12-diabetes mellitus.pdf
TRANSCRIPT
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KEPERAWATAN GAWAT
DARURAT DIABETES MELLITUS
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TUJUAN INSTRUKSIONAL KHUSUS
• Peserta mampu
Menjelaskan patofisiologi kegawatan
DMMenjelaskan tindakan keperawatan
pada hipoglikemia, KAD dan HHS
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POKOK BAHASAN
• Konsep DM
• Komplikasi
Hipoglikemia
Ketoasidosis Diabetik (KAD)
Hyperglycaemic Hyperosmolar State (HHS)
• Penatalaksanaan
• Masalah keperawatan• Intervensi keperawatan
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Manusia secara terus menerus membutuhkan energiManusia makan tidak terus menerus
Kelebihan kalori disimpan:
-glikogen hepar (75g) & otot (300-500g)-trigliserid pada jaringan lemak-protein jaringan
Makan melebihi yang dibutuhkan
HOMEOSTASIS SUMBER ENERGI
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SUMBER ENERGI
KEBUTUHAN ENERGI
MAKANAN PRODUK ENDOGEN
GlukoneogenesisGlikogenolisis
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Hormon Pengendali HomeostasisSumber Energi
• Insulin
Meningkatkan sintesis glikogen, sintesislipid, ambilan glukosa, ambilan asam amino
dan sintesis protein• Counter-insulin hormone
-glucagon
-cathecolamine-growth hormone
-glucocorticoids
lipolisis
glukoneogenesis glikogenolisis ambilan glukosa
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DEFINISI DIABETES MELLITUS
• Kelompok penyakit metabolik yangditandai oleh hiperglikemia kronikakibat kelainan sekresi insulin, aksinya,
atau keduanya (Perkeni, 2006)• Prevalensi meningkat, rural 7,2% dan
urban 14,7%. Indonesia peringkat
keempat negara dengan jumlah DMterbanyak (Perkeni, 2006)
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Kejadian Diabetes di dunia
2000 2030
Ranking Negara Jumlah diabetes
(juta))
Negara Jumlah diabetes
(juta)
1 India 31.7 India 79.4
2 China 20.8 China 42.3
3 US 17.7 US 30.3
4 Indonesia 8.4 Indonesia 21.3
5 Japan 6.8 Pakistan 13.9
6 Pakistan 5.2 Brazil 11.3
7 Russia 4.6 Bangladesh 11.18 Brazil 4.6 Japan 8.9
9 Italy 4.3 Philippines 7.8
10 Bangladesh 3.2 Egypt 6.7
Wild S et al. Diabetes Care 2004;27:1047-53
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PENYEBAB HIPERGLIKEMIA PADA DM
JARINGANPERIFER
(OTOT)
LIVER
GLUKOSA
PANKREAS
GANGGUANSEKRESI INSULIN
PENINGKATAN
PRODUKSI GLUKOSA
reseptor+
Gangguan postreseptor
Summary of the metabolic abnormalities in type 2 diabetes mellitus (T2DM) that contribute to hyperglycemia.Increased hepatic glucose production, impaired insulin secretion, and insulin resistance due to receptor and
postreceptor defects all combine to generate the hyperglycemic state.
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Klasifikasi DM
DM Tipe 1: destruksi sel beta, defisiensi insulinabsolut. Autoimun (1A) danidiopatik(1B)
DM Tipe 2: resistensi insulin dan defek sekresiinsulin
DM Tipe lainDM pada kehamilan (DM gestasional)
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Keluhan DM
PoliuriPolidipsiPolifagi
BB turun
KesemutanGatal di daerah genitalKeputihanInfeksi sulit sembuhBisul hilang timbulPenglihatan kaburCepat lelah
Mudah mengantuk
Khas DM
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Diagnosis DM
Keluhan khas DM + 1 kali kriteria lab. terpenuhi
Tanpa keluhan khas DM dibutuhkan 2 kali kriteria labterpenuhi atau
Kriteria laboratorium
Puasa (mg/dl) 2jPP (mg/dl)
Normal
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Penatalaksanaan DM
• Edukasi
• Perencanaan makan (terapi gizi medik)
• Latihan jasmani• Intervensi farmakologis
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Insulin therapy
Basal insulin + OHAs
Basal plus prandial insulin ± OHAs
T2DM treatment strategies:
stepwise management*
Lifestyle modification
Diet, exercise, weight control
OHA monotherapy
e.g. SU/MG; MF; AGI; TZD
Premixed insulin± OHAs
Mulaipengobatan
atauperubahan
pengobatandilakukan
bila targetkendali gula
tidaktercapai
Combination OHAs**
e.g. MF + SU/MG; MF + TZD;
SU/MG + TZD; MF + SU/MG + TZD
*Individualise; **check localprescribing information.
Adequate insulin
dose usingtitration algorithms
Fix FastingGlucose First
AGI=α-glucosidase inhibitor; MG=meglitinide; TZD=thiazolidinedione.
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TARGET KENDALI DIABETES
BAIK SEDANG BURUK
Gula darah puasa (mg/dl)
Gula darh 2 jam (mg/dl)
A1C (%)
Kolesterol total (mg/dl)Kolesterol LDL (mg/dl)
Kolesterol HDL (mg/dl)
Trigliserid (mg/dl)
IMT (kg/m2)
Tekanan darah (mmHg)
80-100
80-144
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KEGAWATAN DIABETES MELLITUS
• HIPOGLIKEMIA
• KETOASIDOSIS DIABETIK (KAD)
• HYPERGLYCAEMIC
HYPEROSMOLAR STATE (HHS)
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HYPOGLYCEMIA
• Hipoglikemia terjadi bila kadar glukosa darahkurang dari 60 mg/dl
• Secara klinis, hipoglikemia ditandai triad
Whipple yaitu kadar glukosa darah rendah,gejala dan tanda hipoglikemia, dan perbaikangejala dan tanda setelah dilakukan koreksiglukosa plasma
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Gejala dan Tanda
Simptom adrenergik (diperantarai catecholamine):keringat banyak, palpitasi, pucat, takikardia,ketakutan, cemas, lapar, sakit kepala, lemah,restlessness
Simptom Neuroglikopenik:kapasitas intelektual turun, mudah tersinggung,
bingung, perilaku aneh, kejang, coma
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Respons fisiologik terhadap hipoglimia
• Kadar glukosa 56-48 mg/dl
* sekresi adrenalin* keringat banyak, tremor
* Fungsi sistim saraf pusat turun
• Kadar glukosa
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Faktor Risiko
• Kontrol glikemik yang ketat
• Usia ● Durasi diabetes
• Riwayat hipoglikemia
• Saat tidur ● Alcoholism ● Puasa
• Peningkatan sensitivitas insulin: fitness,penurunan berat badan
• Kliren/metabolisme obat: insufisiensi renalatau hepar
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Mekanisme peningkatan efekhipoglikemik sulfonilurea
• Peningkatan waktu paruh karena inhibisikecepatan metabolisme atau ekskresi: etanol,penilbutason, coumarin anticoagulants,kloramfenikol, doksisiklin, sulfonamid, allopurinol
• kompetisi pengikatan oleh albumin: penilbutason,salicsiat, sulfonamid
• Inhibisi glukoneogenesis, peningkatan oksidasi
glukosa, atau stimulasi sekresi insulin:etanol, ß-adrenergic drugs
HIPOGLIKEMIA BERKEPANJANGAN
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Managemen hipoglikemia: Pencegahan
1. Pengenalan dini simptom hipoglikemia
2. Diulang secara periodik
3. Penjelasan hubungan antarapemberian insulin, waktu makan, danolahraga
4. Penjelasan cara penanganan
hipoglikemia secara mandiri
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Managemen hipoglikemia: Treatment
• Hipoglikemia ringan: glucosa oral 15-20 g, tunggu 10-15 mnt, periksa lagi kadar glucosa. Bila tidak naik≥18 mg/dl, beri lagi
• Hipoglikemia berat: beri 50 ml dextrose 50% i.v,periksa lagi dalam 20 min. Bila tetap hipoglikemiaberi lagi
• Glucagon 1.0 mg s.c/i.m/i.v. efek samping berupanausea, vomitus, dan sakit kepala. Kontraindikasibila hipoglikemia karena sulfonlurea. Tidak efektif
pada pasien yang anoreksia, atau hipoglikemiaberkepanjangan
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KETOASIDOSIS DIABETIK
HYPERGLYCAEMIC HYPEROSMOLARSTATE
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PATOGENESIS KAD DAN HHS
• Bila terjadi stres atau infeksi maka kebutuhan insulinmeningkat, hormon hormon anti insulin meningkat(glukagon, katekolamin, steroid, hormon pertumbuhan/GH)
• Peningkatan lipolisis, proteolisis, glikogenolisis,ketogenesis, dan glukoneogenesis
• Peningkatan ketogenesis menyebabkan asidosis danpeningkatan benda keton (ketoasidosis)
• Hiperglikemia menyebabkan diuresis osmotik dandehidrasi. Bila tidak diimbangi minum yang cukupakan terjadi hiperosmolar
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lactic acid↑
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KRITERIA DIAGNOSIS
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• Pencetus umumnya infeksi , pencetus lainnya: CVA, alcohol,pancreatitis, infark miokard, trauma, obat-obatan, terapiinsulin yang tidak adekuat
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Tanda dan Gejala KAD
• Pernafasan cepat dan dalam• Bau pernafasan manis seperti buah-buahan
• Nafsu makan turun
• Nausea• Vomitus
• Demam
• Nyeri abdomen
• Penurunanberat badan
• Fatigue
• Weakness
• Confusion
• Drowsiness
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HHS tanda dan gejala
• Haus berlebihan• Poliuri
• Lemah
• Kram kaki• Bingung
• Takikardi
• Kejang
• Coma
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PENATALAKSANAAN
• Rehidrasi (pilihan cairan?)• Pemberian insulin (infus drip)• Intake kalori
• Koreksi elektrolit• Koreksi asidosis
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Penghitungan Osmolaritas
• Osmolaritas
2 (Na + K) + KGD18
Contoh Gula darah 700 mg/dl, Na 145 mEq/L,
K4,5 mEq/LOsmolaritas = 2 (135+4,5) + 700/18= 299 + 38=
337 mOsm/L
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Pilihan Cairan• Dasar kadar Na terkoreksi (bukan Na hasil
pemeriksaan laboratorium)• Setiap peningkatan 100 mg/dl glukosa diatas100 mg/dl, maka kadar Na dikoreksi denganpenambahan 1,6 mEq/L
• Contoh kadar gula darah 700 mg/dl, Na 145mEq/l, maka Na terkoreksi adalah
145 + [( 700-100) X 1,6] = 145 + 9,6= 154,6 mEq/L
100
Bila normonatremi atau hipernatremia, dipilihNaCl 0,45%. Bila hiponatremia, dipilih NaCl0,9%
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• Kadar gula darah dipertahankan sekitar 200-250 mg/dl (fase 2) sampai kondisi pasien stabil(keadaan umum stabil, intake makanan
terpelihara, stres terkendali)• Kemudian kadar gula darah dikendalikan
sesuai target
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KEGAWATAN PADA TIROID
Hipertiroid
Hipotiroid
Krisis tiroid
Koma Miksedema
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Hyperthyroidism: clinical signs and symptoms
• Skin: warm, smooth, sweating increases, onycholysis,hyperpigmentation, pruritus
• Eyes: lid lag (sclera can be seen above the iris as the patientlooks downward)
• Cardiovascular system: increased cardiac output, tachycardia,
atrial fibrillation (10-20%)• Serum lipid: low total cholesterol, low HDL-C• Respiratory system: dyspnea and dyspnea on exertion (increased
oxygen consumption and CO2 production, respiratory muscleweakness)
•
Gastrointestinal system: weight loss, increased gut motility,hyperphagia, malabsorption, vomiting, abnormality in liverfunction test
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Hyperthyroidism: clinical signs and symptoms
• Hematologic system: normochromic-normocytic anemia• Genitourinary system: frequency, nocturia, in women high
serum estrogen concentrations, oligomenorrhea, anovulatoryinfertility. In men high serum total testosteroneconcentrations, gynecomastia, reduced libido, erectile
dysfunction• Skeletal system: stimulation of bone resorption, osteoporosis
• Neuromuscular system: tremor, deep tendon reflexes arehyperactive, hyperactivity, emotional lability, anxiety,inability to concentrate, insomnia, hypokalemic periodic
paralysis• Hyperglycemia: increased insulin secretion, antagonism to
peripheral action of insulin (increased gluconeogenesis, -glycogenolysis, - intestinal glucose absorption)
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Thyroid Storm/Thyrotoxic Crisis
• Life threatening exacerbation of the manifestationsof thyrotoxicosis
• Precipitating factors: acute infection, surgery, postpartum, radiographic contrast agent, ATD withdrawn,
• Clinical signs: alteration in mental status, high fever,tachycardia/tachyarrhythmias, severe clinicalhyperthyroid signs, vomiting, jaundice, diarrhoea,multisystem decompensation
• Treatment: supportive, PTU, Sol lugol, beta adrenergicantagonist
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Hypothyroidism: clinical signs and symptoms
• Age at onset, duration and severity of thyroid hormonedeficiency
• In infants and children: retardation of growth and braindevelopment, short stature and mental retardation
(cretinism)• In adults: asymptomatic, overt hypothyroidism, mixedema
coma
• Generalized slowing of metabolic processes: fatigue, slowmovement and slow speech, cold intolerance, constipation,
weight gain, delayed relaxation of deep tendon reflexes,bradycardia
• Coarse hair and skin, puffy facies, enlargement of thetongue, hoarseness
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Hypothyroidism: clinical manifestation
• Skin: cool, pale, dry roughness of the skin, decreased sweating,coarse hair and hair loss, nonpitting edema
• Eyes: periorbital edema
• Cardiovascular system: decreased cardiac output, decreased
heart rate and contractility, hypertension (increased peripheralresistance)
• Respiratory system: fatigue, dyspnea on exertion,hypoventilation, sleep apnea (macroglossia)
• Gastrointestinal disorders: constipation, decreased taste
sensation, gastric atrophy• Anemia
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Hypothyroidism: clinical manifestation
• Reproductive system: in women oligo- or amenorrhea orhypermenorrhea-menorrhagia, decreased fertility, earlyabortion
• Neurological dysfunction: sleepiness, slow response to question
•
Myxedema coma• Metabolic abnormalities: hyponatremia,
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MYXEDEMA COMA
• Is the ultimate stage of severe long-standinghypothyroidsm, is an uncommon but potentially lethalcondition.
• Patients with myxedema coma are typically elderlywomen who present during the winter months.
• Patients with hypothyroidism may exhibit a number ofphysiologic alterations to compensate for the lack of
thyroid hormone. If these homeostatic mechanismsare overwhelmed by factors such as infection, thepatient may decompensate into myxedema coma
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…MYXEDEMA COMA
• They often demonstrate classic symptoms ofhypothyroidism: fatigue; constipation; weightgain; cold intolerance; a deep voice; coarse hair;
and dry, pale, cool skin.
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Physical Findings in Myxedema Coma
1. Altered mentation2. Alopecia3. Bladder dystonia & distention4. Cardiovascular
1. Elevated diastolic bloodpressure--early2. Hypotension--late3. Bradycardia
5. Delayed reflex relaxation6. Dry, cool, doughy skin
7. GastrointestinalDecreased motility
Abdominal distensionParalytic ileusFecal impactionMyxedema megacolon-late
8. Hyperventilation
9. Hypothermia10.Myxedematous face
Generalized swellingMacroglossiaPtosis
Periorbital edemaCoarse, sparse hair11.Nonpitting edema
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Addison’s Disease
• Described by Thomas Addison in 1855
• The incidence in the developed world
of 0.8 cases per 100,000 andprevalence of 4 - 11 cases per 100,000population
•Associated with significant morbidityand mortality; can be easily treated
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Essential of D/: Addison’s Disease
• Weakness, easy fatigability, anorexia, weight loss;nausea & vomiting, diarrhea; abdominal pain,muscle & joint pains; amenorrhea
• Sparse axillary hair; increased pigmentation of skin,
esp. of creases, pressure area, and nipples• Hypotension, small heart
• Low sodium (Na), elevated K, Ca, and BUN;neutropenia, mild anemia, relative lymphocytosis
• Low plasma cortisol, elevated ACTH
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Adrenal Crisis
• Dehydration, hypotension, or shock outof proportion to current illness severity
• Nausea and vomiting with a history of
weight loss and anorexia
• Abdominal pain so-called acuteabdomen
• Unexplained hypoglycemia
• Unexplained fever
Ad l C i i
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Adrenal Crisis
• Hyponatremia, hyperkalemia,
azotemia, hypercalcemia, oreosinophilia
• Hyperpigmentation or vitiligo
• Other autoimmune endocrinedeficiencies, such as gonadal failure orhypothyroidism
•If suspected: give hydrocortisone 100-300 mg I.V.; refer to hospital
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