A 17-year-old boy traveled with high speed through a dust cloud and had a collision with a truck. According to the first responders he was alert but dazed before he was brought by helicopter to our emergency department. His neurologic examination was completely normal, and he could clearly describe the sequence of events before and after the accident. CT scan of the brain was normal. He was in severe pain in his left leg and was found to have a significantly displaced femoral fracture. He was admitted to the orthopedic ward after undergoing fixation. He asked for opioids frequently to control his pain but remained alert and oriented. Three days after the operation, he suddenly developed respiratory distress and very shortly thereafter he became comatose with irregular breathing. His neurologic examination reveals small reactive pupils, intact corneal reflexes, but extensor motor responses. CT scan of the brain is unchanged, but the X-ray of the chest reveals diffuse infiltrates (“white-out” lungs) (Figure 19.1). He is emergently intubated and transferred to the surgical intensive care unit. You are asked for an opinion on his neurologic examination and whether this represents “neurogenic” pulmonary edema.
FIGURE 19.1 Note displaced femur fracture. (A) Serial chest X-rays in patient example: B) normal on admission and C) diffuse pulmonary edema 12 hours later.
What do you do now?
Acute pulmonary distress in a patient after significant trauma has multiple causes. In the acute setting, several disorders should be considered, and they include pulmonary contusion, aspiration pneumonitis, and the much less common neurogenic pulmonary edema. Pulmonary emboli are usually seen after a considerable time interval, but they may occur after only a few days of immobilization in predisposed patients. In these patients X-ray is normal but there is a significant hypoxemia not improving with incremental oxygen administration (refractory A-a gradient) because of a large ventilation-perfusion mismatch. A pulmonary embolus should always be considered after neurosurgical procedures, prolonged bed rest, and in patients with hemiplegia in whom the paralyzed leg is particularly at risk of developing deep venous thrombosis. Helical CT angiogram of the chest has become the standard diagnostic test. Acute respiratory distress in a mechanically ventilated patient may have multiple other causes, including acute main bronchus obstruction, inappropriate ventilator settings, pneumothorax, atelectasis, or dislodgement of the tracheostomy tube.
Flash pulmonary edema in a patient with an acute traumatic brain injury is another concerning situation that immediately will lead to intubation and need for high positive end expiratory pressures (PEEP) to open up the collapsed and filled alveoli. The effects of high PEEP on intracranial pressure need to be carefully monitored in patients with head trauma. In hemodynamically unstable patients, high PEEP may reduce cardiac venous return and lead to worsening hypotension. Flash pulmonary edema is usually a result of increased sympathetic activation due to an acute medulla oblongata lesion or due to a rapidly increased intracranial pressure. Pulmonary arterial constriction leads to shunting to other areas that cannot handle pressure, resulting in capillary leak and edema. It can also be seen as a secondary phenomenon of severe stress-induced cardiomyopathy (takotsubo cardiomyopathy). In these patients, there is significant apical ballooning from a major sympathetic outburst associated with acute brain injury, in turn resulting in severe pulmonary edema. Vasodilators and diuretics may be used to relieve pulmonary congestion and reduce ventricular preload. A stress induced cardiomyopathy requires specific treatment to improve ventricular contractility. Fortunately, surviving patients recover quite quickly with a good prognosis.
On paper, this case can be recognized as a classic presentation of fat embolism syndrome. Acute coma and respiratory distress in a patient with a recent femur fracture are sufficient clues to arrive at the diagnosis. In practice, this entity is not always so easily recognized, and reports are infrequently published. Furthermore, the diagnosis is difficult to prove; the “textbook” truncal and axillary petechiae may disappear quickly, fat in bronchial secretions suctioned out by bronchoscopy and fat globules in urine may not be found. (Identification of fat globules requires a special stain such as Sudan red, which is often not readily available.)
Fat embolization syndrome is rare but can be recognized usually about 48 hours after trauma. The treatment of fat embolization syndrome remains supportive and requires hemodynamic stabilization and adequate oxygenation and ventilation with PEEP. Oxygenation goal should be at least an arterial PO2 more than 60 mmHg. Ventilation should maintain plateau pressure less than 30 cm of water and low tidal volumes (6 ml/kg of ideal body weight) to prevent volutrauma.
Fat emboli to the brain may be a cause of sudden neurologic deterioration from injury to the gray and white matter, which may be severe enough to produce coma. Patients may remain comatose for weeks but then may slowly awaken and go on to recover. MRI abnormalities can be particularly severe with numerous lesions reminiscent of a “star field,” and often this has been incorrectly interpreted as an indicator of poor outcome.
Our patient recovered very well with supportive care, and the MRI findings disappeared. This case also taught us that fat emboli to the brain resulting in coma (even with motor extensor responses and episodes of paroxysmal hyperactivity) may have a good outcome against all odds.
All these conditions are not common and we should expect more mundaine causes in a trauma patient who develops sudden respiratory distress. Most patients with decreased level of consciousness cannot handle oral secretions, and a weak cough with pooling will lead to bronchial obstruction. Intubation is needed and bronchoscopy will be most helpful in these cases. Neurogenic pulmonary edema is just as rare as fat embolization syndrome. More likely, patients either develop an aspiration pneumonitis evolving into ARDS or have pulmonary emboli. Both conditions have quite distinctive features that can be distinguished on chest X-ray and CT of the chest. Treatments are specific to those disorders. The differences between pulmonary complications in acute brain injury are shown in Table 19.1.
TABLE 19.1 Acute Pulmonary Conditions after Brain Injury
SAH, subarachnoid hemorrhage; PEEP, positive end expiratory pressure; IVC, inferior vena cava.
KEY POINTS TO REMEMBER REGARDING ACUTE PULMONARY EDEMA AFTER MAJOR TRAUMA
· Acute pulmonary edema after trauma may be due to cardiogenic or neurogenic pulmonary edema, but the pure forms are infrequent. Aspiration is more common, particularly after a seizure, vomiting, and difficult intubation.
· Clinical suspicion of acute pulmonary emboli is based on sudden oxygen desaturation with increased A-a gradient, but normal X-chest.
· Consider fat emboli in a patient with a recent major long bone fracture who develops sudden respiratory failure and neurological decline.
· Treatment may include broad spectrum antibiotics (suspected aspiration), high PEEP (flash pulmonary edema), and repeated bronchoscopy.
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