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DETEKSI DINI KOMPLIKASI DIABETES MELITUS
Harsinen SanusiDivisi Endokrin dan Metabolik Bagian Penyakit Dalam FKUH
RS Wahidin sudirohusodoMakassar
Workshop and symposium DPJS 1 September 2015 clarion hotel
TYPE 2 DIABETES
Characteristics
• Progressive - not stable• Aggressive - not mild• Multipharmacy needed
– antidiabetic– antihypertensive– antilipidaemic– anti-platelet
The Diabetes Numbers
• every 24 hours:–New cases 4,100 cases–Deaths 810 cases–Amputations 230 cases–Kidney failure 120 cases–Blindness 55 cases Derived from NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2005.
Complications of Diabetes Mellitus
• Acute ComplicationsHypoglicemiaDiabetic ketoacidosisHyperglycemic, Hyperosmolar,
nonketotic state• Chronic Complication
Greenspan’s Basic & Clinical Endocrinology 2007:722-5
Microangiopathy 1. Diabetic Retinopathy2. Diabetic Nephropathy3.Diabetic neuropathy
Chronic Complicationt
Macroangiopathy1.CVD2.Stroke3.Peripher Arteri Disease
Greenspan’s Basic & Clinical Endocrinology 2007:722-5
Diabetic microangiopathy
Leading cause blindness (12.5% of cases)
Leading cause of ESRD (42% of cases)
50% of all non-traumatic amputations
• Coronary heart disease (CHD)• myocardial infarction• coronary atherosclerosis (angina)• heart failure
• Cerebrovascular arterial disease (stroke)
• Peripheral arterial disease• intermittent claudication• ischaemic foot ulcer
Diabetic macroangiopathy(cardiovascular disease - CVD)
UKPDS, DCCTRISIKO KOMPLIKASI
MENINGKAT APABILA KONTROL EUGLIKEMIK
JELEK
LESSONS FROM UKPDS:BETTER CONTROL MEANS FEWER COMPLICATIONS
LESSONS FROM UKPDS:BETTER CONTROL MEANS FEWER COMPLICATIONS
EVERY 1% reduction in A1C
Deaths from diabetes
Heart attacks
Microvascular complications
Peripheral vascular disorders
UKPDS 35. BMJ 2000; 321: 405-12.
-37%
-43%
*p<0.0001
-14%
-21%
1%
Target Euglycemic ControllPARAMETER ADA-EASD AACE-ACE IDF PERKENI
FPG (mg/dL
70-130 <110 <100 <100
PPG (mg/dL)
<180 <140 <140 <140
HbA1c (%)
<7.0 6.5 <6.5 <7.0
AACE=American Association of Clinical Endocrinologists; ACE=American College of Endocrinology; ADA=American Diabetes Association;FPG=fasting plasma glucose; IDF=International Diabetes Federation; PPG=postprandial glucose.aReference to a non-diabetic range of 4.0% to 6.0% using a DCCT-based assay.
1. American Diabetes Association. Diabetes Care. 2010;33(suppl 1):S11–S61. 2. AACE Diabetes Mellitus Clinical Practice Guidelines Task Force. Endocr Pract. 2007;13(suppl 1):3–68. 3. Rodbard HW et al. Endocr Pract. 2009;15(6):540–559. 4.
International Diabetes Federation. www.idf.org/webdata/docs/Guideline_PMG.pdf. Accessed September 2, 2010.
TARGETS
Type 2Diabetes
Multiple Defects in Type 2
Diabetes
Adverse Effectsof Therapy
Hyperglycemia
No Hypoglycemia
ImprovesGlycemicControl
Lowers HbA1c to normal levels
Decreases insulin resistance and hepatic glucose production
Increases or preserves
beta-cell mass
Does not cause weight gain
Does not cause edema or
congestive heart failure
Ophthalmopathy 25-30 X DR blind
Kidney 20-30 X CKD HDHeart 2-4 X CVD AMICerebral 2-4 X strokeNeuron 15-40 X parestesi,
amputation
Insulin resistance, DM and CVD–10 0 10 20
IGT Type 2 diabetes mellitus CVD
Diabetes duration (years)
CHD
Amputations
Blindness
Renal failure
Atherosclerosis Advance atherosclerosis
On-going Retinopathy metabolic Nephropathy
derangement Neuropathy
Hypertension
Insulin Resistance
HDL TG
Blood Presure Blood Glucose
Obesity
Macrovascular complications
Microvascular complications
---Eye Complications---
• Higher risk of blindness.• Many have minor eye
disorders.• Early treatments critical• Leading cause blindness
(12.5% of cases)
Diabetic Retinopathy
Microaneurysm
Exudative
Proliferatif Retinopathy
Haemorhargic
Features
microaneurysms
Features
New vessels(also get tortuous vessels and haemorhages)
DIABETES RETINOPATHYPREVENTION AND TREATMENT
• Maintain tight glycaemic and blood pressure, lipid, anemia control
• Regular eye examinations• Treat with laser photocoagulation and vitreoretinal surgery
Klein et al. Ann Intern Med 1996;124:90–6
Diabetic Nephropathy
Definitions of urinary protein abnormalities
Spot collection(µg/mg
creatinine)
Timed collection(µg/min)
24-hour collection
(mg/24 hours)
Normal <30 <20 <30
Microalbuminuria(incipient nephropathy)
30–299 20–199 30–299
Macroproteinuria(clinical nephropathy)
≥300 ≥200 ≥300
American Diabetes Association. Diabetes Care 2004; 27:S79–S83
DIABETES NEPHROPATHYCharacteristics
• Persistent albuminuria
• Diabetic retinopathy
• Hypertension
• Decline in kidney function
KIDNEY DISEASE
• Useful proteins are lost in the urine.• Get a condition known as microalbuminuria.
– There are several treatments at this point that may keep the kidney disease from getting worse.
• When kidney disease is diagnosed later, during macroalbuminuria, end-stage renal disease (ESRD) usually follows.
UKPDS: Patient with survival with time in year
Normal urinary albumin
secretion
Proteinuria
End Stage Renal Disease (ESRD)
Death
Microalbuminuria
50% (5-10 years)
20%(20 year)
- 40%
DIABETIC NEPHROPATHY IS ASSOCIATED WITH CARDIOVASCULAR MORTALITY IN TYPE 2 DM
Normal albumin excretion
Overt proteinuria
Microalbuminuria
Elevated plasma creatinine orRenal replacement therapy
2.0%
1.4%
2.8%
2.3%
4.6%
3.0%
19.2%
Death
Adler et al. Kidney Int 2000;63:225-32
TREATING ALBUMINURIA
• Use ACE-I or ARB in nonpregnant patiens with micro- or macroalbuminuria
• Reduce protein intake to 0.8-1.0 g/kgBW/day in DM & early CKD; 0.8 g/kgBW/day in later CKD
• If ACE-Is /ARBs/diuretics are given, monitor serum creatinine and potassium
• When eGFR <60 ml/min/1.73m2, evaluate for CKD complications
Diabetes Care. 2012
• Prevalence of DN approximately 50% with a clinical course that paraleles the duration and severity of hyperglicemia
• Peripheral neuropathy is one of the most common and disabling diabetic complications.
• Typical clinical manifestations: loss of sensation in the feet, develop.ulcers, deformations and gangrene amputations
DIABETIC NEUROPATHY
• Diabetic neuropathy : diffuse, symmetrical, predominantly sensory peripheral neuropathy, often associated with autonomic dysfunction
• The severity & duration of diabetes etiological factors
DIABETIC NEUROPATHY
Pathogenesis of Diabetic Neuropathy
Risk factors:Prodominace of menIncreasing age, heightSmokingMicroalbuminuriaRetinopati
Clinical manifestation diabetic neuropathy
• Painful diabetic neuropathyPainless diabetic neuropathy
• Patients with painful DN do not usually develop foot ulcers,
• Patients with foot ulcers painful symptom rare
Veves A etal.Diabetes care1993;1611871-189
DIABETIC AUTONOMIC NEUROPATHY
• Erection dysfunction• Gastropharesis• Incontinentia urinae • Atoni buli-buli• Diabetic diarrhae• Hyperhydrosis
OVERACTIVE BLADDER
• Urgensi, frekuensi dan inkontinensia • Tidak mengancam jiwa• Menurunkan kualitas hidupPENGOBATAN:
antimuskarinik:Solifenacin 5 mg, 10 mg (vesicare)Propiverine ( detrusitol)
ATONI BULI-BULI
• Indwelling catheter• Penekanan
Erection Function Disorder( Erection Dysfunction/Impotence )
53,2%
12,9%8,9%
1,0% 1,0%
10,8%6,2%
0,0%
10,0%
20,0%
30,0%
40,0%
50,0%
60,0%
MORTALITY IN TYPE 2 DM
Marble, Joslin Diabetes Center, Boston USA (1974)
CARDIO VASCULAR DISEASE (CVD) IN TYPE 2 DIABETES MELLITUS
• 2.5 x increase risk of stroke• 2-4 X increase of cardiovascular
mortality• DM responsible for 25% of cardiac
surgeries
Framingham Heart Study• Diabetes has been associated 2-4 X CHD• Mortality rate CHD > non diabetic patients• Cardiovascular mortality 2-3 X in DM • After 20 years of followup, CHD mortality in
diabetic patients 2 X non diabetic males and 5 X greater in females
Krolewski AS et al.Am J Med 1991;90(suppl 2A):56S-61S.
Diabetic FootRisk Factors Peripheral nerve disorderPeripheral arterial diseaseFoot deformityTrauma or amputation historyUnfit shoesInfection
Treatment priority
Glucose control as near to normal as reasonably
possible
Microvascular
Control of insulin resistance: hyperinsulinemia, obesity, glucose
intolerance, dyslipidemia, hypertension, procoagulant state
Macrovascular
Summary of recommendations for adults with diabetes (IDF 2007)
• Glycemic controlA1C …………………………………< 6.0%Preprandial plasma glucose……90-100 mg/dlPostprandial plasma glucose… < 140 mg/dl
• Blood pressure………<130/80 mg/dl
• Lipids LDL…………………………….. <100mg/dl
Triglicerides……………………<100mg/dlHDL……………………………… >40mg/dl
The Good News…
5
• By managing the ABCs of diabetes, people with diabetes can reduce their risk for heart disease and stroke.
A stands for A1CB stands for Blood pressureC stands for Cholesterol
The cornerstone of preventing or delaying the progression of macrovascular complications of diabetes
• Aggressive management of hypertension and cholesterol. ACE inhibitors have proven effective in managing hypertension and avoiding other complications of diabetes
• Statins the first-line agents in the management of dyslipidemia.
• Lifestyle modification strategies and • Antiplatelet therapy also remain essential.
Journal of Pharmacy Practice.2009. 22, 135-148
Beckman JA. JAMA. 2002;287:2570-2581
PREVENTION PROGRESSION OF ATHEROSCLEROSIS IN TYPE 2 DM
Beware of Your Blood Pressure
• High blood pressure raises your risk for heart attack, stroke, eye problems and kidney disease.
• Get your blood pressure checked at every visit.
• Target BP = less than 130/80
8
KOMPLIKASI AKUT
• HIPOGLIKEMIA • HIPERGLIKEMIA
KETOASIDOSIS DIABETIKHIPEROSMOLER NON KETOTIK ASIDOSIS LAKTAT
Definisi : Fluktuasi kadar glukosa darah turun
dibawah limit terendah untuk fisiologis normal(Hipoglikemia : GDS < 50 mg%)
Etiologi :Hipoglikemia eksogen insulin, anti diabetik oral, alkohol, obat2 lain:salisilat, beta bloker dllHipoglikemia endogen insulinomaHipoglikemia fungsional H. alimenter, ggn hati berat, aktifitas otot lama,
HIPOGLIKEMIA
Cryer PE. Diabetes. 2008;57:3169-76.
SymptomsSigns
Hypoglycaemia
Pallor Diaphoresis
Neuro-glycopenic
Cognitive impairmentsBehavioural changesPsychomotor abnormalitiesSeizureComa
Neurogenic
Adrenergic: palpitations,tremor, and anxiety/arousal Cholinergic: sweating, hunger, and paresthesia
Symptoms and Sign of Hypoglycemia
High risk Low risk
Insulin Metformin
Sulfonylureas α-glucosidase inhibitors
Meglitinides Thiazolidinediones
GLP-1 receptor agonists
DPP-4 inhibitors
1. Nathan DM, et al. Diabetologia. 2009;52:17-306. 2. Cefalu WT. Nature. 2007;81:636-49.
Oral Hypoglycemic Agents (OHA) (classified by risk of hypoglycaemia)
Criteria for Hypoglycemia
Still can help themselves
Severe hypoglycemia
Need help from others
Mild hypoglycemia
Does not depend on low blood glucose level
HIPOGLIKEMIA Gambaran klinis : Bervariasi, tidak adaa korelasi
gejala klinik dan gula darah. Gejala parasimpatik:
Lapar, mual, tekanan darah turun Gejala simpatik:
Pucat, palpitasi, keringatan, rasa lapar, gelisah, anxiety
Gejala neuroglikopenik: Lemah, lesu, iritabel, skt kepala, konsentrasi
menurun, somnolen, ggn pglihatan, gejala psikiatri,, kejang2, koma
HIPOGLIKEMIA Diagnosis :GD plasma < 70 mg %Riwayat DM tlh dpt obat hipoglikemikTrias Whipple
• Keluhan dan tanda klinis hipoglikemia• Kadar glukose plasma <50 mg/dl• Keluhan menghilang dgn pemberian glukose
HIPOGLIKEMIA Pengobatan:Sadar :
Tablet glukosa 30 gr, sirup, air gula, kue-kue manis, Fruktosa murni dilarang Stop obat hipoglikemik. Periksa GDS
Koma : Dextrose 40 % 50 ml, ulangi setiap 10-20 mnt sp pasien`sadarInfus dextrose 10%, 6 jam perkolf; dipertahankan sp GDS normal atau meningkat sdkt
Glukagon 1 mg IM, madu, kortisol
Management
Mild hypoglycemia Drink sugar solution or glucose tab 15-20 gr, Wait for 20 min Re-check blood glucose If blood glucose is not ≥18 mg/dl, Re-administered glucose solution
Severe hypoglycemia
IV glucose 10-25 gram 1-3 min Or glucagon 1 mg IM/SC
HIPOGLIKEMIA Pengobatan:Respons cepat (5-20 mnt), kecuali
hipoglikemia lama kecuali sdh trjd ggn otak organik, walaupun GDS 200 mg/dl
Bila tidak ada repons hidrokortison 100mg / 4 jam dilanjtkan tiap 12 jam untuk mengurangi edema otak
In elderly people receiving insulin or sulphonylureas, the symptoms of hypoglycemia most commonly
recognized are not specific in nature:
McAulay V, et al. Diabet Med. 2001;18:690-705.
* Transient cerebral ischemia* Vertebrobasilar insufficiency
* Vasovagal attacks* Cardiac dysarhythmia
Unawareness Hypoglycemia
PENCEGAHAN
• Edukasi ps DM yg dpt insulin dosis insulin tepat, kurangi dosis insulin bl kurang makan, olahraga, operasi, melahirkan
• Dosis ADO mulai dosis kecil, ditingkatkan bertahap
• Waspada pada orang tua dan DM dgn CKD
summary• Complication of T2DM : Acute and Chronic• Chronic complication: Micro and
Macroangiopathy • Macroangiopathy = atherosclerosis• Type 2 DM = CHD equivalent• Poor glycemic control increases the risk for CVD
Summary
• Macroangipathy and microangipathy are chronic complication in type 2 DM and can occur earlier before diagnosis.
• Holistic management of type 2 DM such as blood pressure control, blood glucose control and other comorbidity can reduce the chronic complication.
• Hypoglycemia can be caused by OHAs, esp.insulin secretagogue group.
• Be aware for unawareness hypoglycemia in elderly diabetic patient.
Thank you for your attention
Kasuistik
• Seorang wanita 55 tahun datang dengan keluhan gatalgatal, cepat lelah, berat badan menurun , b.a.k. 2-3 kali permalam. Baru mengetahui Diabetes
• Pemeriksaan fisis: berat badan 67 kg, tinggi badan 155 cm, Tensi 140/90 mmHg.pemeriksaan fisis lain-lain normal semua.
• Laboratorium:GDS 250 mg/dL• Apa yang perlu lagi ditanyakan pada anamnesis? • Pemeriksaan fisis apa yang perlu disimpulkan• Bagaimana cara mengetahui gizi?
• Diagnosis : • Kriteria diagnosis :• Pemeriksaan laboratorium yang diperlukan:• Comorbidity pasien ini:• Kapan dikatakan dislipidemia pada DM?• Bila ureum, creatinine diperiksa rumus apa yang
dipakai untuk menentukan fungsi ginjal• Pemeriksaan untuk mengetahui neuropati perifer• Pemeriksaan apa untuk mengetahui neuropati
otonom• Apa yang harus diketahui pada jantung pasien ini.