DIABETIC KETO ACIDOSIS (DKA) &

HYPERGLYCEMIC HYPEROSMOLAR
STATE (HHS)

dr. Leonardo Liswojo

 CHARACTERISTICS OF DKA AND HHS

Hyperglycemic Hyperosmolar State

Diabetic Ketoacidosis (DKA)
(HHS)

Absolute (or near-absolute) insulin Severe relative insulin deficiency,

deficiency, resulting in
•Severe hyperglycemia
•Ketone body production
•Systemic acidosis
resulting in
•Profound hyperglycemia and
hyperosmolality (from urinary free
water losses)
•No significant ketone production or
acidosis

Develops over hours to 1-2 days Develops over days to weeks

Most common in type 1 diabetes, but Typically presents in type 2 or

increasingly seen in type 2 diabetes previously unrecognized diabetes

Higher mortality rate

 Pathophysiology Clinical features
(What’s wrong) (What do you see)

•High lab blood glucose, glucose meter

reading or urine glucose, polyuria,
•Elevated blood glucose
polydypsia

•Sunken eyes, dry mouth, decreased skin

• Dehydration
turgor, decreased perfusion (shock rare)

•Acidotic breathing, nausea, vomiting,

•Metabolic acidosis
abdominal pain, altered level of
(ketosis)
consciousness
 CLINICAL PRESENTATION OF
DIABETIC KETOACIDOSIS

History Physical Exam

• Thirst • Kussmaul respirations
• Polyuria • Fruity breath
• Abdominal pain • Tachycardia
• Nausea and/or • Supine hypotension,
vomiting orthostatic drop of
• Profound weakness blood pressure
• Dry mucous
membranes
• Poor skin turgor
9
 CLINICAL PRESENTATION OF
HYPERGLYCEMIC HYPEROSMOLAR
STATE
• Compared to DKA, in HHS there is greater severity of:
• Dehydration
• Hyperglycemia
• Hypernatremia
• Hyperosmolality

10
 CLINICAL PRESENTATION OF
HYPERGLYCEMIC HYPEROSMOLAR
STATE
Patient Profile Disease Characteristics
• Older • More insidious
development than DKA
(weeks vs hours/days)
• More comorbidities
• Greater osmolality and
• History of type 2 mental status changes
diabetes, which may than DKA
have been
unrecognized • Dehydration presenting
with a shock-like state

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 PRINCIPLES OF DKA MANAGEMENT

1. Correction of shock
2. Correction of dehydration
3. Correction of hyperglycaemia
4. Correction of deficits in electrolytes
5. Correction of acidosis
6. Treatment of infection
7. Treatment of complications
 FLUID THERAPY
• Factors to consider:
• Hemodynamics
• State of hydration
• Serum Na+
• Urinary output

• Plain NSS at 15-20 ml/kg/hr or 1-

1.5 liters during the first hour

• Avoidance of fluid overload

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 PRINCIPLES OF DKA MANAGEMENT

1. Correction of shock
2. Correction of dehydration
3. Correction of hyperglycaemia
4. Correction of deficits in electrolytes
5. Correction of acidosis
6. Treatment of infection
7. Treatment of complications
 INSULIN
THERAPY
• IV infusion of regular
insulin – preferred
• Short half-life
• Easy titration

• Hyperglycemia
• corrected faster than
ketoacidosis

Target is Target is
150-200 mg/dl 200-300 mg/dl

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 PRINCIPLES OF DKA MANAGEMENT

1. Correction of shock
2. Correction of dehydration
3. Correction of hyperglycaemia
4. Correction of deficits in electrolytes
5. Correction of acidosis
6. Treatment of infection
7. Treatment of complications
 POTASSIUM
• Mild to moderate ↑ in
serum K+ despite ↓ in
total-body K+

• Hypokalemia
• Life-threatening arrhythmias
• Respiratory muscle
weakness

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 PRINCIPLES OF DKA MANAGEMENT

1. Correction of shock
2. Correction of dehydration
3. Correction of hyperglycaemia
4. Correction of deficits in electrolytes
5. Correction of acidosis
6. Treatment of infection
7. Treatment of complications
 BICARBONATE TX
At pH 6.9-7.1: failed to show either beneficial or deleterious
• Severe
changes in morbidity or mortality metabolictherapy
with bicarbonate acidosis
1

At pH <6.9: no prospective randomized

• Impairedcontrolled
myocardialtrials
Deleterious effects of bicarbonate therapy: increased risk of
contractility
hypokalemia, decreased tissue •oxygen uptake,
Cerebral cerebraland
vasodilatation
edema, and development of paradoxical
coma central nervous
system acidosis.2 • Severe GI complications
• Controversies in the use of
bicarbonate

1MorrisLR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med 1986;105:836–840
Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N, the Pediatric
23
2Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Risk factors for cerebral edema in children

with diabetic ketoacidosis. N Engl J Med 2001;344:264– 269

 WHEN TO TRANSITION FROM
IV INSULIN INFUSION TO SC INSULIN

DKA HHS
• BG <200 mg/dL and 2 • Normal osmolality and
of the following regaining of normal
• HCO3 ≥15 mEq/L mental status
• Venous pH >7.3
• Anion gap ≤12 mEq/L • Allow an overlap of 1-2
h between
subcutaneous insulin
and discontinuation of
intravenous insulin

Kitabchi AE, et al. Diabetes Care. 2009;32:1335-1343.

CAUSES OF MORBIDITY & MORTALITY

• Shock • Acute respiratory

• Acute renal failure distress syndrome

• During treatment: • Precipitating illness:

• Hypokalemia MI, stroke, sepsis,
• Hypoglycemia pancreatitis,
• Cerebral edema pneumonia
 CONTOH KASUS
NY.F (41 THN)

Anamnesa PF
• (+) lemas, mulut kering • GCS : 15
sejak 10 jam smrs • RR 24x/menit
• (+) Nafsu mkn • TD 100/70 mmHg
berkurang, mual, • HR 108 x/menit
muntah, rasa tidak
nyaman diulu hati • SaO2 97%
• (+) Sempat berobat ke • Mukosa mulut kering
klinik karna sakit maag • Rh -/-, Wh -/-
• Riwayat DM tidak • Turgor kulit menurun
diketahui sebelumnya)
 LABORATORIUM

• GDS: 848 • DL:

• Na:123,K: 7,1,Cl: 89 • 12.9/39,5/26100
N79,8/L11,5 tromb
• AGD 474000
• pH: 7,12
• CXR:
• pCO2: 14,4
• Cor/pulmo dbn
• HCO3: 4,8
• pO2: 106
• UL:
• Be : -24,9 • (+) keton, glukosa +3,
Kuning keruh, darah
• Keton: 6 mmol/l samar (+),
• Cr:1.83 • Laktat 0,9
• Procalcitonin : 0,5
 Na – (Cl + HCO3) =123 – (89 + 4,8)
= 123 – 93,8
= 29,2

2 (Na) + GDS/18 = 2(123) + (848/18)

= 246 + 47,1
= 293,1
30
• BG <200 mg/dL and 2 of
the following
• HCO3 ≥15 mEq/L
• Venous pH >7.3
• Anion gap ≤12 mEq/L