Tuberculosis is a very highly prevalent disease particularly in the developing world. In India one person dies of tuberculosis every minute. It can be a differential diagnosis of any disease ranging from infections to malignancies. But tuberculosis as a primary cause of respiratory failure requiring mechanical ventilation is an uncommon occurrence. Among patients with pulmonary tuberculosis, those with miliary or disseminated disease or having comorbidities like acquired immunodeficiency syndrome (AIDS) are especially prone to develop acute respiratory distress syndrome (ARDS). We present a case of a young female with no comorbidities or immuno suppression who presented with ARDS to us. We initially managed with mechanical ventilation and broad spectrum antibiotics, but there was no improvement. Only after anti tubercular therapy (ATT) and corticosteroids the patient recovered

Ab. Hameed Raina

Abid Bhat

Fayaz Ahmad Bhat

Feroz Ahmad Wani

Ghulam Nabi Dhobi

Khalid Hamid Changal

Manzoor Ahmad Raina

Pervaiz Ahmad Koul

Egyptian Journal of Chest Diseases and Tuberculosis

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Pulmonary tuberculosis presenting with acute respiratory distress syndrome (ARDS): A case report and review of literature

AbstractTuberculosis is a very highly prevalent disease particularly in the developing world. In India one person dies of tuberculosis every minute. It can be a differential diagnosis of any disease ranging from infections to malignancies. But tuberculosis as a primary cause of respiratory failure requiring mechanical ventilation is an uncommon occurrence. Among patients with pulmonary tuberculosis, those with miliary or disseminated disease or having comorbidities like acquired immunodeficiency syndrome (AIDS) are especially prone to develop acute respiratory distress syndrome (ARDS). We present a case of a young female with no comorbidities or immuno suppression who presented with ARDS to us. We initially managed with mechanical ventilation and broad spectrum antibiotics, but there was no improvement. Only after anti tubercular therapy (ATT) and corticosteroids the patient recovered

Raina, Ab. Hameed

Bhat, Abid

Bhat, Fayaz Ahmad

Changal, Khalid Hamid

Dhobi, Ghulam Nabi

Koul, Pervaiz Ahmad

Raina, Manzoor Ahmad

Wani, Feroz Ahmad

Elsevier - Publisher Connector 

Egyptian Journal of Chest Diseases and Tuberculosis (2013) 62, 655–659The Egyptian Society of Chest Diseases and Tuberculosis
Egyptian Journal of Chest Diseases and Tuberculosis
www.elsevier.com/locate/ejcdt
www.sciencedirect.comCASE REPORTPulmonary tuberculosis presenting with acute
respiratory distress syndrome (ARDS): A case report
and review of literatureAb. Hameed Raina a,*, Abid Bhat a, Fayaz Ahmad Bhat a,
Khalid Hamid Changal a, Ghulam Nabi Dhobi a, Pervaiz Ahmad Koul a,
Manzoor Ahmad Raina b, Feroz Ahmad Wani ca Department of Internal Medicine, Sheri-Kashmir Institute of Medical Sciences, Soura (J&K), India
b Department of Clinical Biochemistry, Sheri-Kashmir Institute of Medical Sciences, Soura (J&K), India
c Department of Community Medicine, Sheri-Kashmir Institute of Medical Sciences, Soura (J&K), IndiaReceived 30 July 2013; accepted 8 September 2013
Available online 5 October 2013*
E-
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OpKEYWORDS
Pulmonary tuberculosis;
Acute respiratory distress
syndrome (ARDS);
Miliary tuberculosisCorresponding author. Tel.:
mail address: rainahameed@
er review under responsibil
iseases and Tuberculosis.
Production an
22-7638 ª 2013 Production
en access under CC BY-NC-ND li+91 990
gmail.co
ity of Th
d hostin
and hosti
httpcense.Abstract Tuberculosis is a very highly prevalent disease particularly in the developing world. In
India one person dies of tuberculosis every minute. It can be a differential diagnosis of any disease
ranging from infections to malignancies. But tuberculosis as a primary cause of respiratory failure
requiring mechanical ventilation is an uncommon occurrence. Among patients with pulmonary
tuberculosis, those with miliary or disseminated disease or having comorbidities like acquired
immunodeﬁciency syndrome (AIDS) are especially prone to develop acute respiratory distress syn-
drome (ARDS). We present a case of a young female with no comorbidities or immuno suppression
who presented with ARDS to us. We initially managed with mechanical ventilation and broad spec-
trum antibiotics, but there was no improvement. Only after anti tubercular therapy (ATT) and cor-
ticosteroids the patient recovered.
ª 2013 Production and hosting by Elsevier B.V. on behalf of The Egyptian Society of Chest Diseases and
Tuberculosis. Open access under CC BY-NC-ND license.6650955.
m (A.H. Raina).
e Egyptian Society of Chest
g by Elsevier
ng by Elsevier B.V. on behalf of T
://dx.doi.org/10.1016/j.ejcdt.2013.0Introduction
In most countries, as ours, tuberculosis remains a major public
health problem. One third of the world’s population is esti-
mated to be infected with Mycobacterium tuberculosis. A sig-
niﬁcant proportion of tuberculosis patients still has to be
hospitalized, and in-hospital mortality remains high, with esti-
mates ranging from 2% to 12% [1]. Some decades ago, respi-
ratory failure resulting from tuberculosis was reported mainly
in cases of miliary tuberculosis. In 1977, the ﬁrst case series ofhe Egyptian Society of Chest Diseases and Tuberculosis.
9.008
656 A.H. Raina et al.respiratory failure in 16 patients with tuberculosis and ﬁbro-
cavitary disease was described [2]. The reported frequency of
acute respiratory failure in patients with active tuberculosis
ranged from 1.5% to 5.0% [3,4], although pulmonary tubercu-
losis is rarely the primary cause of this complication. We re-
port a case of a patient presenting with ARDS who
subsequently turned out to be a case of pulmonary
tuberculosis.
Case summary
Our case was a 32 year old female, normotensive, non-diabetic,
presenting with a four week history of severe breathlessness,
cough with expectoration with blood tinged sputum. Initially
she had followed some private practitioner outside but there
was no relief and symptoms got worsened.
On examination the patient was conscious, oriented, febrile
to touch, cyanosed, tachypneic with respiratory rate of 34/min,
pulse of 94b/min and temperature of 100F, BP was 140/
82mmHg. Oxygen saturation was 70% only. Systemic exami-
nation revealed bilateral course crepitations in the lungs. Rest
of the examination was normal. Initial investigations reveal Hb
of 10 g/dl, TLC of 12,000/uL, DLC of 84% neutrophils and
20% lymphocytes. Platelet count of 120,000. KFT of 40 IU
urea and 1.2mg/dl of creatinine. ABG/electrolytes showed
pH of 7.34, po2 = 40mmHg, pco2 = 45mmHg, Hco3 = 22-
meq/L, Na = 143, k= 3.5 depicting Type 1 respiratory fail-
ure. ECG showed sinus tachycardia. Po2/FiO2 = 198. Chest
X-ray (Figs. 1 and 2) showed bilateral dense reticulo-nodular
pattern interspersed with ﬁne inﬁltrates. The patient was
immediately managed with invasive mechanical ventilation
and broad spectrum antibiotics but she did not improve. Inﬂu-
enza retroviral and other virological serologies were negative.
Blood and urine culture came sterile. There was no evidence
of fungal infection. Bedside echo was done which was normal.
Tracheal aspiration showed strong positivity for M. tuberculo-
sis but Monteux test came negative. Subsequently computed
tomography (CT) scan (Fig. 3) showed typical miliary pattern
of the lungs though there was no evidence of disseminated
tuberculosis. So on clinical and radiological suspicion she
was put on anti-tubercular therapy. Fortunately after 7 days
of treatment the patient showed signs of improvement and
she was extubated on 12th day of admission. In the meantimeFigure 1 Chest X-ray showing bilaculture came positive for M. tuberculosis after 2 weeks of cul-
ture in Bactec. Hence she was diagnosed as a case of pulmon-
ary tuberculosis presenting as acute respiratory distress
syndrome (ARDS). She was discharged on 15th day. She is
on our follow up and is doing well. Sputum for acid fast bacilli
(AFB) is now negative and is symptomatically much better.
Discussion
Tuberculosis (TB) has been the scourge of civilization before
recorded history, afﬂicting humans and domestic animals alike
in all parts of the world. The multitude of names including
‘‘the white plague,’’ ‘‘consumption,’’ and ‘‘phthisis’’ that has
been applied to TB attests to its protean manifestations. While
the earliest classical descriptions of TB can be found in the
writings of Hippocrates, it was the experiments of P.F.H. Kle-
ncke in 1843 and Jean Antoine Villemin in 1865 that elucidated
the contagious nature of the disease. The identiﬁcation of the
tubercle bacillus by Kochin in 1882 allowed for the under-
standing of the pathogenesis of TB [2].
Tuberculosis is being increasingly recognized as a cause of
acute respiratory distress syndrome (ARDS) [3–5]. Although
exact ﬁgures as to what percentage of cases of ARDS are
tubercular in aetiology are not available, in the Southeast Asia
tuberculosis accounts for 3–16% of cases of community-ac-
quired pneumonia. Malhotra et al. studied 185 cases of RICU
admissions. Out of a total of 984, 18.8% admissions had
ARDS over an 8-year period of which tuberculosis accounted
for seven (3.8%) [6]. The pathogenesis of ARDS in patients
with pulmonary tuberculosis has not been clearly elucidated.
Postulated mechanisms include massive release of mycobacte-
ria into the pulmonary circulation resulting in inﬂammation,
obliterative endarteritis and damage of the alveolocapillary
membrane [7]. Platelet aggregation in pulmonary capillaries
causing endothelial injury and leucocyte activation resulting
in increased vascular permeability are other hypotheses. In
addition, lipoarabinomannan, a component of the mycobacte-
rial cell wall, is thought to act in a manner similar to lipopoly-
saccharide in bacterial sepsis to activate macrophages to
release tumour necrosis factor-a [TNF-a] and interleukin-1b
[IL-1b] [8]. The activation of macrophages is thought to be a
key step in the causation of lung injury [8]. It is yet to be deter-
mined, whether it is the individual host immunologic responsesteral inﬁltrates (ARDS picture).
Figure 2 Chest X-ray showing features of miliary tuberculosis.
Figure 3 CT scan of the chest showing features of ARDS.
Pulmonary tuberculosis presenting with acute respiratory distress syndrome (ARDS) 657independent of organism burden or differences in the virulence
of different strains of the M. tuberculosis which are the prime
factors in the development of lung injury [6].
Acute respiratory distress syndrome (ARDS) is a life-
threatening reaction to injuries or acute infection to the lung.
ARDS is a severe lung syndrome with direct and indirect
causes. Inﬂammation of the lung parenchyma leads to im-
paired gas exchange with systemic release of inﬂammatory
mediators, causing inﬂammation, hypoxaemia and frequently
multiple organ failure. This condition has a 90% death rate
in untreated patients. With treatment, usually mechanical ven-
tilation in an intensive care unit, the death rate is 50%. It is
diagnosed by the following criteria: [9]
1. Acute onset: It is deﬁned as within 7 days of some deﬁned
event, which may be sepsis, pneumonia, or simply a
patient’s recognition of worsening respiratory symptoms.
(Most cases of ARDS occur within 72 h of recognition of
the presumed trigger.)
2. Bilateral opacities consistent with pulmonary oedema must
be present but may be detected on CT or chest X-ray.3. PaO2: FiO2 ratio < 300. ‘‘Acute lung injury’’ no longer
exists. Under the Berlin deﬁnition, patients with PaO2/
FiO2 200–300 would now have ‘‘mild ARDS.
4. Respiratory failure should not be fully explained by cardiac
failure or ﬂuid overload. There is no need to exclude heart
failure in the new ARDS deﬁnition; patients with high pul-
monary capillary wedge pressures, or known congestive
heart failure with left atrial hypertension can still have
ARDS.
The new Berlin deﬁnition for ARDS has also categorize
ARDS as being mild, moderate, or severe:
ARDS severity PaO2/FiO2* Mortality**
Mild 200–300 27%
Moderate 100–200 32%
Severe <100 45%* On PEEP 5+.
** Observed in cohort.
658 A.H. Raina et al.The following three clinical settings account for 75% ofARDS cases:
1. Sepsis syndrome – most important cause.
2. Severe multiple trauma.
3. Aspiration pneumonia which is due to aspiration of
saliva/gastric contents.
4. Complication of pneumonia if left untreated.
5. Necrotizing pancreatitis. Some cases of ARDS are
linked to large volumes of ﬂuid used during resuscita-
tion post trauma. Other causes include shock, near-
drowning, multiple transfusions and inhalation of irri-
tants or toxic fumes that damage the alveolar epithe-
lium and miliary tuberculosis. But pulmonary
tuberculosis without dissemination causing ARDS
has rarely been mentioned in literature. Our case, there-
fore, represents a unique cause of ARDS.
The leading cause of ICU admission of tubercular patients
was respiratory failure, and Acute Physiology and Chronic
Health Evaluation II (APACHE II) scores ranged from 13 to
23 in most of the studies [1]. Some authors evaluated the fac-
tors associated with the development of respiratory failure
and the need for mechanical ventilation. Gram-negative pneu-
monia or sepsis, COPD, history of poor compliance with
tuberculosis treatment, and cancer were predictors of respira-
tory failure [10]. Our case had none of these. Patients with mil-
iary/disseminated tuberculosis were more likely to require
mechanical ventilation than those having only pulmonary
tuberculosis. In a study conducted in Brazil investigating the
pulmonary histopathological changes found in 3030 autopsies
of patients who died of acute respiratory failure, tuberculosis
was diagnosed as an underlying disease in 110 cases (3.6%).
Among them ARDS was found in very few cases [11]. The
most common radiological ﬁndings are reticular inﬁltrates
and consolidation and cavitation can occur in 27–50% of cases
[1]. The most common laboratory ﬁndings are anaemia, leuco-
penia, leucocytosis, and hypoalbuminemia [12]. Our patient
had only anaemia among these.
Clinical characteristics and chest X-ray remain the main
tools for the early diagnosis of active pulmonary tuberculosis.
Mycobacterial culture takes 6–8 weeks. Therefore, the treat-
ment of intensive care unit (ICU) patients can rarely be based
on culture results. In addition, obtaining material for myco-
bacterial analysis can be difﬁcult, especially in patients with ex-
tra pulmonary tuberculosis and in mechanically ventilated
patients whose parameters preclude diagnostic procedures,
such as bronchoscopy. Although antituberculosis treatment
is potentially toxic, it is recommended that patients admitted
to an ICU with tuberculosis symptoms start receiving the med-
ications before the results of diagnostic tests are available, gi-
ven that delayed treatment initiation can result in death. In
immunocompromised patients, the index of suspicion should
be even higher [1]. Appropriate diagnostic investigation, as
well as knowledge of the clinical and radiological presentations
of severe tuberculosis, can contribute to earlier diagnosis and
treatment initiation. The time from onset of symptoms to ini-
tiation of anti-tuberculosis treatment has been reported to be
over 30 days in 28.8–34.0% of cases [13]. In that retrospective
study, the time from admission to initiation of treatment was
shorter in patients with miliary tuberculosis than in those withtuberculous pneumonia. There can be a delay in diagnosis and,
consequently, in initiation of treatment because it is difﬁcult to
differentiate tuberculous pneumonia from severe bacterial
pneumonia on X-rays. Symptom duration longer than two
weeks and the presence of micronodules or a cavitary pattern
on chest X-ray were signiﬁcantly associated with active pul-
monary tuberculosis [14]. The introduction of new techniques,
including early detection of the aetiological agent by PCR, can
aid in diagnosis and contribute to early initiation of treatment.
In addition, high resolution computed tomography (HRCT)
has been used in situations in which chest X-ray does not con-
tribute to the diagnosis of active disease, such as in cases of
minimal parenchymal changes and in the differentiation of
old ﬁbrotic lesions from those that are characteristic of bron-
chogenic dissemination [15].
Appropriate antituberculosis treatment is an important fac-
tor that can affect patient outcome. Higher mortality is found
among patients who do not receive optimal treatment includ-
ing isoniazid and rifampin.
In the treatment of tuberculosis, corticosteroids are used as
adjuvants, especially in extra pulmonary forms of the disease,
such as meningeal and pericardial tuberculosis. Corticosteroids
act by inhibiting the release of lymphokines and cytokines,
which are responsible for constitutional symptoms and tissue
damage. In addition, they allow antituberculosis drugs to pen-
etrate granulomas, disrupting them [16]. In general, corticoste-
roid use is considered for selected patients with severe forms of
pulmonary tuberculosis, usually for those who develop ARDS
[13]. We used them in our patient and they helped.
Our case is unique in the sense that the patient was young,
had no comorbidities, or superadded infection. She presented
with ARDS and was managed in ICU with mechanical venti-
lation and broad spectrum antibiotics initially. But when she
did not respond other causes were thought of. Further work
up gave the diagnosis of underlying tuberculosis. It was after
putting her on ant tubercular drugs and corticosteroids that
she improved. So tuberculosis should always be kept a possi-
bility of ARDS particularly in the developing world even if
there are no comorbidities or immunosuppression.
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Pulmonary tuberculosis presenting with acute respiratory distress syndrome (ARDS): A case report and review of literature 

Pulmonary tuberculosis presenting with acute respiratory distress syndrome (ARDS): A case report and review of literature

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