1 / 27

A Woman Who Developed Acute Pulmonary Edema During Operation --A Case Report

A Woman Who Developed Acute Pulmonary Edema During Operation --A Case Report. By R2 彭育仁. Brief History (1). This 60 y/o woman was a patient with DM, hyperlipidemia for 20 years and

carl
Download Presentation

A Woman Who Developed Acute Pulmonary Edema During Operation --A Case Report

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. A Woman Who Developed Acute Pulmonary Edema During Operation --A Case Report By R2 彭育仁

  2. Brief History (1) This 60 y/o woman was a patient with • DM, hyperlipidemia for 20 years and • CAD (3-V-D) after PTCA for LAD, LCX and PTCA/stenting for RCA in May 1998. Restenosis of LAD was noted in Sep 1998 after PTCA. • No other systemic disease was noted.

  3. Brief History (2) • She came to our hospital in July 2002 due to chest pain for 6 months and exertional chest tightness progression recently. Cardiac catheterization showed 1. LM diffuse narrowing 2. LAD mild stenosis 3. LCX 80~90% stenosis (prox to middle) 4. PDA 80% stenosis She was admitted for OPCABG on 2002-8-7.

  4. Brief History (3) • After setting up arterial line, induction of anesthesia was accomplished with IV fentanyl 250ug, pentothal 250mg and esmeron 80mg. Endotracheal intubation was performed smoothly and anesthesia was maintained with Desflurane inhalation. Swan-Gans and 14x14 CVC insertions was done over r’t IJV and EJV respectively. The baseline data showed PAP 36/18 and CVP 8.

  5. Brief History (4) • TEE showed hypokinesia at basal and mid posterior, septal and lateral area with LVEF 51%. Mild MR was also noted. NTG small dose infusion was given. • During operation, the hemodynamic was stable from 8AM to 12AM. BP was around 115/65. CVP was around 8 to 10 except N/S 1500ml, HAES 500ml and blood transfusion with whole blood 3u and PRBC 3u. Urine output for 4 hour was 250ml.

  6. Brief History (5) • At around 12:30 AM after LIMA—LAD and SVG1:Ao—PDA, the operating table was adjusted for SVG2: Ao—OM2. 200ml pink frothy fluid was drained from ET tube rapidly. Mild BP drop to around 85/55 was noted. CVP was around 5~8, and PAP was 36/22. TEE showed decreased LV volume, no prominent MR and LV contractility was no different as before. Pre-op BUN/Cre was 15.2/1.0. Pulmonary edema ruled out allergic reaction (increased pulmonary vascular permeability) was impressed.

  7. Brief History (6) • Fluid was then restricted and lasix was given. Blood volume supplementation was replaced by PRBC 4u, FFP 6u and 5% albumin 100ml. Vena and solu-cortef were given for suspected allergic reaction (she received drugs of induction, antibiotics and blood components before reaction). Dopamine, levophed and then bosmine infusion were given for her BP maintenance. PaO2 (FiO2 90%) decreased from baseline 486 to 260 on 12:21 and to 69 on 15:06. The total fluid from ET tube was around 2000ml during operation. U/O 400ml.

  8. Brief History (7) • After sending patient to SICU, ventilator support with high PEEP was given and CVVH was set up to dehydrate the overload volume. CXR showed bilateral pulmonary infiltates. Large amount of pink frothy fluid still drained from ET tube and chest tube for several days. Transfusion-related Acute Lung Injury was highly suspected. Due to low BP and RDS with low saturation under high inotropic agent and ventilator, ECMO was given on 8/13 for circulatory and respiratory support.

  9. Brief History (8) • RLL pneumonia and septic shock was impressed then. Left pupil dilation was noted on 8/14 and brain CT showed multiple ICH, large amount in left hemisphere. She was expired on 8/16 morning.

  10. Transfusion-realted Acute Lung Injury (TRALI) • Clinical findings • Radiologic findings • Laboratory findings • Diagnosis and laboratory confirmation • Distinguishing TRALI from other types of pulmonary edema • Treatment • Implicated donors and prevention

  11. Clinical Findings(1) • Dyspnea, cyanosis, hypotention, fever, chills, cough and production of fluid from ET tube in intubated patients, along with physical findings of bilateral pulmonary edema. • Often develop within 4 hour of a transfusion and resolve within 96 hour. • Indistinguishable from ARDS

  12. Clinical Findings (2) • Severity is related to degree of hypoxemia. • Significant morbidity (72% mechanical ventilation) and mortality (6%). 2nd most common cause of fatal transfusion reaction. • Most associated with WB, PRBC and FFP. There are also reports of granulocytes, platelates and cryoprecipitate even in small amount.

  13. Radiologic Findings • Development of bilateral pulmonary infiltrates after infusion of blood component. • Appear at the time of reaction and resolve within 96hr in about 80% of patients. • More remarkable than physical findings. • Persistence of infiltrates is associated with weaning difficulty from mechanical ventilator support.

  14. Laboratory Findings • WBC antibodies (leucoagglutinating and/or lymphocytotoxic antibodies) in the plasma from multiparous donors direct against the WBC of recipient. • Occasional antibodies in recipient against the WBC of donor. • Interdonor TRALI has been reported.

  15. Diagnosis and Lab Confirmation (1) • Diagnosis of TRALI is based primarily on clinical symptoms and signs, not lab findings. It is important to determine that which type the pulmonary edema is, because it is treated different from cardiogenic or volume overload types. • Presence of non-cardiogenic pul edema following a transfusion should prompt immediate medical treatment with subsequent lab confirmation.

  16. Diagnosis and Lab Confirmation (2) • Lab confirmation. The gender of the donors of all components transfused within the 6h prior to the reaction should be determined. • All female donors are questioned and tested regarding pregnancy and transfusion history. • When antibodies are found, a lymphocytotoxicity crossmatch between donor serum and recipient WBC is performed. • Crossmatch positive: confirmed. • Crossmatch negative: cannot be ruled out.

  17. Distinguishing TRALI from Other Types of Pul Edema (1) • Three types of pulmonary edema: 1. Cardiogenic: secondary to myocardial or valvular heart disease. 2. Overhydration: secondary to excess intake and/or inadequate output of fluid. 3. Noncardiogenic: secondary to increased vascular permeability due to a variety of pathologic, traumatic and infectious causes.

  18. Distinguishing TRALI from Other Types of Pul Edema (2) • TRALI, a form of noncardiogenic pulmonary edema, is clinically distinguished from other forms of pul edema based upon normal to decreased PAWP, normal PAP, absence of JVE, absence of murmers or gallops, normal cardiac silhouette, absence of pul vascular congestion and no evidence of MI on EKG.

  19. Distinguishing TRALI from Other Types of Pul Edema (3) • Intubated patients of TRALI typically produce copious quantities of frothy edema fluid from ET tube. • The ratio of protein in the edema fluid to protein in blood is usually > 0.7 in noncardiogenic and < 0.5 in cardiogenic pul edema. This is due to increased vascular permeability in noncardiogenic pul edema.

  20. Treatment (1) • Corticosteroids, epinephrines and diuretics were traditionally used to treat TRALI. • Studies showed treatment with diuretics that led to decreased PCWP, decreased cardiac output and hypotension might be detrimental. • Corticosteroids remains controversial. • Albumin may increase mortality in critically ill patients compared with crystalloid.(meta-analysis)

  21. Treatment (2) • Maintenance of hemodynamic status is the most beneficial and appropriate therapy. • Ventilatory support and saline infusion are probably the only standard therapies for TRALI.

  22. Implicated Donors and Prevention (1) • Implicated donors are usually multiparous female due to exposure to paternal leucocyte antigens from the fetus during pregnancy. • The percentage of women with antibodies increases with increasing number of pregnencies.

  23. Implicated Donors and Prevention (2) • Blood from implicated donors should only be used as frozen-deglycerolized or washed RBCs, not used as WB, FFP or pheresis Plt. • Implicated donors should be told not to donate again in a recent study. • Particular caution in cases of patient-directed donation of blood from relatives, particularly if the donor is the mother of the recipient. Theoretically, donation of blood from a woman to the father of her children could also result in a TRALI.

  24. Thank You and Have a Nice Day

More Related