12-DIABETES MELLITUS.pdf

8/17/2019 12-DIABETES MELLITUS.pdf

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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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12-DIABETES MELLITUS.pdf

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