A 73-year-old man presented to the emergency department with sudden epigastric and bilateral flank pain after vomiting. Pain and paresthesia worsened rapidly in the lower trunk and both legs within an hour of arrival.
The patient had a history of extensive peripheral vascular disease, having had a left iliac artery thrombectomy with a femoro-femoral crossover graft 2 years previously. He was being investigated for a paraaortic mass; CT abdomen demonstrated a large mass left of the aorta blending with the underlying psoas and disturbing the aortic outline on the left. The diagnostic possibilities included sealed aortic leak following a local dissection, thrombosed saccular aneurysm, a metastatic mass, or lymphoma. A CT-guided biopsy showed necrotic tissue only. He was on aspirin 100 mg daily and smoked heavily.
The patient was distressed by pain with a pulse of 140/min, blood pressure 172/136 mmHg, SaO2 100% on 8 l/min of oxygen, and temperature of 35°C. The abdomen was diffusely tender, guarded, and rigid. The lower abdomen and both lower limbs felt pale and cold. Femoral, popliteal, posterior tibial, and dorsalis pedis pulses were absent including for Doppler signal. He had symmetrical lower limb complete paresis with areflexia. The lower limb muscle compartments were not firm or tender, and active extension of the knee and ankle did not exacerbate pain.
The first EKG showed broad complex sinus tachycardia. The patient then developed monomorphic VT without altered consciousness level, for which he received IV 50 mg lidocaine followed by 300 mg amiodarone over 1 h. This resulted in reversion to sinus tachycardia at 145/min.
Initial serum urea and electrolytes showed no acidemia or hyperkalaemia: [K+] 4.0 mmol/l (3.2-4.5 mmol/l), [Na+] 143 mmol/l (135-145mmol/l), and [bicarbonate] 20 mmol/l (22-33 mmol/l). There was a mild coagulopathy-activated partial thromboplastin time of 41.1 s (22-35 s), prothrombin time of 18.8 s (11-16 s), and fibrinogen of 0.9 g/l (1.5-4 g/l). Urinalysis showed no haemoglobinuria suggestive of myoglobinuria.
His presentation suggested ruptured abdominal aortic aneurysm, and an urgent bedside abdominal USS was arranged. This showed a large non-aneurysmal upper abdominal mass related to the aorta. The abdominal aorta could not be identified below the mass, suggesting distal arterial insufficiency at a high level. CT abdomen with intravenous contrast was then performed, demonstrating a solid mass lying to the left of the aorta (Figure 1). Contrast was seen extending to the level of the mass but not below. Arterial phase perfusion of both kidneys was reduced.
ED management included parenteral narcotic analgesia, IV heparin infusion, and IV fluid resuscitation. A bypass procedure to re-establish perfusion was decided upon. The patient underwent axillo-femoral bypass over 90 min. Hypotension (systolic blood pressure <100 mmHg) throughout the intraoperative period did not respond to a noradrenaline infusion.
The first intraoperative arterial blood gas (ABG) was performed close to establishing bypass re-perfusion: pH 7.13 (7.35-7.45), pCO2 51 mmHg (35-45 mmHg), [bicarbonate] 16 mmol/l (22-27 mmol/l), pO2 165 mmHg (70-100 mmHg), [Na+] 140 mmol/l, and [K+] 4.7 mmol/l. Immediate postoperative ABG showed worsening acidemia and hyperkalaemia (pH 7.025, pCO2 49.6 mmHg, pO2 95.5 mmHg, [bicarbonate] 12.3 mmol/l, [Na+] 143 mmol/l, and [K+] 6.7 mmol/l), which was treated with 10 mmol intravenous calcium chloride.
Soon thereafter, the patient suffered a ventricular fibrillation and subsequent asystolic arrest, which did not respond to advanced cardiac life support measures, an IV 50 ml 50% dextrose with 10 units of insulin, and an adrenaline infusion. A third ABG at mid-resuscitation attempt showed non-life-compatible deterioration in acid-base and potassium status pH 6.959, pCO2 37.1 mmHg, pO2 80.1 mmHg, [bicarbonate] 7.9 mmol/L, [Na+] 137 mmol/l, and [K+] 9.8 mmol/l (not hemolyzed). The time series of perioperative deterioration is demonstrated in Figure 2.