* Senior Lecturer, ** Professor, *** Lecturer, **** Resident, Department of TB and Respiratory Diseases, JN MedicalCollege, AMU, Aligarh-202 002 (UP).

Acute Respiratory Distress Syndrome (ARDS)following Minor Chest Trauma

Zuber Ahmad*, Rakesh Bhargawa**, DK Pandey***, DK Sharma***, Imrana Masood****

Abstract

A 40 year old male patient presented with shortness of breath and restlessness 3-4 hours after a minor blunt chesttrauma. The patient was diagnosed as a case of acute respiratory distress syndrome (ARDS) on the basis of clinical,radiological, and arterial blood gas analysis. Patient was kept in intensive care unit (ICU) and improved withintermittent positive pressure ventilation alongwith steroids and other supportive measures.

C A S E R E P O R T JIACM 2003; 4(2): 166-8

Introduction

ARDS is a syndrome of acute lung injury that can be

initiated due to a wide variety of insults to either direct

(toxic gas inhalation, aspiration of abdominal contents)

or indirect (multiple trauma, sepsis) factors1.

It occurs in an unpredictable fashion often after several

hours or days after the insult. Majority of patients develop

ARDS within first 24 hours of well-defined injuries or

clinical conditions. The risk of ARDS after 72 hours is

negligible. The lung injuries which commonly lead to

ARDS are contusion and blast injuries. The incidence of

ARDS with pulmonary contusion alongwith fractures is

60% and with contusion alone is very low2. This case is

reported keeping in view the rarity of its presentation and

difficulty in diagnosis and management.

Case report

A 40 year old male patient presented in the emergency

department of JN Medical College, AMU with shortness

of breath, restlessness, cough with some streaking of

sputum with blood, and pain in chest and right

shoulder for 2-3 hours. He had a minor blunt chest

injury due to fall from a bicycle 4-5 hours before. There

was no preceding history of breathlessness, fever,

cough, haemoptysis, chest pain, unconsciousness, drug

use, or inhalation of any toxic fumes. There was a past

history of antitubercular treatment for pulmonary

tuberculosis 9 years back.

The patient was a mason by occupation. He was non-

alcoholic. He was a smoker from last 8-10 years with a pack

year of 0.5.

On examination, patient was restless and agitated but

well oriented to time, place, and person. Pulse rate was

110 per min, BP 120/70 mm of Hg, respiratory rate 34

per min.; he was afebrile, mildly cyanosed, and had no

clubbing or oedema. Jugular venous pressure (JVP)

was not raised. Chest examination revealed a small

abrasion in right infraclavicular region. Few bilateral

diffuse crepitations were heard on auscultation. Heart

sounds were normal. The following investigations were

performed: TLC 8,000/mm3, DLC-neutrophils-60% and

lymphocytes-40%, blood-urea 33 mg%, blood sugar

(R)-90 mg%, serum creatinine-0.8 mg%, serum

potassium-4 mEq/L, serum sodium-139 mEq/L. Arterial

blood gas analysis revealed respiratory alkalosis: PaO2

56 mm of Hg, PaCO2 40 mm of Hg and F

iO

2 0.4. Initial

PaO2/F

iO

2 ratio was 140. ECG was within normal limits.

Colour doppler echocardiography revealed normal

functioning hear t. All valves, chambers, and

pericardium were normal. Left ventricular ejection flow

(LVEF) was normal (60%). X-ray chest PA showed

bilateral fluffy shadows (Fig. 1).

Patient was initially put on oxygen therapy. Later, when

hypoxia further increased (PaO2 48 mm of Hg and F

iO

2

0.5), he was shifted to ICU and put on intermittent positive

pressure ventilation (IPPV) with volume cycled mechanical

ventilator in the assist control mode. Initial settings were:

assist control mode; FiO

2 1.0; PEEP 5 cm of water; inspiratory

flow 60 liters/min; initial tidal volume 8 ml/kg body weight.

Fig. 1 : X-ray chest PA view showing bilateral fluffy shadows.

Fig. 2 : X-ray chest PA view showing compete clearance of shadows.

These settings were adjusted from time-to-time on the

basis of patient’s arterial blood gas analysis. Strict fluid

balance was maintained and antibiotics were given to

prevent infection. Hydrocortisone 200 mg tid was also

started after four days which was tapered gradually in

seven days. Initial oxygen saturation of 70% was increased

to more than 90% in 24 hours, which was maintained for

three days when we were able to wean him from

mechanical ventilation. After 3 days, X-ray showed

considerable clearing of shadows. PaO2 reached to 76 mm

of Hg and FiO

2 to 0.3. After 7 days, there was complete

clearing of X-ray shadows (Fig. 2) and arterial blood gases

were within normal limits (PaO2 92 mm of Hg, PaCO

2 42

mm of Hg). He was discharged on the tenth day.

Discussion

ARDS is a potentially lethal condition with a mortality rate

of 50-70%3,4. It is a syndrome of acute inflammatory lung

injury that can be initiated in pulmonary microvessels as

a result of a wide variety of insults to the lung. It is generally

held that 20-35% ARDS cases are due to multiple trauma5,6.

However, a minimal chest trauma is a rare cause of ARDS.

Pulmonary contusion due to blunt trauma to the chest is

responsible for the development of ARDS2. The reported

incidence of developing ARDS following pulmonary

contusion is 17%2.

The first detailed clinico-pathological description of ARDS

was provided by Ashbaugh and colleagues7. It is widely

accepted that neutrophils play a key role in the

pathogenesis of ARDS. Neutrophils generate a range of

reactive oxygen intermediates (ROI) and histotoxic

granule contents such as elastases and collagenase which

cause damage to capillary endothelial cells and airway

epithelial cells8,9. As a result, there is marked increase in

the permeability of the alveolar-capillary membrane to

water, solutes, and plasma proteins. This is the defining

characteristic of ARDS.

The patient develops progressive dyspnoea and often a

non-productive cough. The patient is tachypnoeic, often

cyanosed, and agitated. Tachycardia is likely to be present

but JVP is not raised. X-ray chest typically shows fluffy areas

of opacification.

No specific physical or laboratory findings exist for the

diagnosis of ARDS. Arterial blood gas analysis typically

shows markedly reduced PaO2 with normal or reduced

PaCO2; when fully developed syndrome is present, the

PaCO2: FIO

2 ratio is typically less than 200 mm of Hg. This

consensus criteria alongwith clinico-radiological

presentation is now widely used for diagnosis of ARDS10.

We were also able to reach the diagnosis with this criteria

as our patient had all the above features.

The current treatment of ARDS remains supportive. The

general principles rest on the maintenance of mixed

venous oxygen saturation and function of other organs

and to treat lethal infective complications. Most patients

are supported by intermittent positive pressure

ventilation (IPPV) often combined with positive end-

expiratory pressure (PEEP) which is applied in order to

Journal, Indian Academy of Clinical Medicine � Vol. 4, No. 2 � April-June 2003 167

increase lung volume and keep alveoli open. Fluid intake

is restricted and even diuretics may be used, if possible,

to achieve the lowest pulmonary artery occlusion pressure

consistent with an adequate cardiac output. The role of

corticosteroids is controversial. Anecdotal reports11

suggest that corticosteroids may be useful during the

fibro-proliferative phase of ARDS (5-10 days after onset).

Also, a few patients who have high number of eosinophils

in their blood may benefit from corticosteroids12. We

successfully treated the patient with IPPV and other

supportive measures.

ARDS remains a frequent and dreaded problem in modern

intensive care units. Early identification of the case and its

proper and meticulous management may significantly

decrease its mortality. Our case highlights the fact that

even a minor chest trauma may initiate the ARDS.

Therefoer, even in a previously healthy person, acute onset

of dyspnoea and resetlessness following a minor trauma

should raise the possibility of ARDS.

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