Teaching Case

Young female patient with no significant past medical history presented to the emergency department with asystole.
According to her boyfriend the patient had suffered from severe headache for the last few hours which was not relieved by analgesics. She went to sleep in order to feel better.
The boyfriend awoke to find the patient gasping.

The patient was intubated during resuscitation and portable chest X-ray was performed, which showed endotracheal tube with the distal tip in the right main bronchus.
Bilateral extensive patchy air space opacities with no pleural effusion or pneumothorax.
Based on the patient's history, the findings suggest non-cardiogenic pulmonary oedema.
CT brain correlation was needed.
Findings were conveyed to the referring physician.

Plain CT brain was done immediately and showed a large subarachnoid haemorrhage along with intraparenchymal haematoma in the right basifrontal lobe.
There was also associated interventricular haemorrhage with predominant involvement of both lateral ventricles.
Significant changes of diffuse cerebral oedema were present with effacement of basal cisterns.
No hydrocephalus at present.
No mid-line structures shift.
Bony skull vault was unremarkable.

CT brain angiography was suggested for further and proper evaluation but it was not done due to the patient's condition.

Pulmonary oedema is fluid accumulation in the lung tissue and air spaces which may lead to impaired gas exchange causing respiratory failure. It is differentiated into two types, non-cardiogenic and cardiogenic.
Non-cardiogenic pulmonary oedema (NPE) is caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult. [1]

Distinguishing between non-cardiogenic and cardiogenic causes is difficult, since the clinical symptoms are non-specific. The diagnosis is important, however, because treatment changes considerably depending upon the related cause. [2]

Most patients with non-cardiogenic pulmonary oedema (NPE) are immobile and seriously ill. Chest X-ray is the examination of choice as it is readily, universally available and it has the added advantage of portability. [1]

Neurogenic pulmonary oedema is a rare form of (NPE), which is caused by an increase in pulmonary alveolar and interstitial fluid. It can occur within a few hours of the neurologic insult. Intracranial hypertension is considered an important factor as most common neurological events are associated with high intracranial pressure. [3]

Major causes of neurogenic pulmonary oedema are head injury, cerebral haemorrhage, subarachnoid haemorrhage or epileptic seizures. [3]

Patients most commonly complain of diaphoresis, dyspnoea or orthopnoea. Symptoms are mainly of gradual onset.

Chest X-ray findings of non-cardiogenic pulmonary oedema are:
Bilateral peripheral air space disease with central bat-wing pattern. Normal cardiothoracic ratio. Pleural effusions and Karley B lines are not common. [5]

CT findings:
Ground glass opacifications with air bronchogram and gravity-dependent consolidation are common. [5]
Neurogenic pulmonary oedema usually is generally well tolerated by the patient, although some patients require supportive management.
Mechanical ventilation may be necessary, either non-invasive with a face mask or by an endotracheal tube. The goals of mechanical ventilation are to prevent iatrogenic lung injury and to assure adequate oxygenation. [3]
Diuretics to reduce fluid overload with adequate cerebral perfusion and cardiac output is a reasonable approach. [3]

(NPE) usually resolves within 2-3 days. Prognosis is determined more by the course of the underlying neurological problem rather than by the neurogenic pulmonary oedema, unless significant respiratory complications develop. [3]