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Acute respiratory failure from pulmonary tuberculosis due to head trauma immunosupression.

The course of pulmonary tuberculosis (TB) in immunocompetent patients is commonly benign, progressing slowly unless immunosuppressive factors, such as pharmacologic agents or underlying diseases, adversely affect the immune response. Then, critical deterioration may occur. When this happens, mortality reaches approximately 60% due to respiratory failure (1,2).

We report the case of a 45-year-old male of East European origin, who was admitted to our tertiary hospital after accidental head-injury (Glasgow Coma Scale 7/15). His medical history was unremarkable. Brain computed tomography scan showed an epidural haematoma, multiple haemorrhagic contusions on the right lobe with localised oedema and subarachnoid haemorrhage. After surgical drainage of the haematoma, he was transferred to the intensive care unit (ICU).

Clinical respiratory examination revealed only moderately dense non-haemorrhagic secretions. Arterial blood gases were within normal limits (FiO2 0.35%). Chest X-ray showed a consolidation of the right upper lobe (Figure 1A). On the third ICU day he developed fever and his respiratory function started to deteriorate: bronchial secretions increased and became purulent and diffuse bilateral infiltrates appeared on chest radiography. Microbiologic investigations including smears, cultures, serology of several specimens (blood, bronchial aspirations, bronchoalveolar lavage, urine, bone marrow, cerebrospinal and gastric fluid) for common, atypical pathogens and direct examination for mycobacterium were negative. Tests for HIV and tuberculin skin test were also negative.


[P.sub.a][O.sub.2]/Fi[O.sub.2] gradually declined and on the fifth day Fi[O.sub.2] was 0.75 with [P.sub.a][O.sub.2] 74 mmHg. The patient's clinical deterioration was attributed either to early severe ventilator-associated pneumonia or to acute respiratory distress syndrome (ARDS) secondary to brain injury. However, the location of the initial radiographic findings led also to the hypothesis of active TB despite the negative laboratory results. A chest computed tomography scan revealed a cavity at the right upper lobe and extended consolidation with air bronchograms on both lower lobes (Figure 2). Anti-tuberculous treatment was initiated, and previous antibiotic regimens were ceased on the seventh day. The patient was managed based on ARDS network ventilatory strategy. His deterioration was attributed to active pulmonary tuberculosis. Positive direct smears for Mycobacterium tuberculosis were available later on the seventh day, while positive cultures of bronchial aspirations for TB, taken on his admission, were available on the 12th ICU day. Respiratory function started to improve after 15 days of antituberculous treatment. The patient discharged 35 days after admission with a Glasgow Coma Score of 15/15 and no sign of respiratory failure.

In the present case, slowly progressing active TB was probably accelerated to severe ARDS in the setting of head trauma. We speculate that severe brain injury may have induced immunsupression. To our knowledge, this association has not been underlined so far.

Previous reports suggested that brain injury can affect T-cell immunity and macrophage activation, both important for an intact host response to tuberculosis. T-cell anergy can be seen within hours after brain damage while total circulating numbers of T-cells (T helper, T-supressors, NK, IL-2 receptor-bearing T-cells) are decreased (3). Moreover, reduction of their proliferative response to mitogen stimulation has been noted. IFN-[gamma] and IL-2 production, involved in the host defence mechanism to mycobacterium, are decreased as well (3). The depressed delayed-type hypersensitivity reaction may also explain the negative result of tuberculin skin test seen in our patient. Monocytes exhibit depressed antigen presentation capacity and enhanced secretion of IL-10. IL-10 is an anti-inflammatory cytokine participating in Th2 response which results in reduced resistance to mycobacterial infection (3-5).

One might argue that not brain injury per se, but additional measures for managing brain injury, such as the use of sedation and antiepileptic drugs, may also have immunomodulatory effects contributing in alterations of the immune response of previously immunocompetent patients (6,7). Certainly, this cannot be excluded. Based on positive results for TB from cultures of bronchial secretions sampled on his admission, our patient had most probably active tuberculosis prior to head trauma. Tuberculosis is a chronic infection that progresses rather slowly in otherwise healthy adults. Consequently, either head trauma alone or in combination with the use of sedatives and anti-epileptics might have favoured intrapulmonary spread of tuberculosis, clinically manifested as ARDS.


This report underlines that physicians should be alert for the possibility of fulminant intrapulmonary spread of active tuberculosis in ICU patients with severe head trauma. Clinical suspicion of TB may be important for a favourable outcome in the ICU setting in patients who present risk factors for the disease (origin from countries with increased incidence, suspicious radiology, positive tuberculin test etc.).





Larissa, Greece


(1.) Agarwal R, Gupta D, Aggarwal AN, Behera D, Jindal SK. Experience with ARDS caused by tuberculosis in a respiratory intensive care unit. Intensive Care Med 2005; 31:1284-1287.

(2.) Erbes R, Oettel K, Raffenberg M, Mauch H, Schmidt-Ioanas M, Lode H. Characteristics and outcome of patients with active pulmonary tuberculosis requiring intensive care. Eur Respir J 2006; 27:1223-1228.

(3.) Dziedzic T, Slowik A, Szczudlik A. Nosocomial infections and immunity: lesson from brain-injured patients. Crit Care 2004; 8:266-270.

(4.) Gong JH, Zhang M, Modlin RL, Linsley PS, Iyer D, Lin Y et al. Interleukin-10 downregulates Mycobacterium tuberculosis-induced Th1 responses and CTLA-4 expression. Infect Immun 1996; 64:913-918.

(5.) Boussiotis V, Tsai E, Yunis E, Thim S, Delgado J, Dascher C et al. IL-10 producing T cells suppress immune responses in anergic tuberculosis patients. J Clin Invest 2000; 105:1317-1325.

(6.) Nseir S, Makris D, Mathieu D, Durocher A, Marquette C-H. Intensive care unit-acquired infection as a side effect of sedation. Crit Care 2010; 14:R30.

(7.) Zaccara G, Franciotta D, Perucca E. Idiosyncratic adverse reactions to antiepileptic drugs. Epilepsia 2007; 48:1223-1244.
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Article Details
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Title Annotation:Correspondence
Author:Karapetsa, M.; Makris, D.; Mpaka, M.; Zakynthinos, E.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Geographic Code:9INDI
Date:Mar 1, 2012
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