CDHA Viem Phoi

7/23/2019 CDHA Viem Phoi

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CHN ON HNH NH

NHIM TRNG PHI

BS. NGUYN QU KHONG

BS. NGUYN QUANG TRNG


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DN BI

i cng.

Cc tc nhn gy bnh.

Nhim trng phi do siu vi.

Nhim trng phi do vi trng.

Kt lun.


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DN BI

i cng.

Cc tc nhn gy bnh.



Kt lun.


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I CNG

Nhim trng phi l bnh l thng gp

do nhiu tcnhn gy ra.

Bnh c trng bi tnh trng vim nhim

xut tit

c ph nang v m k.

Nhim trng phi do

siu vi thng c bnh cnh nhhn do vi trng.

Bnh cng c th

khi u nhim siu vi, sau bi

nhim do vi trng.

Nhim vi trng ngoi cng ng hay trong bnh

vin do

nhiu loi vi trng gy nn

.


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DN BI

i cng.

Cc tc nhn gy bnh.



Kt lun.


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TC NHN TRONG CNG NG TRONG BNH VIN

Vi trng 70

-

80% > 90%

Diplococcus pneumoniae 60

-

75% HimHemophilus influenzae 4

-

5% Him

Staphylococcus aureus 1

-

5% 10

-

20%

Vi trng G(

-

) Him >50%

Vi trng ym kh Him 10%Siu vi 10

-

20% Him

Influenzae A, E 8%

Siu vi trng khc (RSV,

Parainfluenzae, Adenovirus,

Varicella zoster, Rubeola).

2

-

8%

Vi khun khng nh hnh 10

-

20% Him

Mycoplasma pneumoniae 5

-

10%

Chlamydia 2

-

3%


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DN BI

i cng.

Cc tc nhn gy bnh.



Kt lun.


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NHIM TRNG PHI DO SIU VI

Hnh nh X quang rt a dng. Tn thng khi u m k, sau c th km tn

thng ph nang.

C th gy TDMP, TDMT, hch v xp phi. Nu din tin thun li, hnh nh X quang gim sau

vi tun, tuy nhin c th c bi nhim do vi trng.

Di chng: X ha m k lan ta.

Vim tiu ph qun tc nghn.


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Varicella pneumonia Healed varicella pneumonia



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Measles pneumonia



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February 10, 2004 12

SARS-SEVERE ACUTE RESPIRATORY SYNDROME

15 MARCH 2003 19 MARCH 2003 20 MARCH 2003



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DN BI

i cng.

Cc tc nhn gy bnh.



Kt lun.


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NHIM TRNG PHI DO VI TRNG

C hai loi tn thng chnh ty bn cht ca tn

thng v cch xm nhp ca vi trng. Vim phi.

Vim ph qun phi.


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Vim phi:

Tn thng h thng ha (gii hn bi rnh linthy).

Rnh lin thy c th b phng (bulging fissuresign): du hiu ny c th gp trong vim phi doKlebsiella, Pseudomonas, Ph cu.


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Vim phi thy gii hn bi rnh lin thy b


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BULGING FISSURE SIGN


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Vim phi:

C th c kh nh ni ph qun (air bronchogram).

Lu rng kh nh ni ph qun khng phi lhnh nh c hiu trong vim phi, vi u phi tacng c th thy du hiu ny (bronchioloalveolarcarcinoma).


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Bng m ng nht thy trn phi (T) vi Kh nh ni ph qun (AirBronchogram) VIM PHI THY


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AIR BRONCHOGRAM


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AIR BRONCHOGRAM / VIM PHI


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K TIEU PHE QUAN-PHE NANG LAN TOA


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Hnh nh X quang khng c hiu cho mi loi vi trng(tr mt s trng hp c bit nh Diplococcus

pneumoniae, Staphyloccus Aureus, Klebsiella.).

Hnh nh X quang gim chm hn lm sng t 1 tun n3 tun.

Mt din bin ko di phi ngh n mt tn thng csn: di vt, ung thdo ,cn ni soi ph qun bng

ng soi mm xc nh nguyn nhn.


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Vim ph qun phi:

Tn thng dng nt, kch thc t vi mm n

vi cm, khng ng nht, b khng u, m. C th tn thng hai bn v km TDMP.

Vim ph qun phi do t cu l mt in hnh.


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mm hthngha

mm rirc

p xe,bngkh

Co ko,xp

Phngrnhlinthy

TDMP Ghi ch

Siu vi + +/-Mycoplasma + + Hch (+/-)

Ph cu ++ + (gi) +/-

T cu ++ + (tr) + Trn m,

trn khLin cu + ++ + + Trn m

ng kn

Klebsiella + + + + Trn mng kn

Pneumocystiscarinii

+

(AIDS)

Tinlng xu

Pseudomonas,VT G(-), VT

ym kh

+ + + BN hisc


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October 31, 2014 27A.J.Chandrasekhar,M.D.Chest X-ray Atlas.

VIEM PHOI THUY TREN (P)


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Pneumococcal pneumonia


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ng c thy trn (T) xa b (T) tim


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Streptococcus pneumoniae


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Staphylococcus aureus

Pneumatocele


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G(-): Hemophilus influenzae



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G (-): Pseudomonas



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Mycoplasma

NHIM TRNG PHI


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Legionella



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Anaerobic infection



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Pneumocystic carinii

NHIM TRNG PHI


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Pneumatocele/Pneumocystic carinii

3 weeks after

NHIM TRNG PHI


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October 31, 2014 41D.Anthoine et al.LImagerie Thoracique.1996-1998.

VIEM PHOI (Legionellose)


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Pseudomonas pneumonia


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Vim phi trn (round pneumonia): Tn thng l mt khi hnh cu d lm vi u

phi. Gp tr em nhiu hn ngi ln. C th gy nn bi: Haemophilus influenzae,

Streptococcus, Pneumococcus. V tr: lun lun pha sau, thng thy di.

Khi hnh cu, b hi nha, c th c airbronchogram, thay i nhanh chng kch thcv hnh dng.


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Bng m trn phn thy nh ca thy di phi (P)VIM PHI TRN


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Bng m trn gia phi (P) Hai ngy sau VIM PHI


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Kh nh ni ph qun trnSiu m.

Phn b ng mch phibnh thng.

VIM PHI TRN


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VIM PHI TRN

13 ngy sau


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C IM X QUANG VI TRNG SIU VI

1. THM NHIM:- Khu tr theo thy, phn thy hoc di phn thy (trn).

- m vi vin khng r.

- M k hoc quanh ph qun.

+2

+1

-1

2. V TR:

- Mt thy.-Nhiu thy nhng b r.

-Nhiu ni, quanh rn phi, khng r nt.

+1+1

-1

3. DCH MNG PHI:

- Gc sn honh t.

- Dch r rt.

+1

+2

4. P XE, TI KH, BONG BNG:

- Cha r.

- R.

+1

+2

5. XP PHI:

- Di phn thy (thng nhiu ch).

- Thy (gia bn (P), thy trn).

-1

-1

SO SNH VIM PHI DO VI TRNG V SIU VI


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SO SNH VIM PHI DO VI TRNG V SIU VI

Nu > + 4,5 Vim phi do vi trng.

Nu < - 2 Vim phi do siu vi.


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MT S C IM

Phn b theo thy: Diplococcus pneumoniae. Phng rnh lin thy: Klebsiella.

Ph phi: Vim phi do virus, Pneumocystis pneumoniae.

Pneumatocele: Staphylococcus.

Nt m ph nang: Varicella, TB.

Vim ph qun-phi: Streptococcus, Staphylococcus,Mycoplasma, Virus.

Tn thng hai bn: Legionella, Virus. Thy di hai phi: Anaerobic pneumonia.

Vim phi ngoi bin: Noninfectious eosinophilic pneumonia.


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Khi u

20 thng sau24 thng sau

42 thng sau

ASPERGILLOMA / HANG LAO(air crescent sign)

Hyae Young Kim, MD et al. Thoracic Sequelae and Complications of Tuberculosis.Radiographics. 2001;21:839-858.


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Aspergillus bronchopneumonia in a liver transplant recipient.


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Air Bronchograms : eosinophilic pneumonia


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Air Bronchograms: Alveolar cell carcinoma


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Pneumonia Alveolar cell carcinoma


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Pneumonia Alveolar cell carcinoma


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Bulging fissure sign: Klebsiella pneumonia


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Bulging fissure sign: pneumococcal pneumonia.


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Bulging fissure sign: Bronchioloalveolar Carcinoma


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Bulging fissure sign: Bronchioloalveolar Carcinoma


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DN BI

i cng.

Cc tc nhn gy bnh.

Nhim trng phi do siu vi. Nhim trng phi do vi trng.

Kt lun.

KT LUN


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KT LUN

Nhim trng phi c th do nhiu tc nhn gy ra.

Hnh nh X quang khng c hiu cho mt vi trng no, nty thuc vo c tnh ca vi trng v sc khng ca bnhnhn.

Nhng cng c vi vi trng cho ra tn thng kh in hnh

nh: Diplococcus pneumoniae, Staphyloccus Aureus,Klebsiella.

Tuy nhin, vic xc nh vi trng gy bnh bng soi trc tiphoc cy l cn thit c th dng khng sinh thch hp.

Hnh nh X quang thng bt chm hn lm sng t 1 n 3tun.

Mt din bin ko di qu 6 tun phi ngh n mt tnthng c sn: di vt, ung th


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Nh th c B Paris, 29/12/2004

CM N S CH CA QU BC S


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TI LIU THAM KHO

Sebastian Lange, MD et al. Radiology of Chest Diseases. 2nd Edition, 1998

Pediatric Chest Imaging.A.L.Baert et al.2002

J. Frija.Radiologie du Thorax. 3e edition .2002 Richard Webb et al. Thoracic Imaging-Pulmonary & Cardiovascular

Radiology. 2005

Wolfgang Dahnert, MD. Radiology Review Manual. 5thEdition. 2003

Mechanisms of lung injury. B

righam

KL

.
http://www.ncbi.nlm.nih.gov/pubmed?term=Brigham%20KL%5BAuthor%5D&cauthor=true&cauthor_uid=6804159http://www.ncbi.nlm.nih.gov/pubmed?term=Brigham%20KL%5BAuthor%5D&cauthor=true&cauthor_uid=6804159http://www.ncbi.nlm.nih.gov/pubmed?term=Brigham%20KL%5BAuthor%5D&cauthor=true&cauthor_uid=6804159


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Abstract

The adult respiratory distress syndrome is pulmonary edema with low heartpressures and hypoxemia. Based on experimental models of the human disease, it is

likely that functional injury to the lung includes pulmonary vasoconstriction, aloss of hypoxic vasoconstriction, increases in resistance to airflow acrossthe lungs, decreases in lung compliance (perhaps both resulting fromairway constriction), and lung microvascular injury resulting in pulmonaryedema. Data accumulated over the last several years strongly suggest an importantrole for both cyclo-oxygenase metabolites and lipoxygenase metabolites of

arachidonic acid in mediating lung vascular injury in this syndrome. Likewise, morerecent evidence suggests a causative role for granulocytes in mediating the lunginjury. Based on what is known about the biological activity of products ofgranulocytes and metabolites of arachidonic acid, it is reasonable to hypothesize asequence of events in which arachidonate metabolites and granulocytes interact toresult in pulmonary vasoconstriction, loss of hypoxic vasoconstriction, airway

responses and capillary injury. It remains possible, perhaps even likely, that otherhumoral mediators, platelets and perhaps even other cellular mediators (forexample, mast cells or lymphocytes) participate in the pathogenic sequence ofevents in ARDS. Specific delineation of the mechanisms of lung injury in thissyndrome must await further research.

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