Sympathetic Crashing Acute Pulmonary Edema in a Postoperative Case of Pituitary Macroadenoma

Abstract

We present a case of 58-year-old male operated for pituitary macroadenoma. On the 7th postoperative day, the patient developed sudden-onset breathlessness and desaturation needing ventilatory support. His cardiac function, which was normal preoperatively, deteriorated (ejection fraction 20%) but cardiac enzyme levels were normal. Chest X-ray was suggestive of pulmonary edema. His condition stabilized with the use of noninvasive mechanical ventilation, high-dose nitroglycerine (NTG) infusion, and furosemide over the next 12 hours. Cardiac functions improved to baseline after about a week.

Sympathetic crashing acute pulmonary edema is life-threatening entity and needs urgent intervention. It should be differentiated from cardiogenic or neurogenic pulmonary edema because treatment involves rapid lowering of blood pressure with the use of high-dose systemic vasodilators like NTG. On initial assessment, clinical condition may be confused with acute decompensated heart failure due to myocardial infarction.

 

MissingLinkText

Keywords

nitroglycerine - pituitary macroadenoma - sympathetic crashing acute pulmonary edema

We had a 58-year-old male patient from Nigeria admitted with complaints of excessive sleepiness, difficulty in walking, and no vision in right eye for 2 to 3 years. Preoperatively, Glasgow Coma Scale score was E3V4M6, drowsy but arousable. He was a diagnosed case of nonfunctional pituitary macroadenoma with diabetes and hypertension for past 10 years on Tab. Metformin 1,000 mg once daily and Tab. Lisinopril 10 mg once daily. Preoperative thyroid function tests, cortisol, and prolactin were normal. Two-dimensional (2D) echo was normal with a left ventricle ejection fraction (EF) of 60% with normal pulmonary artery systolic pressure (PASP) and no regional wall motion abnormalities. Bilateral lower limb venous doppler was negative for any evidence of deep vein thrombosis. Ophthalmological examination showed right eye perception of light as negative and left eye perception of light as positive. He underwent craniotomy and excision of tumor. The intraoperative period was uneventful. However, due to the size of tumor and prolonged surgical duration, the patient was shifted to neuro intensive care unit (ICU) on ventilator for elective postoperative ventilation and sedation. He was extubated on POD-2 and was shifted to room by the 3rd day. The patient's sensorium improved during the postoperative period. On the 6th postoperative day, his Foley catheter was removed as the patient seemed better oriented and responsive.

On the 7th postoperative day, the patient was shifted from ward to ICU with complaints of sudden-onset breathlessness, desaturation, and restlessness. Before this, the patient was observed to be stable and communicating well 2 hours ago by the floor duty doctor. On receiving the patient in the ICU, the patient was found to be tachycardic (heart rate ≈ 170/min), with high blood pressure of 220/110 mm Hg, tachypneic with respiratory rate >40/min, and oxygen saturation maintaining at ≈90% with oxygen supplementation via a face mask at 8 L/min with abdominal distension. He was conscious, obeying commands but restless. His wife gave history that patient was complaining of urinary retention and had not passed urine since the last 6 hours leading to abdominal distension and discomfort. The patient was immediately catheterized but urine output was ≈200 mL. Arterial blood gas was suggestive of severe hypoxia with pH = 7.382, pCO₂ = 30.5 mm Hg, pO₂ = 41.7 mm Hg, HCO₃ = 17.7 mmol/L, Na = 140 mmol/L, K = 4.17 mmol/L, Cl = 110 mmol/L, Glu = 347 mg/dL, and Lac = 4.83 mmol/L at 10 L/min on nonrebreathing facemask. Intubation consent was taken but as the patient was conscious, a trial of noninvasive ventilation (NIV) was given. 2D echo was suggestive of severe left ventricular dysfunction EF of 15 to 20% with global hypokinesia; PASP = 54 mm Hg with moderate tricuspid regurgitation. Inferior vena cava (IVC) was dilated and noncollapsing. Chest X-ray (CXR) was suggestive of flash pulmonary edema ([Fig. 1]). Cardiology reference was done and differentials included an acute cardiac event, likely myocardial infarction leading to pulmonary edema or pulmonary embolism. The patient was started on nitroglycerine (NTG) infusion (≈ 200 mcg/min) and fluid status was adequate as evidenced by full IVC on 2D echo, so Inj. Lasix 40 mg IV (intravenous), Inj. Fentanyl 50 mcg IV, and Inj. Hydrocortisone 200 mg IV was given. Since his previous blood sugar levels were normal, we gave hydrocortisone for the management of pulmonary edema. D-dimer = 2.510 µg/mL and NT-proBNP = 9,087 pg/mL were elevated. Bilateral lower limb venous Doppler was done, which was negative for deep vein thrombosis.

Fig. 1 Chest X-ray on Day 1 of pulmonary edema.

Computed tomography pulmonary angiography was done but came out to be negative for pulmonary embolism ([Fig. 2]). It was suggestive of bilateral mild pleural effusion with underlying atelectasis and perihilar consolidation and interstitial septal thickening with ground glass opacity in bilateral lung fields. Ultrasonography of the whole abdomen was suggestive of grade 1 fatty liver. Cardiac enzymes—i.e. CPK, CPK-MB, and Trop T—were sent and three samples were repeated at 6-hour intervals but were normal. The patient was started on Inj. Enoxaparin 60 mg twice daily and Tab. Ecosprin 75 mg once daily. The patient's vitals and clinical condition improved with NIV over a period of 12 to 24 hours. The patient was kept on Inj. Furosemide infusion (5 mg/h) for 1 day and targeted negative balance for the next 3 days. Procalcitonin done to rule out any underlying infection was also near normal with a value of 0.5 ng/mL.

Fig. 2 Coronal cut of CT chest with pulmonary angiography. CT, computed tomography.

His saturation improved over a period of 3 days and the bilevel positive airway pressure (BiPAP) duration was decreased to 6 h/day. CXR also improved ([Fig. 3]). His NTProBNP came to 1,517 pg/mL by the 4th day of event. His cardiac function improved to EF of 25 to 30% by the 3rd day and coronary angiography done on Day 4 was suggestive of right coronary artery blockage of 70% and left anterior descending artery blockage of 30%, for which no cardiac intervention was advised.

Fig. 3 Chest X-ray on Day 3 (improved).

By the 7th day of event (14th postoperative day), the patient was maintaining well on room air and 2D echo was suggestive of improvement of EF to 40% with mild global hypokinesia and normal pulmonary artery pressure. The patient was discharged on 15th postoperative day on Tab. Torsemide 10 mg once daily and Tab. Ecosprin 75 mg once daily.

Discussion

Acute heart failure due to the SCAPE (sympathetic crashing acute pulmonary edema) phenomenon is a life-threatening emergency.[1] SCAPE develops over minutes and hours and is associated with severe sympathetic response such as hypertension and tachycardia. Bedside 2D echo done at the time of insult may be normal suggesting that underlying presentation is worsening diastolic failure.[2] Cardiac enzyme markers may be elevated. In our case, however, EF was severely reduced but cardiac markers were not elevated and coronary angiography was not suggestive of any significant obstruction of coronary arteries. Treatment of hypertensive cardiac failure with pulmonary edema is high-dose nitrates and mechanical ventilation.[3] The role of diuretics and opioids is not clear but they are used commonly to treat the hypertensive crisis; in our case, we gave diuretics suspecting fluid overload to be the cause of pulmonary edema. In our case, transient systolic dysfunction was due to hypertension. EF depends on the afterload, which is increased in the case of sympathetic hyperactivity. Literature mentions case reports of SCAPE with preserved EF, but our case shows that in extreme cases, EF may get hampered.

A probable labile sympathetic system and hypothalamic–pituitary–adrenal axis post-pituitary surgery along with emotional stress (language barrier and urinary retention) may have led to the SCAPE phenomenon in this patient.

Treatment of pulmonary edema involves application of NIV (BiPAP or continuous positive airway pressure).[1] [4] This helps improve oxygenation and gas exchange, decreases further flooding of the alveoli, and improves cardiac output and work of breathing. Early application of NIV may prevent intubation and mechanical ventilation.

Nitrates are important to decrease the preload and improve cardiac workload. Boluses of NTG are given initially followed by infusion to decrease blood pressure. Care should be taken to avoid hypotension, which can happen in volume-depleted patients. A high infusion rate up to 200–800 mcg/min may be needed.[5] Lower doses of NTG are only venodilatory but to reduce the effect of congestive heart failure, higher doses are needed to bring about both venous and arteriolar dilatation to reduce blood pressure.

Role of opioids in the treatment of SCAPE is controversial. Opioids can cause respiratory depression and sedation; therefore, they may cause respiratory worsening. Their role has been shown to be beneficial in the case of pulmonary edema due to acute myocardial infarction as it decreases the pain due to myocardial ischemia and decreases anxiety and preload. The role of diuretics is also controversial as patients of pulmonary edema due to SCAPE are usually hypovolemic or euvolemic. Diuretics may be useful if the patient has coexistent low EF on 2D echo as in our case as this helps to keep the patient euvolemic.

 

MissingLinkText

Conclusion

The SCAPE phenomenon is a life-threatening event. Prompt active diagnosis and intervention is necessary. Decreasing afterload by giving high-dose nitrates is main line of treatment. Diuretics may be beneficial if there is concomitant low EF. Early application of NIV may prevent intubation. Opioids are not advisable as they may alter sensorium of patient.

 

MissingLinkText

 

MissingLinkText

Conflict of Interest

None declared.

• References

• 1 Agrawal N, Kumar A, Aggarwal P, Jamshed N. Sympathetic crashing acute pulmonary edema. Indian J Crit Care Med 2016; 20 (12) 719-723
• 2 Gandhi SK, Powers JC, Nomeir AM. et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001; 344 (01) 17-22
• 3 Hsieh YT, Lee TY, Kao JS, Hsu HL, Chong CF. Treating acute hypertensive cardiogenic pulmonary edema with high-dose nitroglycerin. Turk J Emerg Med 2018; 18 (01) 34-36
• 4 Howlett JG. Current treatment options for early management in acute decompensated heart failure. Can J Cardiol 2008; 24 (Suppl B): 9B-14B
• 5 Stemple K, DeWitt KM, Porter BA, Sheeser M, Blohm E, Bisanzo M. High-dose nitroglycerin infusion for the management of sympathetic crashing acute pulmonary edema (SCAPE): a case series. Am J Emerg Med 2021; 44: 262-266

Publikationsverlauf

Artikel online veröffentlicht:
22. August 2025