication of diabetes
mellitus characterized by impaired mental
status and elevated plasma osmolality in a
patient with hyperglycemia.

 Occurs predominately in Type II Diabetics

 A few reports of cases in type I diabetics.

 The presenting symptom for 30-40% of Type

II diabetics.
 Mild DKA Moderate DKA Severe DKA HHS

Plasma glucose > 250 > 250 > 250 > 600
(mg/dL)
Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30

Sodium Bicarbonate 15 – 18 10 - <15 < 10 > 15

(mEq/L)
Urine Ketones Positive Positive Positive Small

Serum Ketones Positive Positive Positive Small

Serum Osmolality Variable Variable Variable > 320

(mOsm/kg)
Anion Gap > 10 > 12 > 12 variable

Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma

 Stressful precipitating event that results in
increased catecholamines, cortisol, glucagon.
 Infection (pneumonia, UTI)
 Alcohol, drugs
 Stroke
 Myocardial Infarction
 Pancreatitis
 Trauma
 Medications (steroids, thiazide diuretics)
 Non-compliance with insulin
 Polyuria
 Polydypsia
 Blurred vision
 Nausea/Vomiting
 Abdominal Pain
 Fatigue
 Confusion
 Fruity odor to breath
 Dry mouth and tongue
 Drowsiness
 Deep breathing
 Coma
 Death
 Hypotension, tachycardia
 Kussmaul breathing (deep, labored breaths)
 Fruity odor to breath (due to acetone)
 Dry mucus membranes
 Confusion
 Abdominal tenderness
 Perfusion
 Vital Signs - including weight
 Hydration
 Mental Status
 Evidence for insulin resistance
 Glucose*  Venous pH
 BUN
 Ketones*
 Serum Osmolality
 Sodium  Phosphorus
 Potassium  Calcium
 Anion Gap
 Chloride
 HCO3
*Always perform in an ill child
 Chemistry  CBC
  Glucose  Leukocytosis (possible infection)
  Bicarbonate  Amylase/Lipase
 Anion gap = (Na+) – (Cl- + HCO3-)  To evaluate for pancreatitis
 Frequently seen:  BUT, DKA by itself can also
▪  BUN/creatinine (dehydration) increase them!
▪  potassium  EKG
▪  sodium  Evaluate for possible MI
Pseudohyponatremia: to correct, add 1.6
mEq of sodium to every 100mg/dL of
glucose above normal
 Serum acetones
 Positive in DKA; Possibly small in HNS
 Urinalysis
 Ketones (for DKA); leukocyte esterase,
WBC (for UTI)
 Age <12 yrs
 No first degree diabetic relative
 Lower socioeconomic status
 High dose glucocorticoids, atypical antipsychotics,
diazoxide and some immunosuppresive drugs
 Poor access to medical care
 Uninsured
 Hypophosphatemia
 Occurs after aggressive hydration/treatment
 Monitor phosphorus and replete as needed to keep > 1

 Myocardial infarction, DVT/PE, cardiac dysrhythmias

 Cerebral edema
 Rare, but life threatening
 Usually in pediatric, adolescent patients
 Symptoms: Headache, altered mental status
 Treat with mannitol, hyperventilation

Major cause of death in childhood DKA

 20% with cerebral edema die
 20% with mild to severe neurologic outcomes

 At risk:
 Initial pH < 7.1
 Baseline mental status abnormal
 Newly diagnosed, < 5 years old
 Rapid rehydration (> 50cc/ kg in first 4 hrs)
 Hypernatremia/ persistent hyponatremia
 Headache
 Decreased or worsening level of consciousness
 Slowing of the HR
 Increase in BP
 Sudden onset/return of vomiting
 Warning signs occur before the onset of CE
Diabetes Care 2006 29:1150-1159
 Management of DKA:
 1) Fluids
 2) Insulin
 3) Electrolyte replacement
 HYDRATION!!!
 Normal Saline – 500-1000 cc/hr for 4 hours, then 250 – 500 cc/hr for 4 hours, then
125-250 cc/hr
 Once glucose is < 200, should change fluids to D5 ½ NS until insulin drip is
stopped
 Insulin
 Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hr
 Ideally should decrease glucose 50-100 mg/dL per hour
 In DKA: Change to subcutaneous regimen once anion gap has closed and patient
is ready to eat.
 Need to give long-acting insulin dose several hours prior to stopping insulin drip.

 Accuchecks
 Every 1 hour initially, then every 2 hours, and so on.

 Serial Electrolytes
 Potassium repletion
▪ Should add potassium to IV fluids once potassium < 5
 Hydration!!!
 Even more important than in DKA

 Find underlying cause and treat!

 Insulin drip
 Should be started only once aggressive hydration has taken
place.
 Switch to subcutaneous regimen once glucose < 200 and
patient eating.

 Serial Electrolytes
 Potassium replacement.
 Glucose osmotic diuresis causes dehydration
 Give between 4-6 liters, then reassess (caution in CHF)
 Fluids help decrease the blood glucose levels

 Always start with NS

 Bolus and then steady rate (i.e. 150cc/hr)

 Switch to 0.45% NS when “corrected” sodium within

normal limits
 Add 1.6 mEq to sodium for every 100 glucose is above 100.

 Switch to D5 1/2NS when glucose between

200-250
 IV insulin dripbolus approx 10 units (or .1unit/kg), then
initiate drip at 0.1 unit/kg/hr
 Avoid bolus if K<3.3
▪ Replete K before starting drip
▪ Insulin drive s potassium into the cells so if potassium starts off very low can
make hypokalemia life threatening.
 Switch to SC insulin when anion gap closed signifying acidosis
cleared.
 SC insulin must overlap with insulin drip over 2 hours.
▪ Use patient’s outpatient insulin dose OR
▪ In insulin-naive patients, a multi-dose insulin regimen should be started at a
dose of 0.5 to 0.8 U/kg per day, including bolus and basal insulin until an
optimal dose is established OR
▪ Calculate 24 hour insulin requirements and use 50% as long acting
 Once the AG closes, can feed the patient. Remember to add sliding
scale insulin (preferably lispro) with meals in addition to basal SC
insulin dose.
 Bicarbonate:
 If pH<6.9 (controversial) or K>6 with ECG changes
 Potassium:
 If potassium <5.3
 20-60 meq/L of ½ NS given when K <5.3 with
severe acidosis
 Phosphate:
 If phos <1, especially if muscle weakness
 When needed 20-30mEQ/L of potassium
phosphate can be added to replacement fluids
 Be sure to check q1hour glucose checks and
q2-4hrs bmp to monitor anion gap and
acidosis
 Glucose*  Venous pH
 Ketones*  BUN
 Serum Osmolality
 Sodium
 Phosphorus
 Potassium  Calcium
 Chloride
 HCO3
*Always perform in an ill child
Monitoring
 Management requires close attention to detail
 Use a flowsheet to track vital signs labs, rates of
insulin, fluids, dextrose
 Neurological status
 consider neuro checks q 1 hr
 How does the patient look TO YOU?
 Assess, reassess and then assess again
 Consider ICU admission for closer monitoring if:
 Severe DKA (pH < 7.1 or < 7.2 in young child)
 Altered level of consciousness
 Under age of 5 years
 Increased risk for cerebral edema
 Caution with meds that may alter mental status
 Assume 10-15% dehydration
 Begin with a 10-20 ml/kg bolus of NS
 Replace calculated deficit evenly over 36 hours
- generally 1.5 x maintenance for the next
several hours is appropriate
 Do not exceed 40ml’s/kg in the initial 4 hours,
or 4 L/m squared in 24 hours
 Double bag system
 ¾ NS at 1.5 x M until glucose below 300 mg/dl
 D10 ¾ NS to be mixed with ¾ NS to achieve desired
glucose concentration

 K supplementation
20mEq/L K Acetate + 20mEq/L K Phosphate
 Ionized calcium is low, phosphorous should not be given
 early replacement and frequent monitoring

 Bicarbonate therapy is rarely, if ever, indicated

 IV infusion with basal rate 0.1 U/kg/hr
 No initial insulin bolus – it will decrease time to correction of
the glucose, but does not alter the time to correction of
acidosis
It may decrease the serum osmolality more rapidly than
desirable
 Ideal glucose decline is about 100 mg%/hr
 Continue insulin until urinary (blood) ketones are cleared
 Add potassium when K< 5 and with urination
 K >5.5 – no potassium in IVF
 K 4.5 – 5.5 – 20 meq/L K+
 K <4.5 – 40 meq/L K+
 Prevent depletion of RBC 2,3 DPG which will
improve tissue oxygenation as acidosis is
resolving

 May be useful in patients with anemia, CHF,

pneumonia, hypoxia
 Bicarbonate should be used only when
there is severe depression of the
circulatory system or cellular metabolism...
 Not recommended unless pH <7.0, not even
then, unless above true
 A 24 year old female with past medical history of diabetes
mellitus I is brought to the ER by her mother with
complaints of fatigue and increased thirst and urination.
Of note patient states she ran out of her insulin last week.
She also has had a runny nose and cough for the past
week. She noticed her glucose levels have been running
“very high” and got concerned.
 On Exam:
 BP 101/72; heart rate: 113; respirations: 32; Temperature: 36.8 °C; pulse
oximetry: 100% on room air.
 General: No apparent distress, AA and Ox3.
 HEENT: dry mucous membranes
 CV: tachycardic, normal s1, s2. No murmurs
 Lung: CTAB
 Abdomen: +bs, non distended, slight tenderness to deep palpation, no
HSM no rebound or guarding
 Ext: no cyanosis, clubbing or edema
 What labs do you want to order?
▪ CMP
▪ Complete blood count with differential
▪ Urinalysis and urine ketones by dipstick
▪ Arterial blood gas
 Lab Results:

 EKG sinus tachycardia

 BMP:
 Na: 124
 K: 5.0
 Cl: 95
 CO2: 11
 BUN: 38
 Cr: 1.8
 Glucose 450
 AST:40
 ALT:41
 Alk phos:67
 Arterial blood gas:
pH 6.9, CO2 9, bicarb 10
 WBC 13K, Hb14.4 mg/dL, and Hct 43.5%.
 75% neutrophils
 UA +glucose, +protein, -leuko esterase, -nitrite NO KETONES
 Serum ketones test ordered is positive for
beta-hydroxybutyrate
 What would you do next?
 Bolus 10 units insulin, then start insulin drip
 Bolus with normal saline, then start
maintence
 Blood cultures, chest x-ray to rule out other
sources of infection
 Empiric antibiotics?
 Bicarbonate?
 Q2 hour BMP checks:
 After 6 hours:
 Na: 139
 K: 2.5
 Cl: 108
 Co2: 13
 BUN 28
 Creatinine 1.4
 Glucose 280
 ABG:
 pH 7.2, CO2 of 18 and a bicarb of 12
 What do you do next?
 Switch to 0.45% saline with potassium
supplements
 Repeat BMP in 4 hours:
 Na: 142
 K: 4.5
 Cl: 110
 Co2: 15
 BUN 38
 Creatinine 1.2
 Glucose 230
 Start on d5 ½ NS with K supplements
 Continue insulin drip
 Repeat BMP in 4 hours:
 Na: 140
 K: 4.0
 Cl: 110
 Co2: 23
 BUN 28
 Creatinine 1.1
 Glucose 105
 Continue insulin drip
 Start patient on home regimen of SQ insulin
or calculate last 24 hour total dose and give
50% in form of long acting (i.e lantus)
 2 hours later…
 Stop drip (after 2 hours of starting the SQ
insulin)!!
 Feed patient!
 If anion gap remains closed after meal can
transfer to floor.
 Close monitoring is crucial with glucose
checks and bmps as electrolytes respond
quickly and management depends on these
numbers

 Early fluid resuscitation is important

 Insulin gtt must overlap SQ insulin for 2 hours

prior to discontinuation of the drip
 A 72-year old female with a history of
diabetes mellitus, hypertension, GERD and
obstructive sleep apnea, presents to the
emergency room with nausea/vomiting and
lethargy. Patient states that she skipped “a
few” doses of her lantus, but has otherwise
been good about her insulin. She admits to
blurred vision, and some mild abdominal
discomfort.
 Physical Exam:
 38.1, 110/78, 110, 22, 99% on RA
 Gen: Obese female, alert and oriented x 3; in NAD
 HEENT: very dry mucus membranes
 CV: RRR
 Resp: LCTA bilaterally
 Abd: soft, mildly tender diffusely, no rebound/guarding
 Ext: no LE edema
 Labs:  WBC: 14.3
 Sodium: 130  Hgb: 13.9
 Potassium: 5.9  Hct: 42
 Chloride: 102  Platelets: 291
 Bicarbonate: 18  Urinalysis:
 BUN: 38 ▪ Trace ketones
▪ Trace blood
 Cr: 1.9
▪ Leuk. Est: 4 +
 Glucose: 602 ▪ WBC > 50
 What does this patient have?
 How should you acutely treat this patient?
 What other tests would you send?
 What do you do when the patient’s glucose
falls below 200?
 A 32-year old woman is admitted to the
hospital in a semi-comatose, volume-
depleted state, exhibiting marked air hunger.
She has had type 1 diabetes mellitus for 12
years and ran out of insulin 3 days ago.
 Labs:
▪ Glucose: 1075 mg/dL Serum bicarbonate: 4.5 mEq/L
Potassium: 3.8
▪ ABG: pH 6.90, PCO2: 23 mm Hg
 After 4 hours of treatment that includes
standard doses of insulin (10 units/h) fluids,
intravenous potassium chloride (10 mEq/L)
plus 150 meq/L of sodium bicarbonate, the
patient’s pH increases to 7.10. However, she
suddenly develops respiratory failure
followed by cardiac arrest.
 What is the most likely therapeutic misjudgement?
(A) She was given too much potassium chloride and had suppression of
all cardiac pacemaker activity.
(B) She was given too little potassium chloride and developed
respiratory muscle paralysis followed by ventricular fibrillation.
(C) She was given too little insulin in the face of an unusually high plasma
glucose concentration and developed cerebral edema.
(D) She was given too much bicarbonate, which led to cerebrospinal fluid
acidosis and suppression of the brain stem respiratory center.
(E) She should have been given her potassium as potassium phosphate
in order to prevent respiratory muscle paralysis from
hypophosphatemia caused by insulin administration.
 12 year old admitted with:
 pH = 7.0
 Na= 136, K=3.8, glucose 583mg/ dl
 She is oriented and conversant on admission, you follow
the DKA protocol,
 2 hours later she becomes difficult to arouse and is
responsive only to deep pain. - What do you do?
 Presume cerebral edema
 Decrease fluid infusion to insensible losses
 Give mannitol: 1 gm/kg
 6 y/o boy is admitted in severe DKA. The family
has been traveling and he has been ill for
several days.
 Initial pH=7.0, K+ = 3.7, glucose is 350mg%.
 Despite replacement, his K+ now is 1.9 mg/dl -
what do you do?
 A “bolus” of potassium at TCH is actually an
infusion over an hour. An actual bolus of
potassium into a central vein may be lethal
 16 year old boy is admitted in moderate to
severe DKA (pH=7.23), his weight is 230 lbs, his
BG is 1400, serum osm is 360 mOsm/L, what
do you do?
 Monitor! Everything you can!
 Careful attention to detail
 Careful record keeping
 A detailed flow chart is essential
 Following the data recorded is also essential
 Repeated examination of the patient