Diabetes Mellitus + Gangren Pedis (s) + hipoalbumin...

OBSERVATIONAL ENDOCRINE CASE REPORT

INTERNE-DEPARTMENT/WARD

AUGUST, 1st – 5th 2016

Diabetes Mellitus + Gangren Pedis (s) + Hipoalbumin (membaik) + Anemia (membaik) + Sepsis

DIABETES MELLITUS

Gangguan metabolik kronik, ditandai oleh

hiperglikemia berkaitan dengan abnormalitas

metabolisme karbohidrat, lemak, protein

disebabkan oleh defek sekresi insulin, sensitivitas

insulin atau keduanya

mengakibatkan terjadinya komplikasi kronis termasuk

mikrovaskular, makrovaskular dan neuropati (Tripplitt, 2008; David, G., Basic and Clinical Endocrinology, 2007)

Standard of Medical Care in Diabetes 2010; American Diabetes Association

METABOLIC CHANGES DUE TO DM

Silbernagl, Lang, 2000, Color Atlas of Patophysiology, USA : Thieme Publisher

THE COMPLICATIONS

Silbernagl, Lang, 2000, Color Atlas of Patophysiology, USA : Thieme Publisher

MANAGEMENT THERAPY IN GENERAL

Tripplitt, C.L., Reasner, Diabetes Mellitus, In: J.T. Dipiro, Pharmacotherapy: A Patophysiologic Approach, 7th ed, 2008, USA: The McGraw Hills

Tripplitt, C.L., Reasner, Diabetes Mellitus, In: J.T. Dipiro, Pharmacotherapy: A Patophysiologic Approach, 7th ed, 2008,

USA: The McGraw Hills

DIABETIC FOOT ULCER (The Journal of Foot and Ankle Surgery, vol 39, No 5, Sept. 2000)

RISK FACTORS FOR FOOT ULCER-INFECTION

Lipsky, B.A. et al. Treatment for Diabetic Foot Ulcer, Lancet 2005: 366; 1725-35

Poretsky, L., et al 2009, Principle of Diabetes Mellitus, Springer

PATHOGENS

The Journal of Foot and Ankle Surgery, vol 39, No 5, Sept. 2000

Treatment of Diabetic Foot Infections

Clinical Infectious Disease, 2004;39;885-910


CHOOSING THE PROPER ANTIBIOTICS

INFECTION DEVELOP TO SEPSIS

Sepsis respon sistemik dari host thd infeksi dimana patogen / toksin

dilepaskan ke dalam sirkulasi darah sehingga terjadi proses inflamasi (Balk, R.A., Severe Sepsis and Septic Shock: definition, epidemiology, and clinical manifestation, Crit. Care Clin,

2000;16(2):179-92)

Terjadi pelepasan berlebih mediator inflamasi (TNF, IL), aktivasi

makrofag, neutrofil, limfosit, endotel, sitokin, chemokin,

komplemen (Hack CE., Thjis.L., Role of Inflammatory mediators in sepsis, In: Dhainaut J.F., Thijs, L., Park G., Septic Shock, London: WB Saunders Co, 2000; p. 41-127)

DiPiro, 2008

J.T. Dipiro, Pharmacotherapy: A Patophysiologic Approach, 7th ed, 2008, USA: The McGraw Hills

DEFINITION RELATED TO SIRS - SEPSIS

INFLAMMATORY RESPONSE TO SEPSIS


Data from Dellinger RP, Carlet JM,

Masur H, et al. Surviving sepsis

campaign guidelines for

management of severe sepsis and

septic shock. Crit Care Med

2004;32:858–873

EMPIRIC ANTIMICROBIALS

Crit Care Clin, 24 (2008), 313-334; Gilbert, D.N et al, 2009

DiPiro, J.T., 2008

PATIENT PROFILE AND

THERAPIES

PATIENT PROFILE

Name/ ID

• Tn. W. M. / 12056xxx

Address/ Age / Weight-Height

• Ketintang, Surabaya / 49 tahun / 61 Kg / 160 cm

Hospitalization / Reason & Diagnose

• July, 2016 / 13 July – 2 August

• Reason: luka kaki kiri 1 bulan sMRS 1 minggu sMRS makin sakit, borok hitam terasa cekot-cekot, BB turun, selalu haus.

Other Information

• RPD: MRS di RS “X” 1,5 bulan lalu dengan kelurahan yang sama

• Mata kiri pasien tidak dapat melihat Dx Diabetic Retinopathy

• RPO : Metformin, Glibenklamid

CLINICAL FINDING (July to August)

Clinical

data

Nor. 14

15 16 17 18 19 20 21 22 23 24 25

BP 120/

80

110/

70

110/

80

100/

60

120/

80

110/

70

110/

60

110/

80

120/

70

120/

80

110/

80

110/

60

110/

80

HR (x/m) 80-

100

100 100 100 100 80 80 88 88 96 100 100 88

RR

(x/m)

18-

22

20 18 20 18 18 20 20 20 20 18 18 20

Temp (C) 36,5

-

37,5

37,9 38 38 38 38 37,5 36,5 36,6 36,7 37,9 37,8 36,6

Nyeri kaki - + + + + + + + + + + + +

Mu/munt -/- - - - - - - +/- +/- - - - -

CLINICAL FINDING (July to August)

Clinical data Nor. 26

27 28 29 30 31 1 2 3

BP 120/80 110/60 110/70 110/70 120/80 120/80 120/80 130.80 120/80 110/70

HR (x/m) 80-100 80 84 84 88 90 90 84 80 80

RR

(x/m)

18-22 20 20 20 20 20 20 20 20 20

Temp (C) 36,5-37,5 37,5 37 37,3 37,3 37,5 37,8 37,3 37,8 37,5

Nyeri kaki - + + + + + + + + +

Mual/mun. -/- - - + + + - - - -

LAB FINDINGS

BGA

Data Satuan Normal 13/7 18/7 22/7 27/7

HGB g/dL 12-16 6,7 11,3 10,2 9,76

RBC 106/µL 4,2-5,4 2,5 4,14 3,88 3,66

HCT % 37-47 21,1 11,3 31,4 30,4

MCV fL 81-99 70 81,9 80,9 82,8

MCH Pg 27-31 21,1 27,2 26,3 26,3

MCHC g/dL 33-37 29 33,2 32,5 32,5

PLT 103/µL 150-450 379 439 435 576

MPV fL 7,2-11,1 7,0 7,5 8,0 9,0

WBC 103/µL 4,8-10,8 25 22,5 17,1 14,6

Neu 19,3 13,9 10,1

Lym 1,42 1,84 3,35

Mono 1,52 1,9 0,69

Eos 0,217 0,6 0,174

Baso 0,129 0,2 0,231

APTT/c 25-40/

LAB FINDINGS

Data Satuan Normal 13 14 18 19 20 22 25 26 27 28 29 1

LED mm/h

LAB FINDING (WOUND CULTURE)

Tanggal Pemeriksaan dan Hasil Sensitivitas

14/7 dijawab 20/7

Sampel : DARAH

Jenis : kultur aerob, anaerob

Hasil :

A. Staphyloccocus coagulase negative

hitungan koloni > 105 CFU / ml

B. Tidak ada pertumbuhan kuman anaerob

S : Gentamisin, Eritromisin, Clindamisin,

Azitromisin, Claritomisin, Meropenem

R: Penicilin G, Oxacillin, Cotrimoxazole,

Minocycline, Ciprofloxacin, Ofloxacin,

Levofloxacin, Moxifloxacin

15/7 dijawab 18/7

Sampel : nanah / pus dari pedis (s)

Jenis : kultur aerob

Hasil : E. Coli ESBL (+)

Hit koloni : (-)

S : Amikacin, Imipenem, Meropenem,

Piperacillin-Tazobactam

R : Tobramicin, Gentamicin, Astreonam,

Amoxicillin, Amoxiclav, Ticarcilin-Clav.,

Ciprofloxacine, Azitromisin, levofloxacin,

Ofloxacin, Moxifloxacin, Cephalotin,

Cefazolin, Cefuroxime, Ceftazidim,

Cefotaxime, Ceftriaxone, Cefixime

THERAPIES (July)

TERAPI REGIMENTASI

DOSIS

13 14 15 16 17 18 19 20 21 22 23 24 25 26

PZ 1500cc/24 j 7

tpm

√ √ √ √ √ √ √ √ √ √ √ √ √ √

Apidra®

(insulin

glulisine/rapid

acting)

3X6 U 15’ac √ √ √ √ √ √ √ //

Actrapid®

(human insulin/rapid

acting)

3x10 U 15’ac √ √ √ √ √ √ √

Lantus® (insulin

glargine/long acting)

0-0-14 U √ √ √ √ √ //

Humulin N (insulin

NPH/intermediate

acting)

0-0-14 U √ √ √ √ √ √ √

Metronidazol 3x500 mg iv drip √ √ √ √ √ √ √ √ √ √ √ √ √ √

THERAPIES (July)

TERAPI REGIMENTASI

DOSIS

13 14 15 16 17 18 19 20 21 22 23 24 25 26

Ampisilin -

Sulbaktam

3x1 g i.v √ √ √ √ √ √ √ √ √ //

Meropenem 3x1 g iv √ √ √ √ √

ASA 1x100 mg √ √ √ √ √ √ √ √ √ √ √ √ √ √

Ondansetron 2x4 mg i.v √ √ √ √ √ √ √

Metamizole 3x500 mg i.v

Albumin 100 ml/4 jam

20%

√ √ √ √ √ √ √ √

PRC 2 kolf/hari √ √ √ √ √

Curcuma √ √ √ √ √ √ √

THERAPIES (July to August)

TERAPI REGIMENTASI

DOSIS

27 28 29 30 31 1 2 3 (KRS)

PZ 1500cc/24 j 7 tpm √ √ √ √ √ √ √ //

Actrapid 3x10 U 15’ac √ √ √ √ √ √ √ √

Humulin N 0-0-14 U √ √ 0-0-

16

0-0-

16

0-0-16 0-0-16 0-0-16 //

Metronidazole 3x500 mg i.v drip √ √ √ √ √ √ √ √

Meropenem 3x1 g i.v √ √ √ √ √ √ √ V

ASA 1x100 mg √ √ √ √ √ √ √ √

Dipiridamol 1x25 mg √ √ √ √ √ √ √ √

Ranitidine 2x50 mg i.v √ √ √ √ √ √ √ √

Ondancetron 2x 4 mg i.v √ √ √ √ √ √ √ √

Metamizole 3x500 mg i.v √ √ √ √ √ √ √ √

Multivit 1x1 tab √ √ √ √ √ √

THERAPY

ANALYSIS

CONTROL FOR HYPERGLYCEMIA

Nama Indikasi Monitoring

INSULIN Menurunkan kadar glukosa darah pasien melalui regimentasi

RCI dan maintenance sbg kontrol hiperglikemia pada pasien

dengan infeksi.

Outcome therapy:

Tgl 13/7

GDA 583 RCI 4X4 U GDA 474 (pk. 22.30) RCI

3x4 U

Tgl 14/7

GDA 345 RCI 5X12 U per 24 jam

Tgl 22 /7

GDA 367 RCI 3X4 U GDA 271 post RCI

Tgl 25/7


Tgl 27/7


GDP, GD2PP, GDA,

tanda hipoglikemia

Tripptill & Reanes, 2008

PHARMACOKINETICS OF VARIOUS INSULIN


KOREKSI HIPOGLIKEMIA

Target pemberian glukosa = 15-20 gram

Sediaan larutan glukosa = D5, D10, D40

Apabila koreksi hipoglikemia dengan D40 (target glukosa 15 g):

40% 40 g = 15 g X = 37,5 mL (kemasan: D40, 25 mL)

100 mL X

Apabila koreksi hipoglikemia dengan D10 (target glukosa 15 g):

10% 10 g = 15 g X = 150 mL (kemasan: D10, 500 mL)

100 mL X

Cara Penyiapan D20

Cara penyiapan 100 mL D20 dari D40 dan NS 0,9% atau WFI:

40 (D40) [20] 20 x 100 mL = 50 mL

40

20

0 (WFI/NS) [20] 20 x 100 mL = 50 mL

40 40

NS 0,9% 500 mL dipindahkan volumenya sebanyak 450 mL (secara teknik aseptik di LAFC).

Diambil menggunakan spuit D40 sebanyak 50 mL ditambahkan ke kantong NS 0,9% (secara teknik aseptik di LAFC) yg tinggal tersisa 50 mL total cairan dalam kantong tsb 100 mL campuran D40 dan NS 0,9%.

TREATMENT FOR FOOT ULCERS

Nama Indikasi Komentar dan

Monitoring

Ampicillin-

Sulbactam

Mengatasi infeksi pada pasien dengan gangren pedis, khususnya kuman gram

(+) aerob maupun gram (-) aerob yang patogen pada luka gangren, seperti

Staphyloccocus sp, Streptoccocus, Enterococci, mengatasi bakteri dengan sifat broad

spectrum (cincin beta laktam pada ampisilin mudah didegradasi oleh bakteri

penghasil β-laktamase sehingga dikombinasi dengan sulbaktam untuk

melindungi cincin β-laktam)

Pada pasien ini,

penggantian ampisilin-

sulbaktam menjadi

meropenem karena dari

nilai WBC masih tinggi,

Px sempat mengalami

demam, dan

pemeriksan kultur

nanah didapatkan

bakteri E. coli ESBL (+)

dan kultur darah S.

coagulase (-) yang

sensitif pada

meropenem.

Monitoring terhadap

WBC, tanda SIRS (nadi,

suhu, RR), CRP.

Kondisi pus (basah

dengan gas /

mengering)

Meropenem Merupakan golongan antibiotik karbapenem yang mampu mengatasi infeksi

pada pasien dengan gangren pedis, khususnya kuman gram (+) aerob

maupun gram (-) aerob yang patogen pada luka gangren, seperti

Staphyloccocus sp, Streptoccocus, Enterococci dengan potensi bakterisidal yang

kuat, bersifat broad spectrum

Metronidazole Mengatasi infeksi oleh karena bakteri anaerob, seperti B. fragilis, C. difficile, C.

perfringens pada pasien dengan gangrene pedis


Providing optimal wound care (addition to AB for infection) is

crucial for healing (Level of Evidence A-I)

Select an empirical AB regimen on the basis of severity of infection

and likely etiology agent (Level Evidence B-II) Therapy aimed

solvely at aerob gram (+) may be suffience for patient who have not

recently receveid AB (Level Evidence A-II)

Topical therapy may be used for some mild superficial infection

(Level of Evidence B-I); Suggestion for the duration of AB therapy:

usually 2-4 weeks for severe infection, depending on the adecuacy of

debridement, wound vascularity (Level of Evidence A-II)

For most patient, AB will begin with an empiric regimen while awaiting the result of wound culture should aim to cover the important & common patogens (Staphyloccoci, Streptococci, gram negative bacilli, enterococci, anaerobs)

Minor infections can be treated with narrow spec. AB.

Therapy should parenteral for patient who are systemically ill or have a severe local infection

AB can be discontinued when there are no longer sign and symptom, even if the wound has not completely healed (Lipsky, 1999)

For mild to moderate infection, topical is an additional option such as neomycin, polymixi B, aminoglycoside and mupirocin has been used for soft tissue and infection, but there is no multicenter evidence based data on their efficacy in diabetic foot infection.

Advanced In Therapy, 2005

Clinical Infectious Disease 2010; 50; S16-S23

MTZ is effective for the management of anaerobic infection such us bone-joint infection highly active against gram (+) and (-) anaerob bacteria such as B.fragilis, C.difficile.

MTZ enter the cell as a produg by passive difussion activated in cytoplasm of bacteria. peak plasma occur 1-2 h after administration; prot.binding is low.

MTZ molecule is converted to a short lived nitroso free radical by intracelular reduction inhibit DNA syntesis and damage DNA by oxidation cell death.

The mechanism of resistance to MTZ in Anaerobic bacterial due to: Reducted drug activation; inactivation of drug by alternative pathway; drug efflux; altered DNA repair until 2010, resistance among anaerobic pathogen still generally low

1. Indication (Diagnosis) adherence to G.L.

2. Appropriate to patients physical & physiology

3. Correct in A.M. drug: choice,

4. Correct in dosage regimen, duration, route of

administration

5. Less side effect

6. To be clearly informed to the pts

7. Evaluation of the clinical outcome

Chain of the principles of rationality antimicrobial drug use (Gyssen e.a. 1996)

The pyramid of infectious

disease (Gyssens, 1996) Therapy

Pathogens

Commensals Host Act

ivit

y A

MR

Rheologic Repairment & Vascularization

DM type 2 associated with an increased thrombotic reactivity (Drouet.L, Diabetes, Obesity and Metabolism, 1 (Suppl 2),1999,S37-S47; Cippola, M. et al, Endocrine

Reviews 22(1): 2006; 36-52

The spesific concern for atherothrombotic and diabetic patient is

to ascertain if antithrombotic agent whose efficacy has been

shown

Nama Indikasi

Aspirin Inhibits prostaglandin synthesis, resulting in analgesia, anti-inflammatory

activity and platelet aggregation inhibition

Dipiridamol Antithrombotic action resulting from additive antiplatelet effects.

THROMBOGENESIS & IMPAIRMENT OF

VASCULARIZATION IN DM GANGRENE

Silbernagl, Lang, 2000

EVIDENCE BASED MEDICINE OF ANTIPLATELET IN MANY DM-

COMPLICATION

Aspirin, alone or in combination with dipyridamole, is also being evaluated for potential efficacy in preventing progression of diabetic retinopathy in patients with DM (AHFS, 2008)

Randomized, Comparative Placebo Control Aspirin plus dipyridamole reduced the risk of stroke due to DM and risk of thrombotic by about 23% compared with aspirin alone and by about 25% compared with dipyridamole alone at 2 years of follow-up.

ACCP and AHA recommend that aspirin (50-325 mg daily), or the combination of aspirin and dipyridamole (25 mg aspirin/200 mg extended-release dipyridamole twice daily) are all considered acceptable options for initial antiplatelet therapy for prevention of other vascular events

ADA currently recommends low dosages of aspirin (75-162 mg daily) for the prevention in diabetic men and women who have evidence of large vessel disease

Aspirin alone or in combination with dipyridamole may modify the natural history of intermittent claudication resulting from arteriosclerosis

In one study, combination therapy with aspirin and dipyridamole was considered ineffective and patients receiving the combination had an increased risk of severe bleeding complications;

The combination of aspirin and dipyridamole has been shown to reduce blood concentrations of circulating platelet aggregates and β-thromboglobulin in patients with scleroderma

(Randomized, Double Blind, Placebo Control, Multicenter Study by : The American Heart Association (AHA); European/Australasian Stroke Prevention in Reversible Ischaemia Trial [ESPRIT; The American College of Chest Physicians (ACCP); Second International Study of Infarct Survival; ISIS-2; American Diabetic Association (ADA)); all statements occurs in AHFS Drug Information, 2008)

PREVENTION OF STRESS ULCER –

NAUSEA AND VOMIT

Nama Indikasi Komentar dan Monitoring

Ranitidine Decrease stimulation of histamine on parietal cell

acid secretion Most trials show lower risk

of significant GI hemorrhage (Shuman, RB.

Prophylactic therapy for stress ulcer bleeding. Ann Int

Med 1987; 106: 562-8)

Infeksi kondisi critical

illnes risiko stress ulcer

meningkat. Pemberian

ranitidine dapat mengatasi

acute stress ulcer pada

pasien dimonitoring

setiap hari rasa nyeri

epigastrik, mual, kembung,

perih.

Pasien mengeluh mual tgl

20-22 dan tgl 28-31

sehingga dpt diberikan

antiemetik dan

dimontoring tanda nausea

vomit yang dialami.

Pemilihan antiemetik tidak

sesuai dengan konidis

pasien.

Ondancetron Selective serotonin (5-HT3) receptor antagonist

that inhibits serotonin receptors in GI tract or

chemoreceptor trigger zone prevent nausea

and vommiting with high potencial effect (Tatro,

2003; Katzung, B.G., 2007)

DM GANGRENE-SEPSIS INDUCE ACUTE STRESS ULCER

Curr Med Res Opin, 2005

DRUG RELATED THERAPY

(Prudent Drug Used)

DRUG RELATED THERAPY LIST ADVICE AND MONITORING

Penggunaan ranitidine masih diteruskan pd tgl 1-3 Ags,

namun px sudah tidak mengeluhkan mual/muntah

Sebaiknya pemakaian ranitidine dihentikan karena

tidak terdapat tanda klinis yg mendukung

Penggunaan ondancentron dr tgl 20 Jul-3 Agst

diteruskan, pasien tidak mengeluh mual/muntah

Perlu dipertimbangkan kembali pemakaian ondansentron

Sebaiknya pemakaian ondancetron dihentikan karena

tidak terdapat tanda mual/muntah.

Bisa diberikan metoklopramid

Penggunaan meropenem 12 hari (22 Jul-2 Agst) tidak

dilakukan pemantauan kultur darah ulang, meskipun scr

klinik progesifitas infeksi pasien membaik.

Pemberian meropenem slm pasien sepsis

dipantau tanda klinik pasien; sebaiknya dilakukan

kultur darah lagi (evaluasi) setelah 7 hari terapi.

Pasien merupakan pasien DM gangren-sepsis dengan

ulkus > 2 cm (pro amputasi digiti 2-4), dimana

vaskularisasi obat ke jaringan infeksi jelek

Sebaiknya pasien dilakukan debridement (amputasi

sesuai dg advice BTKV); perawatan luka yg baik

dibilas dg NS dan diberi kanamycin tabur, dmn

aminoglikosida efektif mengatasi kuman gram (-),

(+) aerob yg ada pada superficial luka gangren.

Pemakaian metamizol sebagai antinyeri kurang adekuat

(pasien terus mengeluh nyeri pada kaki)

Pasien mengalami nyeri neuropati yang tidak

adekuat dengan pemakaian NSAID / analgesik

metamizol disarankan terapi analgesik

menggunakan TCA / bila lebih nyeri dapat diberi

tramadol.

Pemberian infus albumin 20% pada saat kadar albumin

masih > 2 g/dL

Pasien belum perlu mendapatkan infus albumin

Pemilihan antiemetik ondansentron tidak sesuai karena

mual muntah Px bukan karena obat kemoterapi

Dipilihkan antiemetik metoklopramide/domperidon

ALBUMIN HUMAN

A low-molecular-weight protein; maintains intravascular oncotic

pressure; responsible for transport of bilirubin, calcium, and

many drugs; indicated for urgent restoration of blood volume;

preparations are derived from pooled human blood, plasma,

serum, or placentas, and contain no blood-clotting factors, Rh

factor, or other antibodies.

Albuked/Albumarc/Albumin

Human/Albuminar/AlbuRx/Albutein/Buminate/Flexbumin/K

edbumin/Macrotec/Plasbumin Intravenous Inj Sol: 5%, 5mL,

25%, 1.0-1.5mg.

DOSAGE & INDICATIONS OF ALBUMIN HUMAN

For the treatment of shock due to hypovolemia dosage should be based on

patient response as indicated by blood pressure, degree of pulmonary

congestion, and hematocrit.

Intravenous dosage in adults Initially, rapidly administer 5% solution IV. As the

plasma volume approaches normal, infuse IV at a rate

≤ 2-4 mL/minute (rate of 25% solution ≤

mL/minute). May repeat initial dose in 15-30

minutes. Continued protein loss may require

administration of whole blood and/or other blood

factors.

Intravenous dosage in

children

0.5-1 g/kg/dose IV. May repeat as needed. Maximum

dosage is 6 g/kg/day.

Intravenous dosage in

neonates

The usual dose is 0.5 g/kg IV as a 5% solution;

however, dosages may range from 0.25-0.5 g/kg IV.

The 25% solution should be avoided in preterm

neonates due to the risk of intraventricular

hemorrhage.

For adjunctive treatment of severe burns.

Intravenous dosage in adults Individualize dosage to clinical goals. Initial

recommended therapy includes administration of a large

volume of crystalloid solution for the first 24 hours,

followed by more albumin and less crystalloid to

maintain electrolyte balance and prevent marked

hemoconcentration. Albumin should not be

administered to patients with severe burns in the first

24 hours following the burn because of capillary

exudation of albumin. Goal of therapy is to maintain

plasma albumin level of 3-4 mg/dL. Duration of

treatment is based on protein loss through renal

excretion, denuded skin, and decreased albumin

synthesis.

For the treatment of nephrosis in nephrotic syndrome.

Intravenous dosage in adults 100-200 mL of 25% albumin IV administered with a

loop diuretic for 7-10 days has been successful in

controlling edema.

For treatment of hypoproteinemia.

Intravenous dosage in adults 25 g IV. May repeat in 15-30 minutes. Alternatively, 200-300

mL (50-75 g) of 25% albumin IV infused at a rate ≤ 2

mL/minute to avoid an excessive increase in plasma volume.

Maximum dosage is 250 g per 48 hours (5 L of a 5% solution

or 1 L of a 25% solution).

Intravenous dosage in neonates,

infants, and children

0.5-1 g/kg/dose IV infused over 2-4 hours. May repeat every

1-2 days. Alternatively, 100 mL (25 g albumin) of 25%

albumin IV infused at rate ≤ 2 mL/minute to avoid too large

an increase in plasma volume. For neonates, the dose may be

added to hyperalimentation and infused over 24 hours.

For adjunctive use with exchange transfusion in the treatment of hyperbilirubinemia

and erythroblastosis fetalis (hemolytic disease of the newborn).

Intravenous dosage (25%

Albumin) in neonates

1 g/kg/dose IV administered 1 to 2 hours prior to or during

exchange transfusion.

Maximum Dosage Specific maximum dosage information is not available.

Individualize dosage based on careful monitoring of clinical

parameters in all patient populations.

Intravenous Administration of Albumin

1. Albumin human 5% or 25% may be given undiluted.

2. The 25% solution may be diluted with 0.9% Sodium Chloride Injection or 5%

Dextrose Injection before administration to give a 20% (200 mL/L) albumin human

solution.

3. The 5% Dextrose solution is oncotically equivalent volume for volume to human

plasma.

4. 50 mL of 25% albumin supplies the oncotic equivalent of 250 mL citrated plasma.

Intravenous (IV) infusion:

1. Use administration set provided by the manufacturer.

2. Administer using a large needle or catheter of at least 20 gauge.

For hypovolemic shock:

1. The initial dose should be administered as rapidly as tolerated.

2. After the initial dose is administered, the rate of administration should be adapted to

the response of the patient.

3. As blood volume approaches normal, the infusion rate should be slow enough (1

mL/minute) to prevent too rapid expansion of plasma volume.

Intravenous Administration of Albumin

For hypoproteinemic patients:

1. Administration rates for the 25% solution vary by manufacturer.

2. Maximum rates of 2 mL/minute and 3 mL/minute are recommended.

3. Too rapid infusion may cause circulatory compromise, including

pulmonary edema.

4. Premature neonates are more prone to intraventricular hemorrhage due

to rapid intravascular volume expansion.

SEKIAN & TERIMA KASIH

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