Neurogenic pulmonary edema

Neurogenic pulmonary edema

The Journal of Emergency Medicine, Vol 11, pp 207-210, 1993 Printed in the USA 0 Neurogenic Pulmonary Edema 0 1993 Pergamon Press Ltd. Examin...

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The Journal

of Emergency


Vol 11, pp 207-210,


Printed in the USA

0 Neurogenic Pulmonary Edema

0 1993 Pergamon

Press Ltd.

Examination of the head, eyes, ears, nose, and throat was largely unremarkable, although the funduscopic examination was deemed unreliable because of lack of cooperation. Pupils were midrange and sluggishly but symmetrically reactive. The neck was supple and there were no carotid bruits. Pulmonary breath sounds were difficult to auscultate because of the loud upper airway sounds; a nasopharyngeal airway was placed and scattered rales were then heard. Cardiac rhythm was regular with an S4 gallop. The abdomen was soft and nontender, and the extremity examination was normal. On neurologic examination, the patient would speak her name when persistently challenged, but otherwise only groaned in response to all stimuli. She periodically abducted both of her upper extremities and held them straight out at the level of her shoulders. There was some shaking of her arms noted, but this appeared more consistent with fatigue than with seizure activity. She would reliably stop this motion and drop her arms to her sides when sternly and loudly commanded to do so. The cranial nerves appeared intact to the limits of her cooperation; there were no gross sensorimotor deficits. Deep tendon reflexes were 2+ and symmetric and Babinski’s reflex was downgoing bilaterally. An intravenous line was established and a rapid bedside check of her serum glucose was 100 mg/dL. Pulse oximetry on 100% oxygen was 87%. There was no response to intravenous naloxone. A trial of intravenous diphenhydramine was given for the possibility of dystonic reaction to the medications given earlier; there was no discernible response. An electrocardiogram revealed left ventricular overload but no acute ischemic changes. A portable chest radiograph (CXR, Figure 1) revealed evidence of pulmonary edema with mild cardiomegaly. She was given 40 mg of furosemide intravenously. Arterial blood gas on 100% oxygen demonstrated pH, 7.28; pOZ, 66 torr; and pCOZ, 55 torr. Other laboratory results were not remarkable. A urine toxicology screen was sent. The patient continued to protect her airway, but was no more responsive after these interventions.

In 1992 we published in this journal four case reports and a review of the syndrome of neurogenic pulmonary edema (NPE) (1). NPE has in the past been associated with diverse etiologies of increased intracranial pressure (ICP), including blunt and penetrating head trauma, intracranial hemorrhage, seizure activity, electroconvulsive therapy, anesthesia induction, and upper airway obstruction. We recently encountered a case that represents a previously unreported etiology - diffuse cerebral hypoxia and edema as a result of drug-induced ventilatory insufficiency.

CASE REPORT A 49-year-old female was brought to the emergency department (ED) by family members who reported she had been unresponsive for 2 hours, since being given “a shot for high blood pressure” in a local physician’s office. They also described intermittent posturing contractions of her upper extremities during the same time period. They did not know what medications she had been given (nor took chronically), but they related that she had a long history of hypertension and frequent severe headaches. Her doctor’s visit earlier that day had been prompted by a headache that the family stated was “no worse than usual.” According to the family, there was no known history of heart disease (other than hypertension), cerebrovascular disease, or pulmonary disease. She had never before had a similar episode of abnormal behavior or movement. Her medications brought by the family included hydrochlorothiazide and cimetidine. Vital signs in the ED were as follows: tympanic temperature, 37.6 OC; pulse, 98 beats/min; respirations, 28 breaths/min; and blood pressure, 1621116 torr. The patient had loud, sonorous upper airway noises, but an intact gag reflex. She responded with groans to persistent, loud verbal stimuli and to pain. = =


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Figure 2. Initial brain CT scan revealing slit-like ventricles and loss of sulcal markings consistent with significantly Increased ICP.

Figure 1. Initial portable chest radiograph in the ED; there is diffuse pulmonary edema and mild cardlomegaly.

After initial difficulty, the treating physician from earlier in the day was contacted and informed us that he had given the patient nalbuphine (Nubaino) and hydroxyzine (Vistarilo) for vascular headache symptoms. Since this information added little to our diagnostic considerations, the patient was taken for an emergency computed tomography (CT) scan of the brain to exclude an acute CNS event. The CT scan revealed diffuse cerebral edema as evidenced by slit-like ventricles (Figure 2) and loss of sulcal markings. There was no evidence of acute hemorrhage or infarct. The etiology of the cerebral edema was unclear, but the consideration that the pulmonary edema was a secondary process representing NPE was entertained. This was at the time felt unlikely, however, because the CXR, which showed cardiomegaly, was more consistent with congestive heart failure than with the noncardiogenic pulmonary edema typically associated with NPE. The patient returned to the ED and was electively nasotracheally intubated so that hyperventilation could be performed in an effort to reduce intracranial pressure. The patient was transferred to the ICU for intensive monitoring and supportive care. She was given diphenylhydantoin to protect against possible seizure activity from her cerebral edema while she was para-

lyzed and being mechanically ventilated. A CXR taken 3 hours after furosemide was given and hyperventilation was initiated revealed remarkable clearing of the lung fields, but no change in cardiomegaly (Figure 3). Twelve hours later, portable electroen-

Figure 3. Portable chest radiograph from ICU, taken 3 hours after furosemide and hyperventilation begun, demonstrating marked clearing of pulmonary edema but unchanged cardiac silhouette.

Letters to the Editor

cephalography was performed that was consistent with hypoxic encephalopathy. At about this time, it was discovered that the dose of nalbuphine given prior to the onset of symptoms was 20 mg, twice the usual maximum dose. She had also received 50 mg of hydroxyzine . Over the next 12 hours, the patient became more alert, was gradually weaned off the ventilator, and was soon extubated. A repeat CT scan on hospital day 3 revealed normal sulcal markings and ventricular architecture (Figure 4). She experienced complete neurologic recovery. A repeat CXR on the day of discharge (Figure 5) revealed a cardiac shadow of essentially identical size to the admission CXR, when there was superimposed pulmonary edema. The patient was discharged with the diagnoses of 1) acute generalized cerebral edema, presumably secondary to ventilatory insufficiency, secondary in turn to nalbuphine overdose, 2) acute NPE, and 3) baseline hypertensive cardiomyopathy.

DISCUSSION There are two forms of NPE: an early form that develops within minutes to hours of the CNS insult, and a delayed syndrome that develops over days (2). This patient appeared to manifest the early form of NPE, with fulminant pulmonary edema developing over the 2 hours between nalbuphine administration and ED presentation. Her hypertension on arrival was also consistent with acute NPE. The atypical CXR initially led us away from the diagnosis of NPE

Figure 5. Baseline chest radiograph, dence of hypertensive cardiomyopathy sation.

demonstrating eviwlthout decompen-

to a dual consideration of CNS insult and acute congestive heart failure, but the patient’s baseline cardiomegaly was responsible for this inconsistency; that it did not resolve supports the diagnosis of NPE. This case also emphasizes that a pure noncardiogenic pulmonary edema pattern need not appear on CXR for the diagnosis to be considered. While this patient’s pulmonary pathology could be explained as a first episode of congestive heart failure, this does not account for her concomitant cerebral edema; the primary neurogenic basis seems more likely. As we discussed in our previous article (l), NPE is best managed by simultaneously treating increased ICP (with diuretics and hyperventilation) and pulmonary edema [with oxygen, diuretics, and mechanical ventilation with positive end-expiratory pressure (PEEP)]. Diphenylhydantoin may be protective in NPE (3); in this patient it was given prophylactically for seizures but may also have contributed to her rapid improvement. CONCLUSION

Figure 4. Repeat brain CT scan (hospital normal ventricles and sulcal markings.

day 3), revealing

Neurogenic pulmonary edema may present in the ED after a variety of CNS insults; to the list of previously documented etiologies, we now add that of diffuse cerebral edema secondary to drug-induced ventila-


The Journal

tory insufficiency. Prompt recognition of NPE (and especially its differentiation from aspiration pneumonia) in the ED is essential to successful management of the CNS, pulmonary, and systemic manifestations of the syndrome. We have previously presented a diagnostic and management algorithm for NPE (I). Charles V. Pollack, Jr., MA, MD* Emily S. Pollack, MD, FAAP~ Departments of *Emergency Medicine and t Pediatrics Maricopa Medical Center Phoenix, Arizona

REFERENCES 1. Pender ES, Pollack CV. Neurogenic pulmonary reports and review. J Emerg Med. 1992;10:45-51. 2. Baigelman W, O’Brien JC. Pulmonary effects of Neurosurgery. 1981;9:729-34. 3. Wohns RNW, Kerstein MD. The role of Dilantin tion of pulmonary edema associated with cerebral Care Med. 1982;10:436-43.

0 Inappropriate Automobiles

edema: case head trauma. in the prevenhypoxia. Crit

Use of Passive Safety Features in

With the rising availability of automobile air bags and other passive restraint systems, it is crucial for health care providers to be aware of injuries that can be caused, either directly or indirectly, by their inappropriate or improper use. In order to disseminate such information, we present the following case report. A 27-year-old male was involved in a motor vehi-

of Emergency


cle accident. He was wearing a lap belt and shoulder harness combination and the car was equipped with an air bag. His car was struck in the left front quarter panel, resulting in deployment of the air bag. The patient stated that the air bag struck him in the face, resulting in hyperextension of his head and neck over the completely lowered head rest. On admission to the emergency department later that day, he complained of pain in the low occipital region and cervical spine. Physical examination was unremarkable except for neck pain with active flexion and extension. His radiographic examination was likewise within normal limits. A diagnosis was made of acute cervical sprain, and the patient was discharged on appropriate therapy. This case points out the need to use all safety features that are built into an automobile appropriately and in proper conjunction with each other. While the air bag functioned flawlessly for this patient, the improper adjustment of the head rest negated, at least in part, the beneficial effects of the air bag. It can be speculated that correct positioning of this head rest might have led to the driver escaping this accident with no injury whatsoever. Every professional providing care in an emergency department setting, we believe, should carefully question patients regarding not only the exact circumstances surrounding the accident, but also the functional condition and correct use of the safety devices installed in the vehicle. This will help us to better evaluate and treat our patients who are victims of motor vehicle accidents. Isaac Dweck, RPA Bernard Beckerman, MD, FACEP Emergency Department Winthrop-University Hospital Mineola, New York