Mortality conference

Reporter: CR Supervisor: CVS

General data
Q102384905 Male 82 100/10/01 100/10/06

Chief Complaint


Low back pain this afternoon, conscious change this evening.

Present illness
    

A 81-year-old man, history of AAA followed at our CVS OPD for 2 years. He was referred to VGHTP for evaluation of aortic stent initially. But he hesitated due to high risk He suffered from low back pain in this afternoon and conscious loss in the evening. He was sent to our ER by ambulance. Conscious recovered on ambulance and he was conscious clear on arrival. However, hypotension and tachycardia were still noted. Abdomen CT showed AAA rupture with massive retroperitoneal hemorrhage. Emergent surgical intervention

Past and Personal History

Vital Signs
     

Body weight: 70kg Height: 165cm BP: 86 / 57 mmHg, PR: 117/ min RR: 20 / min BT: 35.4

Physical Examination
 

Consciousness: alert Skin: normal skin turgor, no skin rash, no pressure sore, jaundice (-) HEENT : Neck: stiffness(-) JVE(-) Chest : No wheezing, no rhonchi, no rales

Heart: regular rapid heart beat Abdomen: Ovoid and distention,

Extremities: Pitting edema(-), deformity(-) Neurological deficit: GCS: E4M6V5, pupil size: 2.0/2.0 Babinski sign: (-)

Lab Data (at ER)

Glu 10/1 202

BUN 17.6

Cr 0.91

GOT 11

GPT 15

Na 141

K 3.86

Cl 106.9

CPK 10/1 73

CKMB 13

TRO-I 0.01

CRP 1.75

PT 15

PTT 25.4

100-10-01

Initial diagnosis


   

1.Infra-renal type abdominal aorta aneurysm rupture with hypovolemic shock. 2.Hyptertensive cardiovascular disease. 3.Coronary artery disease s/p stents. 4.Chronic obstructive pulmonary disease. 5.Benign prostatic hyperplasia.

Operation finding
 1001001

Exploring thoracotomy, Lt chest for decending aorta clamping + abdominal arotic graft replacement (Gelsoft Y graft 22 x 11 mm, Infra-renal abdominal aorta-bilateral common femoral artery)

Operation finding
1. large infra-renal type abdominal aortic aneurysm with maximal diameter about 6.8cm with rupture at left posterior lateral wall about 3x1 cm2 in size and massive retroperitoneal hematoma and mild amount of bloody peritoneal fluid was noted 2. Moderate intra-mural organizing thrombus formation inside the aneurysm wall with multiple focal atherosclerotic calcification and few lumbar branches were ligated 3. Normal appearance of throcic d-aorta with few localized atherosclerosis plaque 4. Inferior mesentric artery was totally occlusion without any back flow 5. Bil common iliac artery aneurysm formation with severe calcifation and atherosclerosis of bil. External and internal iliac atery

Hospital course
1130 Return to ICU Operation Blood loss: 12000 BT PRBC 40U Whole blood 8U Plt 12U, FFP 20U Hypothermia (BT: 30) BT FFP 4U Unstable BP (BP 70110 + dopamie) Wound-> ozzing HgB: 14.3, PLT:63k

10/1

10/2

Hospital course
Conscious drowsy Urine output: 480ml ->Rosis 2amp q6h BP: 80-130mmHg (dopamine) HgB:10.8 -> PRBC 2U BUN/CR: 37.9/2.62 Na/K: 147/5.39 ABG: pH: 7.29 PaO2:76 PaCO2: 49.2 HCO3: 24.2, SaO2: 93.1% (fiO2: 65%)

10/3

Hospital course

Urine output: 80ml->Consult NEP -> on double lumen, HD BUN/CR: 57.5/4.43 Na/K: 143/5.86 Consicous improving, on NG feeding diet-> aspiration Consult INF-> Taro 4.5gm q12h BP: 70-110mmHg (dopamine) HR: 110-130/min ABG: pH: 7.18 PaO2:77 PaCO2: 50.6 HCO3: 18, SaO2: 97.4% (fiO2: 90%) 10/4

Hospital course
Conscious disturbance, air hunger, oligouria-> 10ml -> CVVHD Consult CM-> suspect ARDS HR: 110-130/min SBP: 70-110mmHg (levephed)-> 1100 BP drop-> leveped + dopamine ABG: pH: 7.17 PaO2:73 PaCO2: 52.8 HCO3: 19.7, SaO2: 89.8% (fiO2: 75%) Cr: 4.9, K: 5.77, CRP: 45.1 WBC: 7800, HgB: 12.3

10/5

Hospital course

Persist metabolic acidosis after HD-> suspect organ damage related EKG change (wide QRS) in the morning, pupil dilate and BP drop-> explain to family and sign DNR Bradycardia, VT at 1100 Expired at 1146.

10/6

Lab Data

Lab Data

Final diagnosis


 

   

1.Infra-renal type abdominal aorta aneurysm rupture with hypovolemic shock. 2.Adult respiratory distress syndrome, massive blood transfusion related. 3.Acute renal failure, hypovolemic shock related 4.Chronic obstructive pulmonary disease with respiratory failure 5.Upper GI tract bleeding 6.Hyptertensive cardiovascular disease. 7.Coronary artery disease s/p stents. 8.Benign prostatic hyperplasia

Cause of Death


Adult respiratory distress syndrome, massive blood transfusion related. Acute renal failure, hypovolemic shock related

Discussion

Transfusion-related acute lung injury

Transfusion-related acute lung injury

   

Sudden development of noncardiogenic pulmonary edema after transfusion Epidemiology Etiology and pathogenesis Clinical feature Treatment and prevention

Transfusion-related acute lung injury

TRALI-> most serous complication Less awareness, underestimation Donor antileukocyte antibody Related to shelf life? Review from 2 decades articles, pubmed from 1980

Epidemiology


TRALI-> most common serious complication, major transfusion related mortality in develop countries Incidence-> 0.02% -0.05% blood product unit; 0.08-0.16% per patient In contrast-> HBV (1/20,000); HCV & HIV (1-2/200,000)

Epidemiolgy


 

Antileukocyte antibiotics-> 89% in blood product in most TRALI case (31/36 pts) Most common product-> FFP (50%) TRALI-> underdiagnosed and underreported 8 patient develop severe ALI after received the same multiparous donar-> 2/8 DDX including TRALI

Epidemiolgy


Restrictive transfusion threshold-> Hgb 7 vs 10 g/dL<-> ALI risk (7.7% vs 11.4%) TRALI-> 150,000 each year develop ALI in US each, 1/3 exposed multiple blood products-> TRALI, tip of the iceberg

ETIOLOGY AND PATHOGENESIS

Exact etiology is unknown, 2 distinct mechanism have been suggested 1. antibody-mediated reaction between recipient granulocytes and antigranulocyte antibody from donor (sensitized during pregency, multiparous women! Or previous transfusion) Antibody-mediated increase in pulmonary capillary permeability

ETIOLOGY AND PATHOGENESIS

2. proinflammatory molecules, predominantly lipid products of cell degradation-> accumulate during storage of cellular blood product Lipopolysaccharide-primed-> develop permeability pulmonary edema 2 hypotheses of TRALI-> not mutually exclusive and may act synergistically Initial priming event (first hit)-> sepsis, trauma induced endothelial activation usually require

ETIOLOGY AND PATHOGENESIS

Storage of blood product-> risk? No significant association between storage age of RBC and develop ALI Effect of platelet-> difficult to assess (short shelf life, 5d) Prestorage leukoreduction-> reducing febrile reaction caused by proinflammatory cytokines, but prevent TRALI is unknown

Clinical feature


   

Symptom appear within 2-6 hrs from initiation of transfusion, but TRALI had described up to 48 hrs after BT S/S: dyspnea, tachypnea, frothy sputum, fever hypotension (or hypertension, rarely) Distinguishing TRALI from sepsis, trauma, aspiration, DIC-> almost impossible Lab-> leukocyte antigen-antibody in donor and recipient . Endotracheal tube-> high protein concertration found in edema fluid sampled within first hour of intubation-> DDX from fluid overload, cardiogenic pulmonary edema

Clinical feature


 

No single test for TRALI, most case misdiagnosed or unnoticed. Better short-term prognosis than other ALI < 70% require mechanical ventilation, and hospital mortality is 5-15% Most recover within 24-48 hrs with supportive care

Treatment and prevention

 

Supportive-> as any patient with permeability pulmonary edema, often include ventilator support Lung protective (low tidal volume) Diuretics are unlikely beneficial and even may be contraindicated, unless fluid overload Suspect TRALI-> report to bank-> blood specimen form pt and bags within 6 hrs

Question
 

 

Clinically defined TRALI? Incidence? Antileulocyte antibody, inflammatory cytokine or biologically active lipid-> more present in TRALI compared with control patient? (age, severity of ilness, number of blood transfusion) Important underlying risk (first hit) ? Population likely benefit from clinical trial of specific intervention, washing cellular product, pretransfusion antibody test, avoidance of specific donor product? Short or long term of TRALI?

Conclusion


 

Transfusion-> common and important risk factor for acute lung injury TRALI-> tip of the ice berg Acute lung injury related to transfusion factor-> maybe preventable disease

Thanks for your attetnion!