ACUTE RESPIRATORY

DISTRESS SYNDROME
[ ARDS ]
by: Anastasia D.H.

DEFINITION:
syndrome signed by:
- increase of permeability alveolo capilair
membrane against water, solution & plasma
protein.
- diffuse alveolar disturbance.
- fluid accumulation inside lung parenchym
consist of protein.

 Based Definition by American-Europe ARDS

Coference Committee 1994:
1. Respiratory failure/distress acute onset
2. Ratio of artery vessel oxygen pressure
with inspiration oxygen fraction (PaO 2/
Fi O2) < 200 mmHg Hipoksemia berat.
3. Chest Radiography: bilateral alveolar
infiltrat represent Lung edema
4. Pulmonary capillary wedge pressure <18
mmHg,without clinical signs (rontgen,etc),
presence left atrial hypertension/ without left
heart failure signs.

If PaO2/Fi O2 200-300 mmHg---Acute

Lung Injury, corelation of risk factor ALI
with absence Chronic Lung disease.

RISK FACTORS
Direct injury alveolus epithel:
1. Aspiration of gaster content
2. Diffuse lung infection
3. Lung contusio
4. Drownning
5. Toxic inhalation

 Indirect

injury:
1. Septic
2. Non thoraxic trauma
3. Overload blood tranfussion
4. Pankreatitis
5. Cardiopulmonarry shunt

PATOPHYSIOLOGY
Begin with alveolar epithel & microvascular
disturbance, caused by direct/indirect injury, then
activate cascade inflamation, divided 3 phase:

1.Initiation phase : risk factor condition cause

imune & non imune cells relieves inflamatory
mediators & modulators inside lung towards
systemic
2.Amplification phase : efector cell/netrofil is
activated,pull & persisted inside lung.
3.Injury phase : inside target organ, relieves
inflamatory mediator include oxydase &
protease, directly destroy the lung & stimulate
next inflamatory process.Membran alveolocapilair damage cause increase membrane
permeability & flow of rich protein liquid enter
alveolar space then disturb surfactan integrity
cause further alveolair disturbance

3 Phase Alveolar Disturbance

1.

2.

3.

Exudative phase: interstitial & alveolar

edema, pneumosit cell necrose &
denudation basal membrane, endothel
cell swelling with intercelluler junction
widening, hyalin membrane formed in
alveolar duct & air space, netrofil
inflamation,also found pulmoner
hypertension & decrease of lung
compliance.
Proliferative phase: fastest happened
after 3 days onset, sign: pneumocyte
epithel cel proliferation.
Fibrotic phase: colagen increased, lung
become solid caused of fibrotic

CLINICAL MANIFESTATIONS
Generally,acute onset 3 5 days since condition
as ARDS risk factor is diagnosed.
First sign: tachypnea
Others: hypotension, fever
Auscultation: wet ronkhi

DIAGNOSTIC EVALUATION
Laboratory Findings:
1. Blood Gas Analyzes: hypoxemia, hypocapnea
(secondary cause of hyperventilation), hypercapnea
(in emphysema or further condition).

Alkalosis Respiratory in beginning process replace to

Acidosis Respiratory.
2. Leucocytosis (on septic), anemia, trombosito-penia
(systemic inflamatory reflection & endothelial injury),
increased of amylase level (on pancreatitis)
3. Renal & Liver function disturbances, dissemi-nated
intravasculer coagulation (as part of MDS /multiple
organ dysfunction syndrome)
Imaging:
1. Chest X-Ray: beginning process found lung area
relatively clear,then diffuse radioopaque shadow
seen & no gravitation influence, without heart
congestion description
2. CT scan: heterogenous pattern, infiltrat
predomination on dorsal lung area (supine photo)

DIFFERENTIAL DIAGNOSTIC:
-

Cardiogenic, Neurogenic lung edema

Lung infection: (V,B,F)
High Altitude Pulmonarry Edema (HAPE)
Laryngospasm induce lung edema
Drug induce lung edema (heroin, salicylate, cocain)
Radiation, Hypersensitivity Pneumonitis
Fat embolic syndrome
Mitral stenosis with alveolar bleeding
Vasculitis
Interstitial lung disease

MANAGEMENT
1. Take over respiratory function with mechanical ventilator
2. Agent therapy:
- Corticosteroid on ARDS/ALI advanced phase or
fibroploriferative phase.(severe persistent hypoxemia in
the seventh day ARDS)
- Nitric Oxide inhalation (NO) give selective vasodilatation
effect on distribution lung area
caused decreased pulmonarry artery,repair arterial
oxyganation.Only give for refracter severe hypoxia.
3. Patient position: prone position increased oxygenation but
not change mortality

4. Fluid: must balance between

- needs of optimal organ perfussion
- fluid extravasation problem to lung &
tissue:
increase of intravascular hydrostatic
pressure
caused fluid accumulation in alveolus.
Main focus: defence adequate perfussion
without oxygenation victimize.
Fluid restriction, best monitor by pulmonary
arte-ry catheterization, defence in level:
lowest intra
vascular hydrostatic pressure, but adequat

COMPLICATION:
-- MODS, nosocomial pneumonia, barotrauma,
pneumotorax, trakeomalasia, trakeoesofageal fistule,
inominata artery errosion, death.

PROGNOSE:
mortality : 40 % affected by:
--Risk factors (septic,post trauma,etc), main disease,
malignancy, presence MODS ,age, alcoholism,
presence gas exchange index recovery (Pa O2/FiO2)
in 3 7 day.
-- good response: lung function recovery in 3 months,
max. 6 months post extubation.
-- 50 % patient abnormality persistent, restriction
disturbance & decrease difusion capacity--- decrease
quality of life

MUTIPLE ORGAN FAILURE

PASCA TRAUMA
DEFINITION

MOF :
found 2 / > organ / system failure
1. Cardiovasculair failure:
- HR 54/minute, MAP 49 mmHg, VT & orVF, pH
serum 7,24 dg. PCO2 40 mmHg.
2. Respiratory failure:
- RR 5/min,or 49/min, PaCO2 50 mmHg, on
ventilator in 4th day
3. Renal failure: diuresis 479 ml/24 h or 159 ml/8h,
BUN 100 mg/dl, creatinin serum 3,5 mg/dl

4. Hepatic failure: bilirubin serum 6mg/dl,

PT > 4 sec (without anticoagulant)
5. Central Nervous Systemic failure: GCS 6
(without sedative)
6. Hematological failure: Leuc 1000/ml, Tr 20.000/ml,
Ht 20%
7. Coagulation system failure: trombocytopenia, PT&
APTT,BT memanjang, Hypofibrinogenemia
8. ARDS : history disease, PaO2 / FIO2 < 200 mmHg,
diffuse infiltrat on X-Ray, no pulmonary infection, low
pulmonary compliance, Pulmonary capillary wedge
pressure < 18 mmHg.

9. Acute Lung Injury: PaO2 / FIO2 < 300 mmHg,

+ ARDS criteria

ETIOLOGY:

trauma: multiple trauma, post

operation, visceral ischemia, epileptic status,
heat injury, abdominal compartemen syndr

 PATOGENESIS

- cause of local insult or infection, pro inflamatory mediators released against foreign antigenes
to relieve the wound.

- then followed by anti inflamatory mediators released to

regulate this process,homeostasis reached,patient
recovered.
- if there is severe pathologic insult, local defence
mechanism doesnt success, inflamatory mediators
will enter to systemic sirculation & new leucocyts
recruit in inflamatory area. Stress respon happen in
the whole body. Ones more, anti inflamatory mediators
released to systemic for proinflamatory cascade
recovery till homeostatic reached.

If systemic pro inflamatory respon is severe

or if anti inflamatory respon as its compensated isnt adequate, caused pro inflamatory
respon regulation failed. In this condition, found
SIRS signs,then start to threat organ dysfunction.
- On the opposite, if anti inflamatory respon predominant, caused anergy & immunosupressi, this
condition named Compensatory Antiinflamatory
Respose Syndrome (CARS).
- The progress of life depend on reachment of homeostatic.If failed, last phase patogenic process,
immunological dissonance happened, imbalance
pro & anti inflamatory process --- clinically find
MOF signs
-

Insult
T,B cell,NK cell, macrophage
Anti inflamatory response:
IL-4,IL-10,IL-13

Pro inflamatory response:

IL-1,IL-6,TNF-

into systemic sirculation

Hypoinflammatory condition

Hyperinflammatory condition
SIRS
Systemic Inflammatory Response Syndrome

CARS
(Compensatory Antiinflammatory
Response Syndrome)

Cardiovascular compromised/syok,
apoptosis

Immunocompromised

Lost of homeostatic

MODS

MANAGEMENT
PREVENTION
Well technical surgery is important,cause from research
40% MODS case caused of surgical error.Nosocomial
Infection increase twice mortality.Hand washing, isolation
room, silicon iv cathetherization can reduce MODS insidence.
CAUSE CONTROL
The importance thing: remove presipitate factor & cause or
infection source.
SURGERY
Include bone fracture fixation,burn debridement,ischemic/ necrotic bowel resection,pus removal.Source of inflamatory response not always clear,sometimes surgical exploration need,
especially suspicious intra abdominal source.

ANTIBIOTICS
Maximal effort to find patogen cause infection,include
blood &body liquid culture, serology examination & aspiration percutan. Giving appropriate antibiotic in early process
of infection disease will improve prognostic, prevent secondary infection, nosocomial disease, then reduce MODS
insidence.
SUPPORTIVE MANAGEMENT
If cant find spesific cause:
- Deficit must be corrected
- Support system/organ which suffer dysfunction
- Guard safety system/organ which still functionning

 INOVATIVE

THERAPY
Immune Modulation
Big scale research, monoclonal antibody given
to manipulate immune system (magic bullets)--still not
show decrease of mortality MODS patient

NO inhibitor
Research prove NOS (nitric oxide synthase) inhibitor
Increase mortality.In the future, selective inhibitor to
INOS (Inducible Nitric Oxide synthase) has role in
management MODS
BLOOD FILTRATION ---still not succed
High volume hemofiltration (2 6 filtration/h) may
filtrate cytocines & others inflamatory mediators

Corticosteroid
High dose CS (metilprednisolon 30 mg/kg)
significantly increase mortality septic syok.
Research in physiologic dose, show organ dysfunction & syok recovery, suggest mechanism :
1.Anti inflamation by supression of proinflamatory
cytocines transcription.
2. Replacement therapy in cortex adrenal
insufficiency
3. Improve cathecolamine receptor sensitivity

Manipulation of coagulation cascade

Research of the advantages of activated protein C
& antithrombin III