honk(hiporosmolar non ketotik)

8/10/2019 Honk(hiporosmolar non ketotik)

1/24

HIPOROSMOLAR NON

KETOTIK

Lita Septina

Internal Medicine Dept

Islamic University of Sumatera Utara


2/24

Acute Complication of Diabetes

Mellitus

HyperOsmolar Non Ketotic Coma (HONK)

Diabetic ketoacidosis (DKA) Hypoglycemia


3/24

Hyperosmolar Non Ketotic Coma

In 1957 Summent and Schwarts described a syndrome ofmarked diabetic stupor with hyperglycemia andhyperosmolarity in the absence of ketosis.

The syndrome has been given a number of names :

nonketotic hyperosmolar coma, diabetic hyperosmolarstate, hyperosmolar nonacidotic diabetes andhyperglycemia hyperosmolar state (HHS)(ADA)

17,5 cases per 100.000 person-years and 1 in 1000

admissions to the hospital, in US The mortality rate as high as 12% to 46%. The mortality

rate increases with higher levels of serum osmolarity.


4/24

HONK: Differences from DKA

Patients usually older- typically 60 or more

Major pathophysiologic differences

longer uncompensated osmotic diuresis greater volume depletion

Acidemia (pH > 7.3) and ketosis are mild

Higher mortality -

often 30-50% primarily due to underlying vascular or infectious

event

Occurs in Type 2 diabetics, often mild or unrecognized


5/24

Basic physiology Blood glucose homeostasis involves neural, metabolic, and

hormonal reactions Insulin + glucagon + epinephrine work together to

maintain blood sugar levels initially by glycogenolysis,then through gluconeogenesis

Glucose metabolism in the fed state : Glucose metabolism in the fasting state : Prolonged fasting leads to the non-insulin mediated fuel

source :

1. lipolysis produces glyserol which, when combined withlactat from recycled glucose, can providedgluconeogenesis

2. proteolysis, mediated by cortisol and glucagon,mobilizes amino acids from muscle tissue

Gambar 1Gambar 2


6/24

Insulin acts at the liver by:

1. Supressing endogenous glucose production (gluconeogenesis)2. Increasing glucose storage as glycogen (glycogenesis)

3. Inhibiting glycogen breakdown (glycogenolysis)

NET EFFECT : store glucose as glycogen

Insulin acts at the liver and adipose cells by:1. Produces triglycerides from glycerol and free fatty acids

2. Inhibit breakdown of triglycerids

NET EFFECT : increase lipogenesis in liver

Insulin acts at muscle cells by:1. Stimulating uptake of amino acids

2. Preventing release of amino acids from muscle cells andhepatic protein source

NET EFFECT : increase muscle protein

Regulatory hormone


7/24

Glucagon: promotes hepatic production of glucose andketones

Catecholamines: promotes hepatic glucose output

(glycogenolysis), inhibits mucle glucose uptake,enhances fatty acid mobilization (lipolysis)

Cortisol and Growth Hormone: promotes hepaticglucose production and antagonizes the peripheraleffects of insulin on glucose disposal, primarily in themucle

Counter-regulatory hormones


8/24

Patofisiologi HONK/DKA


9/24

Clinical Presentation of HONK

History Physicalexamination

Laboratory results

Insufficient fluidintake, polyuria

Decreasing polydipsia

Depressed mentation

Mild or undiagnosed

diabetesEvolution over daysto weeks

Stupor in majority

ProfounddehydrationShallow breathing

No acetone odorMultipleneurologicaldisorders

Rare cerebraledema

Normal serum pH

Serum glucose >600mg/dl, glycosuria

Serum osmo >350

Normal anion gap

Normal serumketones

Normal uric acid


10/24

Clinical Findings of Hyperosmolarity

HHS should be suspect : elderly patient with or withoutthe preexisting diagnosis of diabetes who exhibits acuteor subacute deterioration of CNS function and severelydehydrated

Tachycardia Low grade fever

Low or normal blood pressure

Dehydration dry mucous membrane, absent axillary

sweat, poor skin turgor. Nausea, vomiting, distension, and pain-gastroparesis is

due to hypertonicity

Lethargy, hallucinations, and psychosis


11/24

Laboratory Findings in

Hyperosmolarity Blood Glucose: usually > 600mg/dl

AGDA ; pH 7.3

BUN/creatinin : increased

Osmolality >330mOsm/kg Total body sodium low, level high, normal or low.

Potassium high, normal or low.

Leukocytosis 15,000-40,000 even without infection

( response to catecholamine-related stress anddehydration)

Hb,Ht increased due to dehydration


12/24

Hyperosmolar State

Hyperglycemia acts as an osmotic diureticwith obligatory loss of water and

electrolytes. Osmolality = 2(Na) + Glucose/18 + BUN/2.8

(normal 293 )

Ketosis/hyperglycemia stimulate vomiting

with aggravation of dehydration


13/24

Fluid Balance in Diabetic

HyperosmolarityECF = 14 L ICF = 28 L

H2O

ECF ICF

H2O

Osmotic Diuresis

Osmotic Diuresis

ECF hyperosmolar from ICF autotransfusion

ECF and ICF both hyperosmolar


14/24

Precipitating Factors forhyperosmolarity

Medical management of type 2 diabetes, fourthedition. ADA, Clinical Education Series


15/24

Priority in the Treatment of

HONK Replacing volume deficitsnormal saline according

to BP, urine output and CVP value for old age, totaldeficits around 6-9 liters.

Correcting hyperosmolarityto 300 milliosmoles/L

Managing any underlying illnesses

Insulinfor for acidotic, hyperkalameic or renal failurepatients RI 0.15u/kg bolus then0.1/kg/hr infusion untilblood sugar about 250mg/dl or osmo about 315


16/24

Approach to Therapy

Correcting the hyperosmolar state anddehydration is the initial aim of therapy.

Insulin therapy should be undertakenonly after the patient is stablehemodynamically.

Glucose and H2O

H2O lost in urine Loss of ECF, vascular collapse and death


17/24

Rehydration

Bolus fluids until correction of circulatoryfailure.

Correct deficit over 36 to 48 hours. Provide maintenance fluids (1600cc/m2/d) at

the same time.

Subtract resuscitation fluids from deficit.Avoid fluid administration > 4L/m2/d


18/24

Fluid and Electrolytes

Volume 1 l/h 2-3, thereafter adjusted according

to need; usually 4-6 l in first 24 h

Fluids Isotonic saline

Hypotonic saline if plasma Na> 150 mmol/l

(no more than 1-2 l

consider D5W withinsulin if marked hypernatremia)

5% dextrose 1l 4-6 hourly when bloodglucose has fallen to 250 mg/dl.


19/24

Electrolytes

Sodium content varies between 75 to154 mEq/L. Reduce as sodium levels

approach normal. Total body potassium is reduced. When

K levels reach < 3,3 add 20-40 mEq/L

as both KCL and Kphos. Maximum K infusion rate 0.5 mEq/kg/hr.


20/24

Insulin

10-15 U of RI IV bolus

Continuous intravenous infusion:

5-10 U/h (0.1 U/kg/h) initially until bloodglucose has fallen to < 300 mg/dl.Thereafter, adjust rate (1-4U/h) duringdextrose infusion to maintain blood glucose

150-250 mg/dl.When oral intake is resumed, SC insulin is

given, before stop IV insulin.


21/24


22/24

Complications of HONK

Hypoglycemia

Hypokalemia

Cerebral edema


23/24

Glucose metabolism : post-absortive state


24/24

Glucose metabolism : Fasting state

honk(hiporosmolar non ketotik)

Documents