case trali

Case Report

Nama : Ny. Sumirah Umur : 63 th BB : 50 kg RM : 12.23.41.34 Diagnosa pre op : Struma difusa non toksika PS ASA : 2 (Geriatri, special condition airway sulit) OP : Sub total Thyroidectomy k/p Sternotomi Ass Post Op : Sub total Thyroidectomy + Sternotomi + TRALI

Pre Op Anesthesi4/4/13

B1 : A bebas, BM > 3 jari, JMH>6cm, GLB, MP 2, gigi ompong +, gigi goyang -, gigi palsu – R/ asma -, alergi -, URI – SpO2 98 % dg O2 21 % B SR 20-24 x/mnt, sim +/+, ves +/+, rk -/-, wh -/-B2 : p HKM, CRT <2, HR 90 x/mnt reguler. Kuat angkat , TD 130/80 mmHg, temp 36,5 axiler tanda dehidrasi –, tremor -B3 : Alert, GCS 4-5-6, PBI 3/3, RC +/+ , riw/ pusing, mual muntah, pingsan, kejang - .

Pre Op Anesthesi

B4 : BAK spontan +B5 : flat, soepel +, BU + dbn

Pemeriksaan Penunjang

Laboratorium (9/4/13)Hb 12,5 Na/K/Cl 142/ 4,1/101Hct 37,6 BUN/SK 7,2/0,57L 10,3 OT/PT 17/5 Tr 264 Alb 3,6PPT 13/13,6 GDA 166 APTT 23,5/26,6

BGA O2 21 %15/4/13

pH 7,49 pCO2 34,5 pO2 66 HCO3 26,4 BE 2,9SaO2 94 %P/F 314

Pemeriksaan Penunjang

11/4/13Faal Thyroid dBNT3 : 0,66 ( 0,6 – 1,8 )T4 : 4,6 ( 4,5-10 )TSH : 5,5 ( 0,35 - 5,5 )

Thorax 4/4/13

Thorax lateral

Cervical AP/Lat4/3/13

Opasitas berdensitas massa berbentuk bulat, batas tegas, tepi reguler di R Colli D yg terproyeksi setinggi VC5-VTh 7 sisi kanan yang menyebabkan pendesakan trakea ke sisi kanan dan penyempitan lumen trakea bagian distal tanpa gambaran bulging soft tissue mass di R thoracalis dpt mrpk massa R Colli D s/d Retrosternal

CT Scan thorak + kontras11/3/13

Heterougenous enhancing solid lobulated mass di thyroid lobus kanan, kiri, dan istmus yg meluas ke retrosternal mengisi mediastinum anterior dan posterior terutama posterior hemithorak kanan kiri ( dominan kanan) disertai encasement trachea yg menyebabkan penyempitan lumen trachea dan pembesaran KGB pretrachea mengesan struma multinudusa kemungkinan dengan degenerasi maligna

FNAB 28/3/13

Massa di R colli anterior - Nodular Colloid Goiter

Konsul kardio4/4/13Irama sinus 70 x/mnt, axis N CRI klas 1

Komorbid :1. Geriatri2. Special condition airway sulit

Konsultasi

Dr. Maulydia SpAn- Melaporkan pasien dengan PS ASA 2- ACC dikerjakan dg GA Intubasi, dengan

mempersiapkan ETT dg berbagai ukuran untuk mengantisipasi besarnya lumen trakea yg mengalami penyempitan, persiapan difficult intubation, LD sebelum intubasi, Intubasi sleep non apneu.

GBPT OK 51216/4/13

Jam 10.00 Persiapan alat dan obat GA IV line terpasang berjalan lancar, pasang prekordial

stetoskop, pasang monitor onPremed : -Induksi : midazolam 1 mg + 1 mg fentanyl 50 mcg propofol 50 + 20 mg Intubasi oral sleep non apneu ETT no 7.0 cuff + sim + fix +Maintenance : isofluran + O2 , ketamin TIVA

Durante Op

Jam induksi : 10.00 – ( 17.30) insisi I ( SubTotal thyroidectomy ) : 10.30 insisi II ( Sternotomy ) : 14.00 HemodinamikTD S/D : 34-135/ 15-90 mmHgHR : 61-130 x/mntSpO2 : 88-98 %Perdarahan : ± 7000 cc

Durante Op

Perdarahan yang merembes dari tumor bed yang tdk dpt berhenti, ditambah dengan sternotomi yang dilakukan dmn kontrol perdarahan pada tumor bed yang masih belum optimal merupakan kontribusi terbesar perdarahan durante op dan gejolak hemodinamik pada operasi tersebut.

Durante Op

Pemakaian inotropik (dopamin, noradrenalin )Pada saat sternotomi hampir selesai, muncul

irama AF moderate – rapid – moderate respons ( 115-130 x/mnt ), dopamin tapp down- tapp off.

Durante Op

Ditemukan : - struma multinodusa bilateral - struma retrosternal DDilakukan : - Total thyroidectomy (redon drain D/S) - Sternotomy (chest tube D + substernal drain)

EBV dan EBL

EBV 65 x 50 = 3250 Hb 12,5 EBL 10 % : 325 Hb 11,25 20 % : 650 Hb 10 30 % : 975 Hb 8,75

40 % : 1300 Hb 7,5 50 % : 1625 Hb 6,25

Balans cairanInput Output

PO RL 1000 cc PO urine 50 cc jernih

DO WB 4200 cc PRC 400 cc Gelo 1500 cc HES 1000 cc RL 3000 cc PZ 1500 cc

DO perdarahan 7000 cc urine 450 cc

ICU hr 016/4/13 jam 19.00

B1 : A bebas tube in B Ventilator mode bIPAP PASB 16, peep 8, Pins 24, f 15, FiO2 100%- VT 290-350, rate 15 MV 4,3-5,2 sim +/+, ves +/+, rk +/+, wh -/-B2 : p HKM, CRT >2, HR 115-125 x/mnt irama AF, TD 95-125/55-75 mmHg dg support norepinephrin 50 nn, temp 35 axiler B3 : tersedasi, PBI 4/4, RC +↓/ +↓

ICU 5/4/13 jam 16.00

B4 : BAK katB5 : flat, soepel +, BU + dbnB6 : odem -/-

Laboratorium di ICU16/4/13 jam19.30

pH 7,289 Hb 12,6pCO2 54,5 Hct 39pO2 53,4 Na/K/Cl 142/3,39/-HCO3 26,4 Ca/Mg 0,59(1-1,3)/ 0,24(0,4-0,6)BE -0,5 Lactat 2,8SaO2 83 %P/F 53,4

Laboratorium post op(IRD 16/4/13 jam 22.00)

Hb 14,6 PPt 17,2/11,9Hct 43 aPTT 30,1/28,5L 6,7 GDA 132Plt 65.000Bun/Sk 14,1 / 0,66Na/K/Cl /Ca 144/4,7 /100/9Albumin 1,69

Thorak post op16/4/13

ICU hr 0Terapi

Posisi slight head upO2 ventilatorOral n personal hygiene 2x/hrSementara puasaRD5 500 cc s/d jam 07.00 besokDrip neurobion 5000 mg/24jamInj OMZ 1x40 mgInj Vit K 2x1 ampInj Transamin 3x500 mgInj Ca Gluconas 2x1Inj cefazolin 3x1 grInj Tramadol 3x100 mg dripEuthyrax tab 2x100 mg p/sondeMethyl prednisolon 2x125 mg p/sonde

ICU hr 0

Ganti mesin Ventilator karena menit volume yg keluar rendah, di tes dg lung test menunjukkan ventilator error.

ICU hr 016/4/13 jam 21.00

B1 : A bebas tube in, tampak secret pink frotty + B Ventilator mode PCV PC 14, peep 10, f 20, FiO2 100%- VT 280-310, rate 20 MV 5,6-6,0 sim +/+, ves +/+, rk +/+, wh -/-B2 : p HKM, CRT >2, HR 110 x/mnt irama sinus, TD 125/85 mmHg dg support norepinephrin 100 nn, temp 36 axiler B3 : tersedasi, PBI 4/4, RC +↓/ +↓

ICU 5/4/13 jam 16.00


ICU hr 016/4/13 jam 21.00

B1 : A bebas tube in B Ventilator mode PCV PC 14, peep 10, f 20, FiO2 100%- VT 280-310, rate 20 MV 5,6-6,0 sim +/+, ves +/+, rk +/+, wh -/-B2 : p HKM, CRT >2, HR 110 x/mnt irama sinus, TD 125/85 mmHg dg support norepinephrin 100 nn, temp 36 axiler B3 : tersedasi, PBI 4/4, RC +↓/ +↓

ICU hr 016/4/13 jam 21.00


ICU hr 0 17/4/13 jam 06.00

B1 : A bebas tube in B Ventilator mode bIPAP PS 15, PC 14, peep 10, f 16, Tr 2,FiO2 60%- VT 280-320, rate 20 MV 6,3 sim +/+, ves +/+, rk +/+, wh -/-B2 : p HKM, CRT 2, HR 115 x/mnt irama sinus, TD 100/70 mmHg MAP 80, support vascon 50 nn ,temp 36 axiler B3 : GCS 4-x-6, PBI 3/3, RC +/+

ICU hr 0 17/4/13 jam 06.00

B4 : BAK kat urine +B5 : flat, soepel +, BU + dbnB6 : odem-/-

17/4/13 jam06.44mode bIPAP PS 15, PC 14, peep 10, f 16, Tr 2,FiO2 60%- VT280-320, rate 20 MV 6,3

pH 7,43 pCO2 37,5 pO2 103,2 HCO3 25,3BE 0,8SaO2 98 %P/F 172

Balans cairanICU hr 0

Input Output

RL 500 ccRD5 500 ccGelo 250 cc

Urine 1020Drain 120 ccSNI 260 cc

Def 150 cc

ICU hr 1 17/4/13 jam 07.00

B1 : A bebas tube in B Ventilator mode bIPAP PS 15, PC 14, peep 10, f 16, Tr 2,FiO2 60%- VT 280-320, rate 20 MV 6,3 sim +/+, ves +/+, rk +/+, wh -/-B2 : p HKM, CRT 2, HR 120 x/mnt irama sinus, TD 120/80 mmHg MAP 91, support vascon 50 nn ,temp 38,3 axiler B3 : GCS 4-x-6, PBI 3/3, RC +/+

ICU hr 1 17/4/13 jam 07.00


Laboratorium 17/3/13 jam 18.00

PPt 20/12,4aPTT 30/30,7Bili D/T 0,39/ 0,85--------------------------------------------------------------Hb 11,1 Na / K/ Cl 146/3,6/103Hct 32,7L 8,6Plt 24.000

ICU hr 1 ( 17/3/13)Terapi

Posisi slight head upO2 ventilatorOral n personal hygiene 2x/hrSonde D5 6x50 ccInf KaenMg3 1000 ccInf RD5 500 cc Lasix 2x1 ampDrip neurobion 5000 mg/24jamInj OMZ 1x40 mgInj Vit K 2x1 ampInj Transamin 3x500 mgInj cefazolin 3x1 grInj Tramadol 3x100 mg dripTransf albumin 20 % 100 cc, transf TC 10 bagEuthyrax tab 2x100 mg p/sondeMethyl prednisolon 2x125 mg p/sonde


Input Output

Sonde D5 300 ccKaenMg3 1000 ccRD5 500 ccTC 500 ccAlbmn 100

Urine 1190ret 285 ccSNI 525 ccDrain 280

Ekses 120 cc

ICU hr 2 18/4/13 jam 07.00

B1 : A bebas tube in B Ventilator mode Spontan PS 9, peep 8,FiO2 50%- VT , rate, MV sim +/+, ves +/+, rk -/-, wh -/-B2 : p HKM, CRT 2, HR 110 x/mnt irama sinus, TD 110-130/70-80 mmHg MAP 80-95 ,temp 38 axiler B3 : GCS 4-x-6, PBI 3/3, RC +/+

ICU hr 2 18/4/13 jam 07.00


Laboratorium18/4/13

Hb 8,8Hct 26,6L 16,9Plt 85.000Alb 2,86


Posisi slight head upO2 ventilatorOral n personal hygiene 2x/hrSonde PE 6x50 ccInf KaenMg3 1000 ccInf kalbamin 500 cc Ivelip 10% 100 ccLasix 3x1 ampInj Metamizole 3x 1 grDrip neurobion 5000 mg/24jamInj OMZ 1x40 mgInj metoklopramid 2x1 Inj Vit K 2x1 ampInj Transamin 3x500 mgInj cefazolin 3x1 grEuthyrax tab 2x100 mg p/sondeMethyl prednisolon 2x125 mg p/sonde


Input Output

Sonde PE 300 ccKaenMg3 1000 ccKalbamin 500 ccIvelip 100 ccObat 100 cc

Urine 1280ret 60 ccSNI 525 ccDrain 380 cc

Def 245 cc

ICU hr 319/4/13 jam 07.00

B1 : A bebas tube in B Ventilator mode Spontan PS 8, peep 5,FiO2 30%- VT 300-320 , rate 18- 28 , MV 9,5 sim +/+, ves +/+, rk -/-, wh -/-B2 : p HKM, CRT 2, HR 110 x/mnt irama sinus, TD 120-130/60-70 mmHg MAP 80-90 ,temp 36 axiler B3 : GCS 4-x-6, PBI 3/3, RC +/+

ICU hr 3 19/4/13 jam 07.00


19/4/13 jam09.30mode Spontan PS 8, peep 5,FiO2 30%- VT 300-320 , rate 18- 28 , MV 9,5

pH 7,45 Hb 11,7 pCO2 35,8 Hct 35 pO2 71,9 HCO3 25,1BE 0,8SaO2 95,4%P/F 230


Posisi slight head upO2 ventilatorOral n personal hygiene 2x/hrFisiotx nafasSonde PE 6x150 ccInf KaenMg3 500 ccInf kalbamin 500 cc Ivelip 10% 100 ccLasix SP 5 mg/jamInj Metamizole 3x 1 grDrip neurobion 5000 mg/24jamInj OMZ 1x40 mgInj metoklopramid 2x1 Inj Vit K 2x1 ampInj Transamin 3x500 mgInj cefazolin 3x1 grTranf albumin 20 % 100 cc, Transf PRC 2 kolfEuthyrax tab 2x100 mg p/sondeMethyl prednisolon 2x125 mg p/sonde


Input Output

Sonde PE 750 ccKaenMg3 650 ccAlbmn 100 ccPRC 200 ccObat 100 cc

Urine 1275ret 149 ccSNI 525 ccDrain -

Ekses 51 cc

ICU hr 3 19/4/13

Jam 23.00TD turun, disertai dengan desaturasi, resusitasi

cairan dan inotropik (dopamin, norepinephrin, adrenalin )

Jam 06.30arrest

Hb Hct L Plt PPt Aptt BUN SK Na K Cl Ca Mg alb GDA Lac

16 12,6 30 6,7 65 17,2/11,9

30,1/28,5

14,1 0,66 142 3,39 100 9 0,24 1,69 132 2,8

17 11,1 32,7 8,6 24 20/12,4

30/30,7

146 3,6 103

18 8,8 26,6 16,9 85 2,86

19 11,7 35

Tgl 16/4/13 17/4/13 19/4/13

Ventilator mode bIPAP PASB 16, peep 8, Pins 24, f 15, FiO2 100%- VT 290-350, rate 15 MV 4,3-5,2

mode bIPAP PS 15, PC 14, peep 10, f 16, Tr 2,FiO2 60%- VT280-320, rate 20 MV 6,3

mode Spontan PS 8, peep 5,FiO2 30%- VT 300-320 , rate 18- 28 , MV 9,5

BGA pH 7,289 pCO2 54,5 pO2 53,4 HCO3 26,4 BE -0,5 SaO2 83 %P/F 53,4

pH 7,43 pCO2 37,5 pO2 103,2 HCO3 25,3BE 0,8SaO2 98 %P/F 172

pH 7,45 pCO2 35,8 pO2 71,9 HCO3 25,1BE 0,8SaO2 95,4%P/F 230

Transfusion-Related Acute Lung Injury (TRALI)

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TRALI: Medical History • 1951:

– Syndrome was first described by Barnard• 1983:

– Transfusion-related Acute Lung Injury (TRALI) coined by Popovosky et al.

• 2004: – Canadian Consensus Panel

Transfusion-related acute lung injury (TRALI)• What Is TRALI?

– Transfusion related noncardiogenic pulmonary edema– Differential Diagnosis

• Circulatory overload (TACO)• Allergic/Anaphylactic• Bacterial• Acute hemolytic reaction

– Clinical presentation (“classic”, severe form)• Acute respiratory distress• Pulmonary edema• Hypoxemia• Hypotension• Transfusion usually within 6 hours (majority of cases during

transfusion or within 2 hours of transfusion)

Comparison TRALI TACO

Blood Pressure Hypotension Hypertension

Onset Up to six hrs post transfusion

Usually occurs during or immediately after a transfusion

Chest X-Ray Bilateral pulmonary infiltrates, normal heart

Bilateral pulmonary infiltrates, enlarged heart

Lab tests BNPTNI

<250pg/ml Normal

>250 pg/ml Elevated

temp Normal to elevated Normal

PAWP ≤ 18 higher

Respons to fluid improves worsen

TRALI• Clinical criteria

– Insidious, acute onset of pulmonary insufficiency - Profound hypoxemia PaO2/FiO2 < 300 mmHg Hg regardless of PEEP or O2 saturation of < 90% on room air

– CXR b/l fluffy infiltrates c/w pulmonary edema– Cardiac PA wedge pressure 18 mmHg– No clinical evidence of LA HTN

TRALI: Clinical Presentation

Diffuse Bilateral Pulmonary Infiltrates

TRALI• Syndrome of TRALI (Weber KE et. al., Transfusion Med

Rev, 2003)– Very common

• Dyspnea, hypoxemia, pulmonary edema, hypotension, fever (1-2°C increase)

– Common• Tachycardia, cyanosis

– Uncommon• Hypertension

– ?• Leukopenia, hypocomplements, monocytopenia

TRALI• Implicated Blood Products

– RBCs, FFP, apheresis platelets, platelet concentrates– Rare cases of IVIG, cryo-– No cases of albumin reported

TRALI

• Clinical Course– 100% TRALI patients require O2 and 72% require ventilation

support– 81% resolves within 4 days and 17% resolve within 7 days

• Most pts. recover with 72 hours– Mortality rate 6% (subsequent series up to 14-25%)– No long term sequela

• Treatment– Respiratory support– No role for treatment w/ steroids or diuretics

TRALI• Why Is TRALI Important?

– Between 2001 – 2003, FDA report on causes of transfusion related deaths

• TRALI 16.3%• ABO/Hemolytic transfusion reaction 14.3%• Bacterial contamination 14.1%

– UK SHOT Data 7 years experience (from 1996)• Total 155 cases

– 32 Deaths

TRALI: Pathogenesis

• Activated neutrophils cause damage to pulmonary endothelial cells which allows for leaky capillaries and pulmonary edema

TRALI: Histopathology1) Neutrophil

sequestration within pulmonary capillary vasculature

2) Extravasation of neutrophils into interstitial and air spaces

3) Interstitial and intra-alveolar edema

4) Hyaline membrane and pulmonary architectural destruction

http://ccforum.com/content/15/1/R4/figure/F2?highres=y

TRALI: Pathogenesis

• Two leading hypothesis: – Anti-neutrophil Antibody Hypothesis – Two Event Hypothesis: Neutrophil Priming

TRALI: Pathogenesis Hypothesis I: Anti-neutrophil Antibody Hypothesis

◦ Concept: An Antigen-Antibody reaction triggers the events leading to TRALI

1) Passive transfusion of donor antibodies directed against antigens on the surfaces of recipient neutrophils

OR

2) Infusion of donor neutrophils into a recipient with antibodies directed against donor neutrophils

◦ Activation of Neutrophils

Antibodies can be against ◦ Human Leukocyte Antigens (HLA) Class I or II◦ Human Neutrophil Antigens (HNA)

TRALI: Pathogenesis • Hypothesis II: 2-Hit Hypothesis • First: Underlying Inflammatory Condition

– Pulmonary Endothelial Cell Activation

– Sequestration and priming of neutrophils in the pulmonary microvasculature

Bux. Br J Haemotol. 2007.

TRALI: Pathogenesis • Second: Transfusion

– Infusion of substances in the plasma of the transfused product

• HLA Antibodies • HNA Antibodies • Biologically Activated Lipids

– Activation of Primed Neutrophils

Acute Lung InjuryEndothelial DamageDestruction of Alveolar Vasculature Capillary LeakFlooding of Air-Space with protein rich fluid Pulmonary Edema

FIRST: Underlying Inflammatory Condition

Second: Transfusion

How can we prevent TRALI?

• We have evidence that antibodies are responsible for TRALI in a primed host

• How can we identify a primed host?• Fresher product for the primed host?

How can we prevent TRALI?

• TRALI reduction strategies have focused on donors with antibodies and specifically plasma containing products

– Secondary – Measures taken to identify the cause of a reaction that has occurred and prevent it from happening again

– Primary – Preventive measures taken to eliminate the risk before it happens in the first place

How can we prevent TRALI• Secondary…defer implicated donors

– Donors associated with a reported TRALI are investigated for anti HLA and anti neutrophil antibody and deferred if positive

– Pilot 2001 – 2006, SOP 2006• Primary…avoid donors with anti HLA or anti neutrophil

antibody• what have blood suppliers done and what has the effect

been– Donor loss– Reduction of TRALI

Which donors develop WBC antibodies?

• WBC alloimmunization may occur following previous exposure to WBCs through pregnancy or transfusion – 332 female plateletpheresis donors – 17% had detectable anti-HLA antibody– Frequency of HLA antibodies increased with pregnancy:

0 pregnancies: 7.8%1-2 pregnancies: 14.6% 3 or more: 26.3%

Densmore et al. Transfusion 1999;39:103-6

Primary Prevention

• 2003 – UK changed component production policy moving to predominantly male plasma for transfusion

2003 2004 2005

TRALI 36 23 23

Highly likely/probable

22 13 6

Chapman et al. Vox Sang 2006;91(Suppl 3):227

SHOT data• 10 years hemovigilance in UK and impact of preferential

use of male donor plasma• Risk of highly likely/probable TRALI due to FFP decreased

– 15.5 per million units 1999-2004– 3.2 per million units issued 2005-2006 (p= 0.0079)

• Risk of highly likely/probable TRALI due to platelets decreased– 14 per million to 5.8 per million

– Chapman.Transfusion 2009;49:440-452

TRALI reduction measures CBS-predominantly male plasma

• CBS moved to predominantly male plasma for transfusion Oct 2008

• Female plasma diverted fractionation

TRALI Reduction Measures – Platelet Apheresis

• On July 20, 2009 CBS started asking all female platelet donors if they’d ever been pregnant

• Any responding positively redirected to whole blood

Donor Loss YTD

• June 2009 there were 2394 female apheresis platelet donors

• By Nov 2009 only 300 active female apheresis platelet donors

• 32% of the remaining donors converted to whole blood or plasma (approx 765 donors)

• Net loss of approx 1329 donors

Summary Primary Prevention

• Transfuse blood or blood components only if absolutely necessary

• Donor screening for leukocyte antibodies• Avoidance of multiparous female FFP donors• Use of fresh cellular components – as biologically

active lipids accumulate in blood products with storage, fresh cellular components may reduce the risk by preventing exposure of recipient neutrophils to neutrophil-priming agents

Summary Primary Prevention

• Use of solvent detergent plasma – the pooling process decreases the titre of responsible antibodies

• Leukodepletion – prevents complement activation

case trali

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