Rohat Ak et al.
BOĞAZİÇİ TIP DERGİSİ; 2017; 4 (1): 35-36 doi: 10.15659/bogazicitip.17.02.663
Case Report
Acute Dyspnea After Subarachnoid Hemorrhage:
Is It Neurogenic Pulmonary Edema?
Subaraknoid Kanama Sonrası Akut Dispne: Bu Nörojenik Akciğer Ödemi mi?
Fatih DOĞANAY 1, Rohat AK 1, Tevfik PATAN
1
1. University of Health Sciences, Fatih Sultan Mehmet Training and Research Hospital, Emergency Medicine Clinic
ABSTRACT
INTRODUCTION
Neurogenic pulmonary edema (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. NPE is
defined as an increase in pulmonary interstitial and
alveolar fluid caused by an acute central nervous
system injury. Pulmonary edema in patients with
subarachnoid hemorrhage (SAH) has been associated with high-grade SAH, increased mortality.
Early infiltrates, which treated effectively, did not
affect mortality, mostly . In this case report, we aimed to present a patient who developed NPE due to
SAH in the emergency department.
Neurogenic pulmonary edema (NPE) is
defined as an increase in pulmonary interstitial and alveolar fluid caused by an acute central
nervous system injury (1). It has been reported in patients with subarachnoid hemorrhage
(SAH), traumatic brain injury, intracerebral
hemorrhage, status epilepticus, meningitis, spinal cord injury, intracranial tumors, ischemic
stroke and multiple sclerosis (2). But still NPE
is underdiagnosed after serebrovascular accidents although it may course mortally if it is
not treated early. We presented a patient who
developed NPE in emergency department due
to SAH and we revealed the presentation and
diagnosis for ED doctors in this case report.
Keywords: neurogenic pulmonary edema; subarachnoid hemorrhage; dsypnea
ÖZET
Nörojenik pulmoner ödem (NPE), uygun ortamda pulmoner ödem oluşumuna ve daha olası
bir alternatif neden bulunmadığına dayalı klinik bir
tanıdır. NPE akut merkezi sinir sistemi hasarının
yol açtığı pulmoner interstisyel ve alveoler sıvıda
bir artış olarak tanımlanır. Subaraknoid kanamalı
(SAK) hastalarda pulmoner ödem, yüksek dereceli
SAK ile ilişkili olup mortaliteyi arttırmaktadır. Etkili bir şekilde tedavi edilen erken infiltratlar çoğunlukla mortaliteyi etkilemez. Bu olgu sunumunda
acil serviste SAK nedeniyle NPE gelişen bir hastayı
sunmayı amaçladık.
Anahtar Kelimeler: nörojenik pulmoner ödem; subaraknoid kanama; dispne
Contact
Corresponding Author: Rohat AK
Address: Istanbul Fatih Sultan Mehmet Training and Research Hospital, Icerenkoy, 34752 Atasehir, Istanbul, Turkiye
Phone Number: +90 (506) 821 31 36
E-mail: [email protected]
Submitted: 03.01.2017
Accepted: 04.01.2017
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CASE
A 82-year-old man presented to emergency department (ED) with fatigue and headache. His symptoms began about 5 hours ago.
On initial presentation, his Glascow Coma Scale (GCS) was 15; blood pressure was 170/90
mmHg, pulse rate was 78 bpm, oxygen saturation 98%, body temperature was 36,4°C.
His physical and neurological examination
revealed no pathology including normal breath sounds. His electrocardiography and his
laboratory results were normal, too. He was
sent to computed tomography (CT) of brain
for intracranial hemorrhage because of having
the worst headache in his life. His CT scan in
the emergency department revealed diffuse subarachnoid hemorrhage (Figure 1). During his
wait in angiography, after an hour in his followups, suddenly he had dyspnea. In his repeated
physical examination, bibasillary crepitant rales were developed in his lung auscultation. His
vital signs were as his presentation except oxygen saturation measured 88% and respiratory
rate was 32/min. He had oxygen therapy, he
was sent to CT for scaning thorax. Thorax CT
revealed bilateral pulmonary edema (Figure 2).
Half an hour later, his GCS score regressed to
8 in spite of supportive therapy. After endotracheal intubation, the patient was sent to intensive care unit for further therapy and follow-up.
Rohat Ak et al.
BOĞAZİÇİ TIP DERGİSİ; 2017; 4 (1): 35-36
Figure 1: Brain CT scan of subarachnoid hemor- Figure 2: Thorax CT scan of pulmonary edema.
rhage.
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<300
mm Hg simultaneously (7). Definitive diagnosis is hard because diagnostic tests are nonspecific. The clinical diagnosis is based upon the
occurrence of pulmonary edema, neurological
pathology and absence of a more likely alternative diagnosis (6). The clinical findings of NPE
may be confused with aspiration pneumonitis,
ARDS. NPE tends to develop more rapidly
than aspiration pneumonia. The mortality rate
is high, but surviving patients usually recover
very quickly.
CONCLUSION
Pulmonary edema in patients with SAH
has been associated with high-grade SAH, increased mortality. Early infiltrates, which treated
effectively, did not affect mortality, mostly (8).
Optimal oxygenation and avoidance of hypoxia
are essential. So early recognition by ED doctors and appropriate treatment are necessary to
decrease mortality.
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