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Edukasi Perawatan Kaki Diberikan Secara Rinci Pada Semua Orang Dengan Ulkus Maupun Neuropati Perifer Atau Peripheral Arterial Disease (PAD)
Edukasi Perawatan Kaki Diberikan Secara Rinci Pada Semua Orang Dengan Ulkus Maupun Neuropati Perifer Atau Peripheral Arterial Disease (PAD)
Edukasi perawatan kaki diberikan secara rinci pada semua orang dengan ulkus maupun neuropati perifer atau
(PAD)
1. Tidak boleh berjalan tanpa alas kaki, termasuk di pasir dan di air.
2. Periksa kaki setiap hari, dan dilaporkan pada dokter apabila kulit terkelupas,
kemerahan, atau luka.
3. Periksa alas kaki dari benda asing sebelum memakainya.
4. Selalu menjaga kaki dalam keadaan bersih, tidak basah, dan mengoleskan
krim pelembab pada kulit kak
5. Potong kuku secara teratur.
6. Keringkan kaki dan sela-sela jari kaki secara teratur setelah dari kamar
mandi.
7. Gunakan kaos kaki dari bahan katun yang tidak menyebabkan lipatan pada
ujung-ujung jari kaki.
8. Kalau ada kalus atau mata ikan, tipiskan secara teratur.
9. Jika sudah ada kelainan bentuk kaki, gunakan alas kaki yang dibuat khusus.
10. Sepatu tidak boleh terlalu sempit atau longgar, jangan gunakan hak tinggi.
11. Hindari penggunaan bantal atau botol berisi air panas/batu untuk
menghangatkan kaki.
Kapan digunakan?
- Secara fisiologis terdapat 2 macam pola sekresi insulin : Basal dan Prandial.
- Ketika terjadi defisiensi maka insulin eksogen dapat mensubsitusi terhadap defisiensi
- Def. insulin basal = peningkatan KGD puasa
- Def.insulin prandial = peningkatan KGD setelah makan
- Untuk mengatasi Def. insulin basalterapi oral/insulininsulin kerja sedang/panjang
o Apabila KGD sudah tercapai namun HbA1c belum mencapai target, bisa
dikendalikan insulin prandialnya dengan insulin kerja cepat yg disuntikan 5-10
menit sebelum makan dan insulin kerja pendek yg disuntikkan 30 menit
sebelum makan
- Bisa dikombinasikan dengan obat oral
DKA
- A consensus statement from the International Society for Pediatric and Adolescent
Diabetes (ISPAD) in 2014 :
o Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND
o Metabolic acidosis – Defined as a venous pH <7.3 or plasma bicarbonate
<15 mEq/L (15 mmol/L)AND
o Ketosis – Determined by the presence of ketones in the blood or urine.
Serum beta-hydroxybutyrate is a more accurate measure of ketosis
and should be used whenever available. Beta-hydroxybutyrate
concentrations ≥3 mmol/L (31 mg/dL) are consistent with DKA
- Pencetus
o Poor metabolic control/missed insulin doses
o Strestmeningkatkan sekresi katekolamin, kortisol, glucagonoeningkatan
produksi glukosa dan ketoacid
o Vomiting and dehydrationpenyakit yg terjdai bersamaaan mengganggu
intake makananpenurunan dosis insulin oleh keluarga
o Obatkortikosteroid, antipsikotik atipikal
o Alkohol
- Gejala
o Onset akut (rapid)
o Tripoli, takikardi, fatigue, nocturia
Polyphagia usually occurs early in the course of the illness. However,
once insulin deficiency becomes more severe and ketoacidosis
develops, appetite is suppressed. Some patients present with
anorexia, nausea, vomiting, and abdominal pain, which at times can
mimic appendicitis or gastroenteritis
o Napas kussmaul
o KU : bisa mengantuk, lethargy hingga komaderajat hiperosmolalitas atau
derajat asidosis
HH
- Keadaan kegawatdaruratan yang ditandai dengan :
o Hyperglikemi >600 mg/dl
o Serum bicarbonate >15 mmol/L
o Asidosis minimal (ph vena >7.25)
o Absent or small ketonuria
- Gejala
o Onset insidious
FR 22nya :
- Infeksi pneumonia or UTI dan berhenti intake insulin atau terapi tidak adekuat
- Gejala neurologis umum di HHS, gejala hiperventilasi dan nyeri perut hanya di DKA
o nausea, vomiting, and abdominal pain
Possible causes of abdominal pain include delayed gastric emptying
and ileus induced by the metabolic acidosis and associated electrolyte
abnormalities
Clinical features
DKA usually evolves rapidly over a 24-hour period.
Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and
hyperventilation. The earliest symptoms of marked hyperglycemia are polyuria, polydipsia,
and weight loss.
As hyperglycemia worsens, neurologic symptoms appear and may progress to include
lethargy, focal deficits, obtundation, seizure, and coma.
Common causes of DKA include: infection; noncompliance, inappropriate adjustment, or
cessation of insulin; new-onset diabetes mellitus; and myocardial ischemia.
Evaluation and laboratory findings
Assess vital signs, cardiorespiratory status, and mental status.
Assess volume status: vital signs, skin turgor, mucosa, urine output.
Obtain the following studies: serum glucose, urinalysis and urine ketones, serum
electrolytes, BUN and creatinine, plasma osmolality, mixed venous blood gas,
electrocardiogram; add serum ketones if urine ketones present.
DKA is characterized by hyperglycemia, an elevated anion gap* metabolic acidosis, and
ketonemia. Dehydration and potassium deficits are often severe.
Serum glucose is usually greater than 250 mg/dL (13.9 mmol/L) and less than 800 mg/dL
(44.4 mmol/L). In certain instances (eg, insulin given prior to emergency department arrival),
the glucose may be only mildly elevated.
Additional testing is obtained based on clinical circumstances and may include: blood or
urine cultures, lipase, chest x-ray.
Management
Stabilize the patient's airway, breathing, and circulation.
Obtain large bore IV (≥16 gauge) access; monitor using a cardiac monitor, capnography,
and pulse oximetry.
Monitor serum glucose hourly, and basic electrolytes and venous pH or bicarbonate every
two to four hours until the patient is stable.
Determine and treat any underlying cause of DKA (eg, pneumonia or urinary infection,
myocardial ischemia).
Replete ECF volume and free water deficits:
• Give several liters of IV isotonic (0.9%) saline as rapidly as possible to patients with signs
of shock.
• Give IV isotonic (0.9%) saline at 15 to 20 mL/kg per hour (ie, 1 to 1.5 L per hour for an
average-sized adult), in the absence of cardiac compromise, for the first few hours to
hypovolemic patients without shock.
• After intravascular volume is restored, give one-half isotonic (0.45%) saline at 4 to 14
mL/kg per hour if the corrected serum Na+¶ is normal or elevated; isotonic saline is
continued if the corrected serum Na+¶ is reduced.
• Add dextrose to the saline solution when the serum glucose reaches ~200 mg/dL (11.1
mmol/L).
Replete potassium (K+) deficits:
• Regardless of the initial measured serum K+, patients with DKA have a large total body K+
deficit.
• If initial serum K+ is below 3.3 mEq/L, hold insulin and give potassium chloride 20 to 40
mEq/hour IV until K+ concentration is above 3.3 mEq/L; rarely, additional potassium
supplementation may be necessary to avoid life-threatening muscle weakness and cardiac
arrhythmias.
• If initial serum K+ is between 3.3 and 5.3 mEq/L, give potassium chloride 20 to 30 mEq per
liter IV fluid; maintain serum K+ between 4 to 5 mEq/L.
• If initial serum K+ is above 5.3 mEq/L, do not give potassium; check serum K+ every 2
hours; delay administration of potassium chloride until serum K+ has fallen to 5 to 5.2
mEq/L.
Give insulin:
• Do not give insulin if initial serum K+ is below 3.3 mEq/L; replete K+ and fluid deficit first.
• Give all patients without a serum K+ below 3.3 mEq/L regular insulin. Either of two
regimens can be used: 0.1 units/kg IV bolus, then start a continuous IV infusion 0.1 units/kg
per hour; OR do not give bolus and start a continuous IV infusion at a rate of 0.14 units/kg
per hour.
• If serum glucose does not fall by at least 50 to 70 mg/dL (2.8 to 3.9 mmol/L) in the first
hour, double the rate of insulin infusion.
• When the serum glucose reaches 200 mg/dL (11.1 mmol/L), it may be possible to
decrease the infusion rate to 0.02 to 0.05 units/kg per hour.
• Continue insulin infusion until ketoacidosis is resolved, serum glucose is below 200 mg/dL
(11.1 mmol/L), and subcutaneous insulin is begun.
Give sodium bicarbonate to patients with pH below 6.90:
• If the arterial pH is below 6.90, give 100 mEq of sodium bicarbonate plus 20 mEq of
potassium chloride in 400 mL sterile water over two hours; may be repeated if venous pH
remains below 7.00.