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Medicine

ARDS + PTE

Lecture 36

د. ﺪ ن اﳉﺒﻮري

Acute Respiratory Distress Syndrome)

It is also called "Shock Lung“

Definition

: It is a syndrome in which there is pulmonary oedema without

increment in the pulmonary capillary venous pressure.
Unlike the Lt. sided heart failure, in which there is pulmonary oedema
due to increase pressure in the Lt. atrium which causes increase in the
pulmonary  venous  pressure  →  oozing  of  fluids  to  the  lung  tissue  →
pulmonary oedema; but here, the pulmonary oedema is due to oozing
of  fluids  through  the  capillaries  without  increase  in  venous  pressure
which means that the defect is related to the capillaries themselves
This syndrome is caused by variety of causes that are either directly or
indirectly cause damage to the lung tissue, directly: bullet injury, blast,
embolus,  infections…etc.,  indirectly:  haemolytic  anaemia,  fractures
(e.g. in the lower limb.)…etc.

· There are many processes that precipitate ARDS:

1) Pulmonary infection: whether viral, for e.g. *SARS because

one of it is complication is ARDS, *Influenza virus which
causes a wide spread lung infection or mycoplasma infections
or bacterial infection like Tuberculosis

2) Injuries: either directly by bullet or blast…etc. or

indirectly by fractures or haemolytic anaemia…etc.

3)  Fractures
4)  Head injury
5)  Surgery – if prolonged- cause ARDS
6)  Septicemia  &  septic  shock,  in  fact  all  shock  states

can cause ARDS, that is why ARDS is called "Shock
lung"

7) Acute pancreatitis

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 2

8) Burn
9) Embolization:

either

fatty

embolus,

pulmonary

thrombo-embolus, air embolus, & amniotic fluid embolus...
**  usually,  embolization  is  due  to  small  embolus  that  blocks
small  tributary  of  pulmonary  artery;  but  the  patient  may
develop  ARDS  (unknown  cause)  or  by  large  embolus  →
massive pulmonary embolization → ARDS

10) Direct damage to the lung by acids (due to vomiting or

regurgitation) → ARDS

11) Drowning: water is detrimental to the lung & can initiates

ARDS

12) Hanging: either suicidal or execution, if the patient –for

example- survive after hanging himself → develop ARDS

13) Inhalation of chemicals & toxic materials: as in the wars, which

cause ARDS & serious respiratory problems to the soldiers, or
it can happen to the workers (who works in water refinery
system) where chlorine is used for water cleaning, but chlorine
is very irritant to the lung & cause damage to the lung tissue →
ARDS also happen in housewives who use detergent in large
conc.

14) In cardio pulmonary bypass in cardiac surgery
15) Multiple blood transfusion
16) Gastric aspiration

17) Toxic gases that cause this syndrome, one of which is O

Though O

is used in the treatment of this syndrome, it is an

irritant gas if given in high conc. So it is mandated not to give
high conc. for more than 24 hours, & this could happen in
mechanical ventilators, if you breath into close circuit &
getting pure O

(100% conc.), so if you need O

, you should not

use pure O

over 24hs because it may lead to this syndrome.

Pathophysiology

Regardless of the cause of ARDS, it will lead to destruction of the lung
tissue & this tissue contains endothelium of the blood vessels & the
epithelium in the alveoli which constitute the respiratory membrane.

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 3

Hence,  the  process  will  lead  to  damage  to  both  epithelium  &  the
endothelium or to any one of them, & once the capillaries get damaged
it  will  lead  to  oozing  of  oedema  fluid  to  the  alveolar  spaces,  this  is
actually a pulmonary oedema, (such thing can occur in left sided heart
failure)  &  there  will  be  oozing  of  fluid  from  the  capillaries  to  the
air-spaces of the lung tissue.
Hence,  damage  to  the  epithelial  &  endothelial  layers  due  to
inflammatory process of ARDS will lead to stiffness of the lung.

Severe ALI
B/L radiographic infiltrates
PaO2/FiO2 <200mmHg (ALI 201-300mmHg)
No e/o L Atrial P; PCWP<18

Acute Phase

· Pulmonary oedema with normal vascular pedicle Associated with

no cardiomegaly or upper lobe blood diversion
When pulmonary vessels can be distinguished they are often
constricted

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 4

· Septal lines usually absent because capillary leak occurs directly

into alveolar spaces (cardiogenic pulmonary oedema)

· Progressive lung destruction and transition from alveolar to

interstitial opacities

Chronic phase

· Fibrosis
· Focal emphysema

Activation of inflammatory mediators and cellular components resulting
in damage to capillary endothelial and alveolar epithelial cells
Increased permeability of alveolar capillary membrane
Influx of protein rich edema fluid and inflammatory cells into air spaces
Dysfunction of surfactant

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 5

Clinical Features
Any patient having severe medical or surgical problem & he developed
severe RF. Within 1 or 2 days, you should think about ARDS. Again the
clinical features of the cause

Complications

· Bacterial super infection, because there is very good medium for

infection by many M.O.

· Multiple organ failure, because there will be septicemia which can

leads to liver, kidney, heart, or brain failure this is why mortality
rate is high even in best centers

· Mortality rate in best centers is about 50%, here in our country

the mortality rate is about 90%!! Because of lack of sophisticated
equipment, the average mortality rate is about 70%.

· If the patient survive, he will undergo "pulmonary Fibrosis"

Summary of finding

1) Progressive SOB (1-2 days) following any medical or surgical

problem.

2)  Central cyanosis (resistant to treatment).
3)  Hypoxia & hypocapnia.
4)  Wide-spread shadowing (bilateral) on chest X-ray.
5)  If  there  is  pulmonary  edema,  we  check  the  pulmonary  venous

pressure by using a catheter & it will be normal (i.e. there is normal
pulmonary wedge pressure, yet there is pulmonary edema).

6) Fibrosis.
7) Fine crepitation, due to pulmonary edema

Treatment

The patient should be cared in an "Intensive Care Unit" ICU, with
facility for mechanical ventilator & Rx is directed toward:

A: cause (medical or surgical)
B: General measures

· General measures that include the following

1- O2

therapy: it is general Rx or therapy for all causes; but not

pure O

because it is irritant to the lung tissue

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 6

2- Mechanical ventilation: in ARDS, there is damage to type-2

pneumatocyte → decrease amount of surfactant, so you need
always a +ve pressure to keep the lung inflated & push the
fluids away from the airspaces

B: General measures that include the following

1- O2

therapy: it is general Rx or therapy for all causes; but not

pure O

because it is irritant to the lung tissue

2- Ventilation: in ARDS, there is damage to type -2- pneumatocyte

→

decrease amount of surfactant, so you need always a +ve

pressure to keep the lung inflated & push the fluids away.

There are 2 types of assisted ventilation to keep this +ve pressure:

1) IPPV “intermittent positive pressure ventilation”
2) PEEP “positive end expiratory pressure”

Other general measures that include

1)  Dealing with infection.
2)  IV nutrition may be needed in ICU
3)  Cleanliness
4)  Prevent bed sore
5)  Electrolyte balance must be carefully controlled.
6)  Use of Steroids

End of ARDS

Sabeeh & CHW

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 7

Pulmonary Thrombo-Embolism

It is a blockage of the pulmonary artery or its tributaries by an embolus
coming from DVT in 90% of cases, while the other 10% comes from the
heart

The burden of PTE

PM finding:
5% of hospital deaths are due to PTE
While 40-50% who die in hospital were found to have DVT.
This indicates that PTE is a common problem in hospital practice

DVT

Clinical Features
Unilateral pain in the thigh & calf muscles
O / E:
They are swollen, tender, hot & pitting edema.
DVT + PTE = ????????????

ﯾرﺟﻰ ﻗراءة اﻟﻣﻼﺣظﺔ ﻓﻲ

ﻧﮭﺎﯾﺔ اﻟﻣﺣﺎﺿرة

P.T.E. (pulmonary Thrombo-Embolism)
** Diagnosis (DX): the Dx of PTE is by clinical suspicion & you should
diagnose it early, because it is a fatal condition..
  ≥  It  occurs  mainly  in  hospitalized  patient  because  of  prolonged  bed
rest  especially  after  surgery  because  of  increased  risk  of  DVT  that  is
usually complicated by PTE.
So,  you  must  know the  Dx  of  DVT:  Pain  in  the  thigh  &  calf  muscles  7
they are Swollen, Tender & pitting oedema (Unilateral).
Or from the history of the patient if he had past PTE, so he more liable
for another attack of PTE
**  The  Dx  of  PTE  depends  on  the  clinical  feature  of  it  is  types  that
mentioned  previously.  There  are  many  diseases  affecting  respiratory
system & cardiovascular system that mimic PTE:

1) Massive PTE mimic Acute MI, dissecting aortic aneurysm, &

massive pulmonary collapse

2) Pulmonary infarction (occlusion of 1 branch of pulmonary artery)

mimic T.B., pulmonary abscess, acute asthma, bronchiectasis,
bronchogenic CA.

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 8

3) Recurrent small pulmonary emboli → primary pulmonary

hypertension → Rt. Sided heart failure mimic secondary
pulmonary hypertension (mitral stenosis or other causes of Lt.
sided heart failure) & other causes that leads to Acute respiratory
failure..

** Investigation:

A. Radiological: 90% of PTE is caused by DVT, so we do venogram to

calf veins, thigh veins or pelvic veins, so we can detect filling
defect in the veins.

B. Ultra-sound (Doppler): we can use it for the same area of above.
C. Chest X-ray: it is helpful in most cases, in which the chest x-ray is

abnormal. The effect of recurrent small emboli or pulmonary
infarction of small/medium emboli may be not seen; but later on
you may see lung collapse (at the affected site), linear opacities or
any type of opacity, wedge-shape opacity suggest collapse of one
of segments.

- Also, you can see effusion because pulmonary infarction will

affect the overlying pleura → effusion (usually haemorrhagic)

- Sometimes you see Elevated hemidiaphram only suggested

Hidden collapse segment.

- Increase in hilar shadow because of pulmonary hypertension
- The lung is oligemic at the area of infarction if the PTE is

massive → the whole lung is oligemic.

D. C.T. scan & Angiogram : they are very much confirmative of this

disease by pulmonary angiogram you can detect the pulmonary
artery & it is branches

E. Radioactive scanning procedures : Technitium scan can show PTE

but bronchogenic CA, pneumonia, & pulmonary oedema mimic
the PTE, so it will be confused … So, it is better to do ventilation
scan & ventilation-perfusion scan using radioactive xenon, then
matching them → not matched.

F. E.C.G. changes : would be specific for the Rt.side of the heart,

sinus tachycardia & evidence of Rt. Sided ventricular hypertrophy
& classical pattern ( S

, Q

3 )

· Deep S in lead 1

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 9

·  T-wave is inverted in lead 3
·  Q – wave in lead 3
·  Rt. Bundle branch may appears
·  If the embolus is small, the E.C.G. may be normal or there is

very small changes.

G. Arterial blood gases: the pattern is of type -1- respiratory failure

(hypoxia, normocapnia, or hypocapnia) that indicate
ventilation-perfusion problem..

** Treatment (Rx):
Preventive measures:

1) Prevention of prolonged bed rest, use stockings to prevent DVT

(usually the patient is in faulty posture due to trauma or fatigue.
So change the position frequently by the patient himself or the
companion).

2) Also treat other risk factors for DVT like dehydration & treat

congested heart failure.

3) Prophylaxis is offered to any patient have problem & needs

operation, if he has  past PTE or DVT in the next surgery he  will
have  a  high  incidence  of  PTE,  therefore  we  we  must  give  the
patient  prophylactic  measures  like  :  Anti-coagulants  (leads  to
increase bleeding time, so in this case the surgeon must block all
the bleeding vessels that are usually left to block themselves)
We  give  –  Heparin  –  5000  IU/12  hr  (very  low  dose)  helpful  to
prevent DVT or we give – Dextran – I.V. during the operation

4) If the patient has DVT & recurrent pulmonary embolism &

resistant  to  Rx  ,  so  mechanical  measures  used  as  Inferior  Vena
Cava    PLICATION or other devices to allow blood to go on; but
prevent emboli to come to the heart.

** Treatment (Rx) of established cases:
IF the patient has massive PTE use thrombolytic agents which lysis
thrombus (for e.g.: Streptokinase, starting with loading dose 250,000 –
500,000 IU, then every hour 150,000 IU for 2 days with no complication
(like : brain haemorrhage or G.I.T. bleeding – contraindication-)

· Tissue Plasminogen Activator (TPA) by catheter is injected into

the thrombus, directly leading to it is lysis.

Lecture 36

Medicine

Dr. Adnan

ARDS + PTE

Page 10

· Anti-coagulant given to the patient by special device that

produce stable conc. of blood like that for Heparin 1000 IU/ hr,
so in 24 hr. there is 24000 IU. This will lead to smooth circulation
& we can follow up this by PTT (Partial Thromboplastin Time),
2-3 times than normal control.

· The Warfarin orally gradually taken before stopping heparin,

because it is effect appears after 3 days the PTT must be 2-3
times than normal control.

· The Rx must be from 6 weeks to 6 months depending on the

patient

’

s status, age (young 6 weeks, old or ill 6 months), & the

degree of embolization.

· Also supportive measures like good nutrition

ﻣﻼﺣﻈﺔ

ﲞﺼﻮص ﳏﺎﴐة:

PTE

... دﻛﺘﻮر ﺪ ن ﻋﺮض ﺑﻮرﺑﻮﯾ ﺖ ﻣﺎ

ﰷﻣﻞ و ﳊﺪ ﻋﺒﺎرة

DVT + PTE =

إ ﻜﻄﻢ اﳊﺠﻲ و ﻓ ﺢ دو ﯿﻮﻣ ﺖ وورد ﺑﯿﻪ ﳬ اﶈﺎﴐة ﺲ ﰷل ﻫﺎي اﶈﺎﴐة ﻣﻮ ﻣ ﻘ ﺔ و ﳱﺎ ا ﻼط و

ﺪ )اﻟﯿﻮم( ﻋﺴﺎس رح ﯾﻨﻄﻲ اﶈﺎﴐة ﺑﻮرﺑﻮﯾ ﺖ ﰷﻣ و ﻣ ﻘ ﺔ و ﺎﻻ ﻠﺐ ﲆ ﻣﻮﻗﻊ اﻟﳫﯿﺔ

إذا ﺣﺼﻠﺖ اﶈﺎﴐة رح ا ﺰﻟﻬﺎ ﲆ ﺮوب اﳌﺮ

و ﻫﺎي اﻟﺼﻔ ﺎت ذﺑﻮﻫﺎ و اذا ﻣﺎ ﺣﺼﻠﳤﺎ او ﻣﺎ ﺰﻟﺖ ﲆ

ﻣﻮﻗﻊ اﻟﳫﯿﺔ

...

ﻫﺎي وراق ﲤﴚ ﺷﻐﻞ ﻠﻤﻮد ﻣ ﺎن

ﻫﺎي آﺧﺮ ﳏﺎﴐة ﲠﺎﻟﻔﺼﻞ و ﰻ ﳏﺎﴐات دﻛﺘﻮر ﺪ ن دا ﳌﺪ

ًو ﺷﻜﺮا

The end of this lecture

Sabeeh & CHW