Upload
others
View
14
Download
0
Embed Size (px)
Citation preview
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
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
J.T. Dipiro, Pharmacotherapy: A Patophysiologic Approach, 7th ed, 2008, USA: The McGraw Hills
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
GDA 513 RCI 4X4 U GDA 234 post RCI
Tgl 27/7
GDA 300 RCI 3X4 U GDA 189 post RCI
GDP, GD2PP, GDA,
tanda hipoglikemia
Tripptill & Reanes, 2008
PHARMACOKINETICS OF VARIOUS INSULIN
J.T. Dipiro, Pharmacotherapy: A Patophysiologic Approach, 7th ed, 2008, USA: The McGraw Hills
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
Clinical Infectious Disease, 2004;39;885-910
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