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Acute Complication of

Diabetes Mellitus

Hermina Novida

Department of Internal Medicine


Dr. Soetomo Teaching Hospital-Faculty of Medicine Airlangga University
SURABAYA
Hypoglycemia

Hyperglycemic Crisis
Diabetic Ketoacidosis (DKA)
Hyperosmolar hyperglycemic state (HHS)
Ketoacidosis Lactate (KAL)
Hypoglycemia In Diabetes Mellitus
 The ADA Workgroup recommended that people with
insulin secretagogue or insulin treated diabetes
become concerned about the possibility of developing
hypoglycemia at a self-monitored (or device estimated)
plasma glucose concentration of ≤ 70 mg/dL (≤ 3.9
mmol/L).

 PERKENI, 2011 defined hypoglycemia as a decreased


blood glucose level < 60 mg/dL.
Risks of severe hypoglycaemia associated with
different diabetes treatment

50
Patients affected per year (%)

40

30

20

10

0
Sulphonylurea- Insulin- “Standard” insulin Intensively
treated type 2 treated type 2 therapy in type 1 Treated in type 1
diabetes diabetes diabetes diabetes (DCCT)
Factors that Precipitate or Predispose to Hypoglycaemia :
Excessive insulin level
Excessive Error by patient, doctor or pharmacist
dosage

Increased Accelerated absorbtion (exercise, injection into


insulin abdomen, change to human insulin)
bioavailability Insulin antibodies, Renal failure, Honeymoon periode

Increased Counter-regulatory hormon deficiencies (Addison,


insulin Hypopituitarism)
sensitivity Weight loss, physical exercise, postpartum,
menstrual cycle variation
Inadequate Missed, small or delayed meals
carbohydrate Anorexia nervosa, Vomiting (gastroparesis), breast
response feeding, failure to cover exercise

Other factors Exercise, alcohol, drugs


Heller SR. Textbook of Diabetes 1, 2003, p.33.1
WHIPPLE’S
TRIAD

HYPOGLYCEMIA
HYPOGLYCEMIA

Low Plasma Glucose Levels


The signs and symptoms of hypoglycemia can
be divided into two categories :

• Autonomic

• Neuroglycopenic
Common Symptoms of Acute Hypoglycaemia
in Diabetes Mellitus

Autonomic Neuroglycopenic Malaise


Sweating Confusion Nausea
Pounding heart Drawsiness Headache
Tremor Speech difficulty
Hunger Incoordination
Atypical behaviour
Visual disturbance
Circumoral paraesthesia

Heller SR. Textbook of Diabetes 1, 2003, p.33.1


Hypoglycaemia aware
Blood glucose (mmol/L)
4
Epinephrine Start of brain
release dysfunction
3
Confusion/loss
Sweating, of concentration
Glycaemic thresholds for tremor 2
release of epinephrine and
1 Coma/seizure
activation of autonomic Permanent brain damage
symptoms and for
Hypoglycaemia unaware
neuroglycopenic effects in
Blood glucose (mmol/L)
diabetic subject who are 4
aware or unaware of Start of brain
dysfunction
hypoglycaemia Epinephrine 3
release Confusion/loss
of concentration
2
Sweating,
tremor
1 Coma/seizure
Permanent brain damage
Principal metabolic effects of counter-regulation
in response to acute hypoglycaemia
Hypoglycaemia

+
+

ACTH

Glucagon Vasopressin Growth Cortisol


hormone

+
Established
Capillary blood sample
diagnosis

Oral glucose
(15-20 gram)

Evaluation

Intramuscular glucagon
0.5 – 1 mg Repeat
after 10 ‘
Maintainance
180 – 200 mg%
10% Dextrose Intravenous glucose
20 – 30 ml 50%
dextrose
Practical Guidelines of the Treatment of Hypoglycemia with
Formula 3-2-1-1 for Pts with DM to Avoid “Honey Moon” Phenomena
(Clinical Experiences : Tjokroprawiro 1996-2014)

GlLUCOSE Treatment of Hypoglycemia with GLUCOSE 40%


LEVEL 1 VIAL: 25 mL
(mg/dL) FORMULA 3-2-1-1 with 10 g Glucose

< 30 mg/dL *) : I.V GLUCOSE 40%, BOLUS 3 VIALS FORMULA - 3


30-50 mg/dL *) : I.V GLUCOSE 40%, BOLUS 2 VIALS FORMULA - 2
50-70 mg/dL *) : I.V GLUCOSE 40%, BOLUS 1 VIAL FORMULA - 1
70-90 mg/dL **): I.V GLUCOSE 40%, BOLUS 1 VIAL FORMULA - 1
If 15 (fifteen) minutes After Treatment the Blood Glucose < 100 mg/dL,
I (one) VIAL IV Glucose Should be Repeated
*) True Hypoglycemia : The 4 (Four) Hormones CGCG may be
Secreted (Catecholamine, Glucagon, Cortisol, Growth hormone)
**) Reactive Hypoglycemia : If Plasma Glucose Rapidly to be Lowered
and Drops Steeply f.e. from 400 to 70-90 mg/dL
Hyperglycemia In Diabetes Mellitus
Diabetic Ketoacidosis
• DKA consists of the biochemical triad of
ketonaemia (ketosis),
hyperglycaemia, and
acidaemia.

• DKA has been considered to be indicative, or even diagnostic,


of type 1 diabetes, but increasingly there are cases of ketone-
prone type 2 diabetes being recognized.

However, the initial treatment is the same !


Hyperosmolar hyperglycemic state
These are:
• Hypovolaemia
• Marked hyperglycaemia (30 mmol/L or more) without
significant hyperketonaemia (<3 mmol/L) or
acidosis (pH>7.3, bicarbonate >15 mmol/L)
• Osmolality usually 320 mosmol/kg or more

N.B. A mixed picture of HHS and DKA may occur.


PRECIPITATING FACTORS

• Infection (20% - 40%) → urinary tract and lung


• CVA
• Myocardial infarction
• Pancreatitis
• Discontinuation of or inadequate insulin therapy
• Drugs (steroids, sympathomimetics, thiazides)
Pathogenesis DKA and HHS
DIAGNOSIS

• History and physical examination

• Laboratory findings

• Differential diagnosis
History and Physical examination

• History of polyuria, polydipsia, weight loss, dehydration,


weakness, and mental status change.
• Physical findings : poor skin turgor, kussmaul respiration
(DKA), tachycardia, and hypotension, mental status
change (full alertness to profound lethargy or coma).
Focal neurologic signs and seizures  HHS
• Naussea, vomiting, diffuse abdominal pain are frequent
in pts with DKA (>50%).
Laboratory findings
• plasma glucose, serum and urine ketones,
electrolytes (with calculated anion gap), osmolality,
arterial blood gases
• blood urea nitrogen/creatinine
• urinalysis
• complete blood count with differential
• electrocardiogram
• bacterial cultures of urine, blood, and throat, etc.
• chest X-ray
Diagnostic criteria for DKA and HHS
DKA HHS
Mild Moderate Severe
Plasma glucose (mg/dl) > 250 > 250 > 250 > 600
Arterial pH 7.25–7.30 7.00–7.24 < 7.00 > 7.30
Serum bicarbonate (mEq/l) 15–18 10 to 15 < 10 > 18
Urine ketones (+) (+) (+) Small
Serum keton (+) (+) (+) Small
Effective serum osmolality Variable Variable Variable >320
(mosm/kg)
Anion gap > 10 > 12 >12 Variable
Alteration in sensoria and Alert Alert/drowsy Stupor/coma Stupor/coma
mental

Anion gap : (Na+) - (Cl + HCO3) (mEq/l). ADA, 2009


Osmolality : (2Na+ + glucose + urea)
Terapi insulin pada krisis hiperglikemia
A. Definisi dan diagnosis (krisis hiperglikemi)

KAD SHH glukosa


plasma >600
Ringan Sedang Berat
mg/dl
pH arteri 7.25-7.30 7.00-<7.24 <7.00 >7.30
Bikarbonat serum 15-18 10-<15 <10 >18
mEq/L
Keton urine Positif Positif Positif Kecil
Keton serum Positif Positif Positif Kecil
Osmolaritas serum Bervariasi Bervariasi Bervariasi >320 mOsm/kg
efektif
Anion Gap >10 >12 >12 Bervariasi
Status menatal Siaga Siaga/menga Stupor/kom Stupor/koma
ntuk a

Perkeni 2015
HHS (HONK) – ESSENTIALS OF DIAGNOSIS
(ADA-2009, Kitabchi et al 2009, Tjokroprawiro 2009-2013)

1 Yes - Severe Hyperglycemia (>600 mg) TETRALOGY HONK :


2 No History of DM
1 Yes & 3 No
3 No Kussmaul’s Breathing
4 No Ketonuria or Ketonemia; Sometimes : Mild Ketonuria (Tjokroprawiro 2009)

5 No Metabolic Acidosis (pH >7.3)


6 Serum Bicarbonate >18 meq/l
7 Anion Gap <12
8 Serum Osmolality ≥ 320 mOsm/kg
Serum Glucose mg/dl
2 [ Measured Na (meq/l) ] + = > 325 mOsm/kg
18
Clinical Experiences (Tjokroprawiro 1991-2009), Clinical Dx of HHS
The TETRALOGY of HHS (HONK) : 1 Yes & 3 No
1 Yes : Glycemia >600 mg/dl
2 No : No History of DM HHS HONK
3 No : No Kussmaul’s Breathing
4 No : No Ketonuria or Ketonemia
Hyper Osmolar Non Ketotic
TREATMENT

• IV fluid (NS)
• Insulin (Continuous IV drip/im)
• K+
• Bicarbonate (pH < 7)
……..General management issues !!!!

Fluid administration and deficits

There is universal agreement that the most important initial


therapeutic intervention in DKA is appropriate fluid
replacement followed by insulin administration.

The main aims for fluid replacement are:


• Restoration of circulatory volume
• Clearance of ketones
• Correction of electrolyte imbalance
• This should be replaced as crystalloid.

• In patients with kidney failure or heart failure, as well as the


elderly and adolescents, the rate and volume of fluid
replacement may need to be modified.

• Typical deficits in DKA in adults :


Water 100ml/kg
Sodium 7-10mmol/kg
Chloride 3-5mmol/kg
Potassium 3-5mmol/kg
IV Fluids
Hydration Status ?

Severe hypovolemia Mild dehydration Cardioogenic shock

0.9% NaCl (1 L/h) Hemodynamic


monitoring

Evaluate corrected serum Na+

Serum Na high Serum Na normal Serum Na low

0.45% NaCl (250 – 500 ml/h) depending 0.9% NaCl (250 – 500 ml/h)
on hydration state depending on hydration state

When serum glucose reaches 200 mg% (DKA) or 300 mg/dl


(HHS), change to 5% dextrose with 0.45% NaCl at 150-250 ml/hr
INSULIN
A fixed rate intravenous RI 0.1 u/kg/h/iv infusion
insulin infusion (FRIII)

If serum glucose does not fall by at least 10% in first hour,


give 0.14 U/kg as IV bolus, then continue previous Rx

When serum glucose reaches 200 When serum glucose reaches


mg/dl, reduce RI infusion to 0.02-0.05 300 mg/dl, reduce RI infusion to
U/kg/hr IV, or give rapid acting insulin at 0.02-0.05 U/kg/hr IV. Keep serum
0.1 U/kg SC every 2 hrs. Keep serum glucose between 200 and 300
glucose between 150 and 200 mg/dl mg/dl until px is mentally alert
until resolution of DKA

Insulin has several effects, but the following are the most important when treating
DKA :
• Suppression of ketogenesis
• Reduction of blood glucose
• Correction of electrolyte disturbance
J.Goguen, J. Gilbert / Can J Diabetes 42 (2018) S109–S114
Terapi insulin pada krisis hiperglikemia
 Langkah pertama: melakukan resusitasi cairan untuk memperbaiki
deplesi cairan tubuh, bila kadar kalium <3.3 mEq/L, harus diberikan
pemberian kalium terlebih dahulu sebelum pemberian infus insulin
secara kontinyu diberikan
 Pada umumnya infus insulin intravena diberikan dengan dosis 5-7 U/jam
(yang mampu menurunkan gluosa darah sebesar 50-70 mg/dL/jam)
 Bila penurunan gluosa darah <60 mg/dL/jam perlu diperhatikan
kemungkinan adanya rehidrasi yang kurang atau asidosis yang
memburuk
 Bila kadar glukosa darah telah mencapi <250 mg/dL dosis insulin
dikurang menjadi 50% dari dosis sebelumnya. Infus insulin tetap
diberikan sampai ketosis teratasi dan pasien sudah dapat makan/minum

Perkeni 2015
TERAPI KETOASIDOSIS DIABETIK (KAD) - REVISI 2010 68
(Clinical Experiences and Illustrated : Tjokroprawiro 1991-2014)

1 REHIDRASI : NaCl 0.9% atau RL, 2 L / 2 jam pertama, lalu 80 tt/m


selama 4 jam, lalu 30 tt/m selama 18 jam (4-6 L/24 jam),
diteruskan sampai 24 jam berikutnya ( 20 tt/m) : FORMULA KAD : 2,4,18-24
2 IDRIV (NovoRapid®) : 4 unit/jam i.v (FORMULA MINUS SATU)
FASE-I 3 INFUS KALIUM : 25 mEq (bila K+ = 3.0-3.5 mEq/l), 50 mEq (K+ = 2.5 - 3.0),
PER 24 JAM 75 mEq (bila K+ = 2.0-2.5), dan 100 mEq (bila K+ < 2.0 mEq)
4 INFUS : bila pH < 7.2 atau BIK <12 mEq/l : 50-100 mEq / 500ml / 24 jam
BIKARBONAT Bolus BIK 50 mEq / 10 menit diberikan bila pH < 7.0
dan sisanya (50 mEq) diberikan dengan drip selama 2 jam
5 ANTIBIOTIK : HARUS RASIONAL dengan DOSIS ADEKUAT
Glukosa Darah + 250 mg/dl atau Reduksi Urine + IDRIV : INSULIN DOSIS RENDAH INTRA VENA
1 MAINTENANCE NaCl
: 0.9% atau Pot. R (INS 4-8u), Maltosa 10% (INS 6-12u)
bergantian : 20 tt/m (Start Slow, Go Slow, Stop Slow)
FASE-II 2 KALIUM : p.e (bila K+ < 4 mEq/l), atau per os (air tomat/kaldu)
3 NovoRapid® : 3 x 8-12 U sc (ingat : FORMULA KALI DUA)
4 MAKANAN LUNAK : KARBOHIDRAT KOMPLEKS PER ORAL

FORMULA : 2,4,18,24–Time ; FORMULA : 2,80,30,20–Fluid *) F4 : 25 meq K+, dlm 100 ml RL, drip 5 jam

2 4 18 24 TIME
Koreksi HIPOKALEMIA gunakan FORMULA sbb : FORMULA KAD : 2 80 30 20 FLUID
HIPO K: F1, F2, F3, F4 (251005) *)
Hati hati pada pasien CKD dan GAGAL JANTUNG IDRIV AMAN pada kasus HIPOKALEMIA
Monitoring
• Capillary blood glucose - hourly

• Serum electrolytes and bicarbonate– 2 hourly


initially

• Urine output

• Blood pressure/heart rate

• Mental status
Resolution of DKA is defined as :

pH > 7.3 units;


bicarbonate > 15.0mmol/L; and
blood ketone level < 0.6mmol/L
(rather than < 0.3mmol/L),
Thank You

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