ACUTE COMPLICATIONS OF

DIABETES MELLITUS
PATIENTS

dr. Rensa, Sp.PD

Departemen llmu Penyakit Dalam- FK UNIKA

OUTLINES
Diabetic

Ketoacidosis (DKA)
Hyperglicemic Hyperosmolar
Syndrome (HHS)
Hypoglicemia

DIABETIC KETOASIDOSIS
(DKA)

KASUS

Pasien, Wanita, usia 42 tahun.

Keluhan utama (chief complain) : panas, sesak

(Kussmaul), lemah, kesadaran menurun.

Menderita DM sejak usia 26 tahun,

Terapi injeksi insulin, jenis: Novomix 10-0-10 units,

Lab: Gula Darah Sewaktu : 480 mg/dl, WBC 24.000,
analisis gas darah (AGD) : pH 6.98, K 3.6 meq/l,
Keton urine (+), Thorax foto : paru/jantung : normal

Kesimp : KAD, DM tipe1

Foto Pasien

DIABETIC KETOACIDOSIS
Mortality : 5-10% (western), Indonesia 10-20%
higher in elderly
Avoidable
Affects : T1DM, can accur in T2DM during severe
intercurrents illness as a precipitating factors

PRECIPITATING
FACTORS
Infections 28%
New cases of IDDM 10%
Treatment errors 13%
Miscellaneous 5%
Myocardial infarction 1%
No diagnosis established 43%

Source : John Pickup,Williams G, 39.0-39.23, 1997

KETOACIDOSIS
(DEFINITION)

Severe uncontrolled diabetes

requiring emergency treatment with insulin and
intravenous fluids and with a blood ketone body
(acetone, acetoacetate and 3-OH butyrate)
concentration of > 5 mmol/l

Source : Alberty, 1974

KETOACIDOSIS
Cardinal biochemical features : TRIAD
(DEFINITION)

hyperketonemia,
metabolic acidosis and
hyperglicaemia
Metabolic acidosis : HCO3(-) concentration
(arterial/cap) 15 mmol/l,
Dehydration, defisit in fluid and electrolytes.
significant ketosis (urine ketostix ++ or plasma
ketostix + or more)

Source : Diabetes Care 24(1),2001

PATHOGENESIS
Intercurrents illness raised concentration of catabolic
counter regulatory hormone : glucagon, cathecolamines,
cortisol, growth hormone
Relative deficiency of insulin

HYPERGLICAEMIA
KETOACIDOSIS
DEHYDRATION
ELECTROLIT DISBALLANCE

Metabolic
decompensation

METAB. DECOMPENSATION
(HYPERGLICAEMIA,
KETONEMIA)
HYPERGLICEMIA

Increased glucose production

(hepatic glycogenolysis,
gluconeognesis,renal gluconeognesis)
Reduced glucose disposal
(by periph. tissue : muscle, fat)

LIPOLYSIS

FFA, NEFA keton bodies

(OH butyrate, acetoacetate, acetone)

Fig : Pathofisiology Keton Bodies production

Ins deficiency (abs/rel) + stress hormone stimulates lipolysis

acetyl CoA production : incr lipolysis Ac CoA keton bodies synthesis
(adapt. QJ Med 2004,97:773-780)

CLINICAL FEATURES OF DKA

Poliuria
Weight loss
Weakness
Blurred vision
Acidotic (Kussmaull) respiration
Abdominal pain (sp. in children)
Leg cramps
Nausea and vomiting
Confusion and drowsiness
Coma (10% of cases)

DIAGNOSIS
DKA

: medical emergency !
Hyperglicaemia glucose oxidase reagent
strip
Urine (ketones) : keton testing (acetest
tab/ketostix dip sticks), plasma keton body
concentration (ketostix or acetest)
Venous blood : glucose, urea, electrolytes,
full blood count
BGA (blood gas analysis)

DIAGNOSTIC CRITERIA FOR DKA AND

HHS
PG (mg/dl)
Arterial pH
HCO3(-)
Urine keton
Osm (mOsm/kg)
Anin gap
Sensorium
stupor/

DKA
HHS
Mild
moderate severe
> 250
>250
>250
>600
7.25-7.30 7.0-7.24 <7.0
>7.30
15-18
10-<15 <10
>15
(+)
(+)
(+)
small
(+/-)
(+/-)
(+/-)
> 320
>10
>12
>12
<12
alert
alert/
stupor/
drowsy

coma

coma

HHS : hyperglicemic hyperosmolar syndrome

Adapted:clinical diabetes 19(2):82;2001

LABORATORY TEST
RESULTS AND
DIFFERENTIAL
DIAGNOSIS
Lab test that would be routinely
monitored in
the setting of DKA
Hb, leucocyte, diff count.
Glucose, electrolyte, BUN, creatinine
Changes in Na,K,Cl,P,BUN,creatinine
Uraemic acidosis

The sine qua-none of DKA

Acidosis (due to prod. and accum. of ketone),
HCO3 < 10 meq/l anion gap > 14meq/L

ANION GAP

Anion gap = sodium (chloride + bicarbonate)

Most pts DKA: > 20 - < 40 mEq/L

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)

FLUID AND ELECTROLYTES

INSULIN
OTHER MEASURES

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)
FLUID AND ELECTROLYTES
Volumes : usually 4-6 Litres /24 h
Fluids : isotonic salines, hypotonic (not more then 2-4
l) if Na >150mmol/l,
D5 %if BG < 270 mg/dl (15 mmol/l) (simultane with
saline if indicated), sodium bicarbonates if pH<7.0
Potasium *: prevent hipo K
< 3.5 mmol 40 mmol KCl,
3.5-5.5 mmol 20 mmol KCl,
> 5.5 mmol NO KCl

*KCl to be added from 2nd litre onward

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)
ASSESS NEED FOR BICARBONATE

pH < 6.9
NaHCO3, (100 mmol/l) in 400 cc H2O drips
200cc/hrs.
Repeat adm every 2hrs until pH >7.0 and monitor K.
pH 6.9-7.0
NaHCO3, (50 mmol/l) in 200 cc H2O drips 200cc/hrs.
Repeat adm every 2hrs until pH >7.0 and monitor K.
pH >7.0
NO HCO3- (bicarbonate)
Source : Diabetes Care 26(suppl1):S109,2003

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)
POTASSIUM
K <3.3 meq/l : HOLD insulin, give 40 meq/l K per
h, (2/3 KCl, 1/3 KPO4) until K >/=3.3 meq/l
K 5.0 meq/l : dont give K, but check every 2 hrs
K 3.3 5.0 meq/l : give 20-30 meq/l / liter of IV
fluid (2/3 KCl, 1/3 KPO4) keep serum K at 4.5
meq/l

Source : Diabetes Care 26(suppl1):S109,2003

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)
FLUID AND ELECTROLYTES
INSULIN
Continuous intravenous infusion.
5-10 u/h (avrg 6 u/h) BG < 270 mg/dl (15 mmol/l)
adjust rate (usually 1-4u/h) with D5 to maintain BG
90-180 mg/dl (5-10 mmol/l ) until pts eating again.
Intramuscular injection
20 u immediately IM, then 5-10 u/h untill BG fallen to
180-270 mg/dl (10-15 mmol/l), then change to 10 u/h
SC untill pts eating again together with D5 infusion

Source : Diabetes Care 26(suppl1):S109,2003

TREATMENT

(GUIDE TO INITIAL TREATMENT OF DKA IN

ADULTS)
FLUID AND ELECTROLYTES

INSULIN
OTHER MEASURES
Tight recording
Search for and treat precipitating cause
Hypotension / dehidration
CVP monitoring
NG tube
Urine cathether
ECG monitoring
Cerebral edema : manitol, dexamethazone, brain imaging
ARDS
Thromboembolic complications
Consider mechanical ventilation (to accelerate CO2

elimination)

HYPOGLICEMIA

FREQUENCY OF
HYPOGLYCEMIA
Type1 diabetes

Hypoglicemia is a fact of life for people with type1 diabetes.

Many episodes of asymptomatic hypo.
PG levels < 50-60 mg/dl, may be 10% of time
2 episode of symptomatic hypoglicemic per week.
Severe hypo (at least temporary disabling) once a year.
2-4% death due to hypoglicemia

Type2 diabetes
Difficult to assess.
During intensive therapy : 10-73 episode per 100 pts/years.
Severe hypoglicemia about 10% of those in type 1 diabetes (even in
aggressive ins th/).
Major hypoglicemia in UKPDS : 2.4% metform groups, 3.3% SU
and 11.2% insulin groups.
DCCT : 65%

adapted : Cryer PE et al, Diabetes Care 2003, 26(6):1902,

Cryer PE Diabetologia, 2002;45:937-48

HYPOGLYCAEMIC EPISODES
IN ELDERLY DIABETIC PATS
10/29 cases (34.48%)
6 pats (20.68%) on OHA therapy, 4 (13.79%) on insulin
therapy
4 (13.79%) pats (half on insulin and half on OHA
treatment) severe and need hospital admission.

Astika N, et al. Geriatric div, Dept of Medicine, RSUP Denpasar 2007

HYPOGLYCEMIA
(CLINICAL MANIFESTATION)
Whipples triad
Hypoglycemic symptom (+)
Low PG (plasma glucose) concentration
Sympt relief when PG raised

SYMPTOMS OF HYPOGLYCAEMIA
Divided into 2 categories
Neurogenic (autonomic ) symptoms.
Neuroglycopenic

SYMPTOMS OF HYPOGLYCEMIA
(COMMON SYMPTS OF ACUTE
HYPOGLYCEMIA IN DIABETIC PTS)

Neurogenic / Autonomic cathecolamine release

Sweating
Pounding heart
Shaking (tremor)
Hunger
Neuroglycopenic
Confusion
Drawsiness
Speech dificulty
Incoordination
Atypical behaviour
malaise

SYMPTOMS OF HYPOGLYCAEMIA
NEUROGENIC / AUTONOMIC
Autonomic response due to : Falling BG and
derangements of CNS functions.
Neurogenic sympts : Catecholamine release :
tachycardia, pallor, anxiety, tremulousness,
sweating.

Attenuated / absent in
blocker th/, autonomic neuropathy and chr
hypoglicemia,

SYMPTOMS OF HYPOGLYCAEMIA
NEUROGLICOPENIC SYMPTOMS
Neuroglycopenic symptoms (neuro hypoglicemic
sympts) due to CNS neuronal deprivation :
confusion, lightheadedness, headache, aberrant
behaviour, blurred vision, loss of consciousness,
seizure

RISK FACTORS FOR SEVERE

HYPOGLYCEMIA
Insulin treatment regimen
Intensified regimens and tight glycemic control
High ins dosages
Impaired awareness of hypoglycemia
Chronic (central autonomic failure)
Acute (induced by proceeding hypoglycemia)
Long duration of diabetes
Increasing age of pts
Sleep
Excessive alcohol consumption

TREATMENT
Pts

conscious oral glucose (20-30 gr) or

sucrose
Pts unconscious IV glucose 50% (30-50 ml),
glucagon 1 ml/SC or IM

Check BG after 15-20 min

Confirm recovery

No recovery D5/D10 IV
Recovery identify cause, re-educate, take
measures to avoid hypoglycemia

GLUCAGON
Dosis : 1mg, SC or IM or IV or intra nasal (spray)
Act within minuts (IV > SC)
Primary actions : hepatic glycogenolysis,
stimulate insulin release (CI in SU induced
hypoglycemia)
SE : nausea, vomiting, head ache.

PREVENTION
Pts education
Frequent SMBG (self monitoring blood glucose)
Flexible insulin and other drug regimens
Individualized glycemic goals
Professional guidance and support.

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