Boğaziçi Tıp Dergisi

Rohat Ak et al.
BOĞAZİÇİ TIP DERGİSİ; 2017; 4 (1): 35-36
Figure 1: Brain CT scan of subarachnoid hemorrhage.
DISCUSSION
NPE is a clinical diagnosis based upon the
occurrence of pulmonary edema in the appropriate
setting and in the absence of a more
likely alternative cause (3). In our patient sudden
dyspnea and hypoxia developed after 6
hours of SAH symptoms. The lack of diagnostic
markers for special etiologies contributes
to poor recognition and diagnosis wordwide.
The reported prevalences for NPE after SAH
are changing between 10%-40% (4). This range
may be minimized by more recognition of
ED doctors. The pathophysiologic mechanisms
are thought to be pulmonary capillary pressure
increase by transient pulmonary vasoconstriction
after cerebrovascular accident, and/or in
the pulmonary capillary bed, increased permeability
reproduced by inflammatory mediators.
In addition contributions of the hypothalamus,
elevated intracranial pressure, and activation of
the sympathoadrenal system may play role (5).
In emergency departments, physicians should
be alert of clinical presentation consisting of
signs of oxygenation failure, such as dyspnea,
tachypnea, tachycardia, cyanosis, pink frothy
sputum, and crackles and rales on auscultation
in patients with SAH (6). NPE must be kept
in mind if bilateral, symmetric, smooth and
diffuse, alveolar edema-like infiltrates were
present in the chest radiography or thorax CT
and PaO2/fraction of inspired oxygen is