In patients with brain injury, the lungs can get affected from either a direct lung injury or from secondary effects of brain injury. Lung injury also has a significant bearing on the overall outcome of patients with brain injury. This paper will discuss the neurological conditions affecting the lungs, lung pathology that can occur in patients with brain injury and the management strategies in patients with dual injuries. 
Various neurological conditions like traumatic brain injury (TBI), status epilepticus, meningitis, stroke, intracranial hematomas, subarachnoid hemorrhage (SAH) etc can affect the respiratory system and contribute to poor outcome. The most severe forms of lung injury following brain injury are acute respiratory distress syndrome (ARDS) and neurogenic pulmonary edema (NPE). The lung mechanics following secondary lung injury also influence the intracranial pressure (ICP) and cerebral perfusion pressure (CPP).  
Trauma to the chest and underlying lung can occur in patients with TBI. This can result in fractured ribs, flail chest, pneumo- and hemothorax, broncho-pleural fistula, airway trauma, lung contusion etc which can secondarily affect the brain due to compromise in oxygenation and ventilation. Pain and injury to the respiratory muscles can also impede breathing, compromising the normal respiratory mechanics. Quick assessment of lung injury with a chest radiograph or lung ultrasound will facilitate early and simultaneous intervention for lung problem along with management of brain injury. Pneumo- and hemothorax require emergent placement of an intercostal drain even before any intervention for the brain. Adequate pain control with regional blocks prevents pooling of secretions and atelectasis. Lung contusion requires intubation and mechanical ventilation with low tidal volume.
Respiratory physiotherapy procedures like chest vibration, postural drainage with tapping and endotracheal aspiration/suctioning maneuvers affects ICP without significantly changing CPP in intensive care unit (ICU) patients. Increase in intrathoracic pressure, which is directly related to the alveolar pressure, decreases the rate of venous return to the heart and decrease cardiac output and mean arterial pressure, which compromises cerebral venous return, leading to increased ICP. [1]
ARDS develops in up to 20% of patients with severe head injury. This complicates the treatment of head-injured patients because lung-protective strategies such as high PEEP and permissive hypercapnia may increase ICP and reduce CPP. High-frequency percussive ventilation (HFPV), a hybrid of conventional mechanical ventilation and high-frequency oscillatory ventilation, is an alternate mode of ventilation that may improve oxygenation for head-injured patients while also lowering ICP. In a study in 10 patients with severe TBI and ARDS, there was an increase in PF ratio (91.8 +/- 13.2 vs. 269.7 +/- 34.6; p < 0.01), PEEP (14 +/- 2.5 vs. 16 +/- 3.5), and mean airway pressure (20.4 +/- 4.8 vs. 23.6 +/- 6.8) 16 hours after institution of HFPV from conventional ventilation. There was a decrease in ICP (30.9 +/- 3.4 vs. 17.4 +/- 1.7; p < 0.01), PC02 (37.7 +/- 4.1 vs. 32.7 +/- 1.1; p < 0.05), and PIP (49.4 +/- 10 vs. 41 +/- 7.9; p < 0.05) at 16 hours. Overall mortality was 10%. [2]
In a prospective study involving 362 TBI patients, 28 (7.7%) developed ARDS. There were no differences between TBI + ARDS vs TBI alone group with respect to age, sex, ISS, Glasgow coma score (GCS), head, abdomen and extremity AIS. TBI+ARDS group had significantly more patients with chest AIS> or =3 (57.1% versus 32.1%, p=0.03). There was no difference with respect to mortality between TBI+ARDS group (50.0%) and TBI group (51.8%). There were significantly more complications in TBI+ARDS group (42.9%) compared to TBI group (16.1%). TBI+ARDS group had mean ICU length of stay of 15.6 days vs 8.4 days in TBI group. TBI+ARDS group had significantly higher hospital charges than TBI group. [3]
In a retrospective study involving adult patients with TBI and ARDS/ALI from 1988 to 2008, prevalence of ARDS/ALI increased from 2% in 1988 to 22% in 2008. ARDS/ALI-related mortality after TBI decreased from 33% in 1988 to 28% in 2008. Predictors of in-hospital mortality after TBI were older age, male sex, white race, chronic kidney disease, hypertension, chronic liver disease, congestive heart failure, ARDS/ALI, and organ dysfunctions. [4]
Mean ICP increases up to 14.5 ± 7.7 mmHg in response to as little as 10 cm H2O of
PEEP.  [5] Patients with normal pulmonary compliance generally demonstrate no elevation in ICP with increases in PEEP. Patients with normal ventricular compliance and decreased pulmonary compliance normally do not experience great increases in ICP. If patients have both, they are at greater risk for elevated ICP in response to changes in PEEP. Head elevated positioning can reduce the impact of increased PEEP on elevated ICP. [6] In patients with various brain injuries such as stroke, TBI, and intracranial hemorrhage, no direct effect of inverse ratio ventilation was demonstrated on elevations of ICP. [7] There is not much evidence on permissive hypercapnia in neurological injury, but it should be done with monitoring of ICP and CPP if it is likely to help improve lung condition and thereby improve cerebral oxygenation.
In a study to evaluate the influence of positive end-expiratory pressure (PEEP) on ICP and CPP in patients with acute stroke, the authors increased PEEP from 4 to 8 and then to 12 mm Hg. The authors did not observe significant change in the ICP. The observed decreases in CPP as detected by decreased Vm MCA were associated with decreased MAP. They conclude that, PEEP application should be safe, provided that MAP is maintained.  [8]
Sixty of the 133 (45%) patients with severe TBI acquired VAP with incidence density of 42.7/1000 ventilator days. Patients with polytrauma were at higher risk of VAP than those with isolated head injury. VAP was associated with greater degree of non-neurological organ system dysfunction. Although VAP was not associated with increased hospital mortality, patients who developed VAP had a longer duration of mechanical ventilation (15 vs 8 days, p < 0.0001), longer intensive care unit (17 vs 9 days, p < 0.0001) and hospital (60 vs 28 days, p = 0.003) lengths of stay, and more often required tracheostomy (35 vs 18%, p = 0.003) [9]
Stroke-associated pneumonia (SAP) has been implicated in the morbidity, mortality and increased medical cost after acute ischemic stroke. The annual cost of SAP during hospitalization in the United States approaches USD 459 million. The incidences of SAP in the following settings were: NICUs 4.1-56.6%, MICUs 17-50%, stroke units 3.9-44%, mixed studies 3.9-23.8% and rehabilitation 3.2-11%. The pathophysiology of SAP is explained by aspiration combined with stroke-induced immunodepression through complex humeral and neural pathways that include the hypothalamic-pituitary-adrenal axis, parasympathetic and sympathetic systems. [10]
Severe brain damage, such as cerebral and subarachnoid hemorrhage, head injuries and seizures, represents a risk factor for developing NPE. Misdiagnosis and inappropriate management may worsen cerebral damage because of secondary brain injury from hypoxemia or reduced CPP. These factors may increase morbidity and mortality. NPE is characterized by the acute onset of pulmonary edema following a significant central nervous system (CNS) insult. The etiology is thought to be a surge of catecholamines that results in cardiopulmonary dysfunction. The early form of NPE is most common and is characterized by the development of symptoms within minutes to hours following neurologic injury. In contrast, the delayed form develops 12 to 24 hours after the CNS insult. Patient becomes acutely dyspneic, tachypneic, and hypoxic within minutes. Pink, frothy sputum is commonly seen and bilateral crackles and rales are appreciated on auscultation. Sympathetic hyperactivity is common and the patient may be febrile, tachycardic, and hypertensive. Chest radiograph will reveal bilateral hyperdense infiltrates consistent with ARDS. Symptoms often spontaneously resolve within 24 to 48 hours; however, in patients with ongoing brain injury and elevated ICP, the NPE often persists. Diagnostic criteria for this subset of NPE: 1) Bilateral infiltrates; 2) PaO2/FiO2 ratio < 200; 3) no evidence of left atrial hypertension; 4) presence of CNS injury (severe enough to have caused significantly increased ICP); 5) absence of other common causes of ARDS (e.g., aspiration, massive blood transfusion, sepsis). For those patients who meet the above NPE criteria, measurement of serum catecholamines may be helpful. The management is primarily to treat the underlying neurologic condition. [11] Alpha antagonists have shown to be useful in some patients; else, the management remains largely supportive with mechanical ventilation aiming at maintaining oxygenation and elimination of CO2.

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