Honk(hiporosmolar non ketotik)
-
Upload
raja-alfian-irawan -
Category
Documents
-
view
238 -
download
1
Transcript of 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
-
8/10/2019 Honk(hiporosmolar non ketotik)
2/24
Acute Complication of Diabetes
Mellitus
HyperOsmolar Non Ketotic Coma (HONK)
Diabetic ketoacidosis (DKA) Hypoglycemia
-
8/10/2019 Honk(hiporosmolar non ketotik)
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.
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
8/24
Patofisiologi HONK/DKA
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
14/24
Precipitating Factors forhyperosmolarity
Medical management of type 2 diabetes, fourthedition. ADA, Clinical Education Series
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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
-
8/10/2019 Honk(hiporosmolar non ketotik)
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.
-
8/10/2019 Honk(hiporosmolar non ketotik)
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.
-
8/10/2019 Honk(hiporosmolar non ketotik)
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.
-
8/10/2019 Honk(hiporosmolar non ketotik)
21/24
-
8/10/2019 Honk(hiporosmolar non ketotik)
22/24
Complications of HONK
Hypoglycemia
Hypokalemia
Cerebral edema
-
8/10/2019 Honk(hiporosmolar non ketotik)
23/24
Glucose metabolism : post-absortive state
-
8/10/2019 Honk(hiporosmolar non ketotik)
24/24
Glucose metabolism : Fasting state