Flash pulmonary oedema following arteriovenous fistula surgery: rapid assessment and treatment is key to break the vicious cycle

Background

Flash pulmonary oedema (FPE) is a life-threatening clinical condition that causes acute respiratory distress. It is characterised by the development of acute dyspnoea due to the rapid accumulation of fluid in the interstitial and alveolar spaces of the lungs. FPE is a common term used to describe the dramatic form of acute decompensated heart failure.1 The prevalence of heart failure is around 40% in patients with chronic kidney disease.2 FPE can occur in any condition that disrupts pulmonary fluid homeostasis, for example, excessive activation of the renin–angiotensin system.3

In the literature, there are many cases of FPE caused by a variety of reasons, but to our knowledge, this is the first case of FPE that occurred immediately following the creation of an arteriovenous fistula (AVF) in a patient with prior heart disease. This study emphasises the importance of a multidisciplinary team (MDT) approach instituted immediately to break the vicious cycle of hypertensive crisis, myocardial dysfunction and impending ventilatory failure.

Case presentation

An early adolescent boy with a known case of end-stage kidney disease had been on haemodialysis (HD) for 4 months and was referred to the surgery clinic for the creation of an AVF. His medical history revealed that he was taking medicines for hypertension, dilated cardiomyopathy with systolic dysfunction and extrapulmonary tuberculosis. He has been undergoing maintenance HD through the right internal jugular vein catheter since 4 months. Prior to the surgery, the patient’s haemoglobin was 85 g/L, whole blood cell count was 8.7×10⁹/L and platelets were 230×10⁹ /L. His blood urea was 108 g/dL, and his serum creatinine was 8 g/dL, his serum sodium was 146 mmol/L and his potassium was 5 mmol/L. The patients’ ECG showed a strain pattern with left ventricular hypertrophy. His echocardiogram showed dilated cardiomyopathy, left ventricular hypertrophy, an ejection fraction of 30% and moderate systolic dysfunction. His chest X-ray showed minimal pleural effusion on the right side. He had undergone HD 2 days prior to vascular access surgery. His preoperative haemodynamics showed a heart rate of 88 beats per minute; blood pressure was 140/80 mm Hg; respiratory rate was 18 breaths per minute and saturation was 99% on room air. The left Brachio-Cephalic AVF was performed under local anaesthesia and was completed in 55 min. The patient was stable throughout the procedure, and the AVF was functioning with a good thrill after declamping the vessels. About 10 min after completing the procedure, the patient began having cough and dyspnoea in the supine position. His heart rate was 110 bpm, blood pressure was 188/96 mm Hg, respiratory rate was 24; Spo2 was 93% on room air and 99% on face mask 4 L/min. Immediately, a team of intensivists and nephrologists were informed. About 20 min following surgery, the patient had progressive desaturation from Spo2 of 99% on 4 L/m oxygen to 88% on 10 L/min oxygen in the postsurgery recovery room. His haemodynamic parameters at the end of 60 min following surgery showed a heart rate of 122 beats per minute, blood pressure of 220/136 mm Hg, a respiratory rate of 40 breaths/min and Spo2: 88% on 15 L/min oxygen by non-rebreathing mask (NRBM). On auscultation, the patient had crepitation on bilateral chest examination. A provisional diagnosis of acute PE with accelerated hypertension was made.

Investigations

Arterial blood gas analysis showed respiratory acidosis (figure 1), and his Chest X-ray showed massive PE in bilateral lung fields (figure 2). His ECG showed strain pattern with left ventricular hypertrophy, no ST elevation (figure 3).

Differential diagnosis

Sudden fall of saturation made us keep acute myocardial infarction and pulmonary embolism as differentials. But on evaluating further no ST changes were seen on ECG. Cardiac markers troponin I and T were normal. Bedside echocardiogram was also done which revealed no embolus.

Treatment

An MDT approach was used, and management included ongoing assessment and treatment to maintain airway, breathing, circulation, neurological disability and hypothermia prevention. Initially, the patient was put on a non-invasive ventilator (NIV) machine as he was not maintaining saturation on NRBM (oxygen flow rate of 15 L/min). He was administered injection esmolol 4 mg, injection lasix 40 mg and injection diltiazem 10 mg to normalise his blood pressure. His haemodynamic parameters at the end of one and a half hours were: heart rate of 118 bpm; blood pressure was 180/96 mm Hg; respiratory rate was 35 breaths per minute and saturation was 93% on NIV. Subsequently, injection nitroglycerin 50 mg/10 mL 1 mL/hour was started. As the patient began desaturating on NIV at the end of 2 hours, he was put on a mechanical ventilator. Subsequently, the patient was put on HD and 2 L of ultrafiltrate fluid was drained. The patient was kept on a ventilator for 1 day and was extubated on postoperative day 2. He was stable on room air, maintaining 93% saturation, PR: 80; RR: 18; BP: 126/78. PE resolved on chest X-ray on postoperative day 4. (figure 4)

Outcome and follow-up

The patient was discharged the day following admission (figure 5). He was advised to have HD three times a week and to have a regular check-up. He was followed up 6 months later. He is doing well, undergoing HD through the same AV fistula. He also got registered for renal transplant and is waiting for suitable donor.