Post on 26-Jan-2017
* 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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