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Vasopressin for the treatment of catecholamine-resistant hypotension during a phaeochromocytoma resection in a 6-year-old child

Thillaivasan, Ayngara; Arul, G Suren; Thies, Karl-Christian

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European Journal of Anaesthesiology: November 2010 - Volume 27 - Issue 11 - p 991-992
doi: 10.1097/EJA.0b013e32833ade4f


There are multiple reports of the use of vasopressin with phaeochromocytoma resections in adults. Support for vasopressin in the paediatric patient, however, is not quite as substantiated. We report such a case to add to the limited evidence for its use in a young child.

Case report

A 6-year-old boy, weighing 21 kg, was admitted to a local District General Hospital with severe headaches not responding to simple analgesics. His initial blood pressure was recorded as 166/91 mmHg. This was persistently elevated and, subsequently, he developed vomiting, photophobia and bilateral papilloedema. He was referred to our institution for further investigation and treatment. Tests showed raised urinary levels of catecholamine metabolites over 24 h and a subsequent computed tomography (CT) scan confirmed a left-sided adrenal phaeochromocytoma. He was started on gradually increasing doses of phenoxybenzamine and atenolol, and a laparoscopic adrenalectomy was planned for within 6 weeks. In the meantime, his blood pressure was controlled with phenoxybenzamine, 20 mg twice daily, and atenolol, 30 mg once daily. Cardiac workup included electrocardiography and echocardiography, which were both normal.


The boy was admitted to our hospital 48 h before surgery when he was noted to have an increased BP of 140/80 mmHg. In addition to the phenoxybenzamine and atenolol, he was started on hydralazine 10 mg three times daily; all three of which were continued until the morning of surgery. As a premedication, he was given midazolam (0.5 mg kg−1 orally) 30 min prior to coming to theatre. The BP before induction of anaesthesia was 105/68 mmHg.

Induction of anaesthesia

Anaesthesia was induced with intravenous propofol (4 mg kg−1) and fentanyl (slowly titrated up to 5 μg kg−1), and he was paralysed with rocuronium (1 mg kg−1). After endotracheal intubation, large bore peripheral intravenous catheters, an arterial line, a central venous line and an epidural catheter (L1/2) were inserted. The epidural was dosed with 10 ml of 0.25% ropivacaine over a period of 30 min. The patient remained normotensive with blood pressure readings around 100/50 mmHg. Anaesthesia was maintained with oxygen, air and isoflurane.

Operative procedure

The operation was performed in the right lateral position via a laparoscopic retroperitoneal route, using three 5 mm operative ports and gas insufflation with CO2. The ventilation was adjusted to maintain normocapnia throughout. Dissection of the adrenal gland was kept to an absolute minimum until its blood vessels were identified. It was clear that any contact with the adrenal gland did cause major spikes in blood pressure. As soon as these vessels were clearly identified, the adrenal vein was double clipped and divided, the remaining vessels were then divided. The adrenal gland was removed intact with no damage to the surrounding structures, and there was no significant bleeding or breach of the peritoneum.

During the operation, sodium chloride 0.9% was infused at a rate of 10 ml kg−1 h−1 for maintenance. The blood pressure rises during tumour manipulation peaked at around 170 mmHg systolic and were controlled with intravenous sodium nitroprusside and colloid boluses of gelofusine. Central venous pressure (CVP) was maintained around 10 mmHg. Urine output during the operation remained around 1.5 ml kg−1 h−1. After dissection of the tumour and ligation of its venous drainage, the blood pressure dropped to 50/35 mmHg, which did not respond to a fluid bolus of 20 ml kg−1 of gelofusine. Two boluses of noradrenaline (5 and 20 μg) also failed to produce any effect. A vasopressin infusion was started at a rate of 0.02 units kg−1 h−1 and gradually increased to 0.24 units kg−1 h−1 within the following 10 min, which stabilized the blood pressure immediately.

After conclusion of the operation, ketamine (0.5 mg kg−1) was administered epidurally before the catheter was removed.


The patient was admitted to the paediatric intensive care unit (PICU) at 14:00 h and his vasopressin infusion was weaned off at 23:00 h. Subsequently, his blood pressure dropped to a systolic of 69 mmHg with an elevated heart rate of 150 bpm. A fluid bolus of 20 ml kg−1 of gelofusine was administered, but had no response. The vasopressin infusion was, therefore, recommenced at a rate of 0.1 units kg−1 h−1, which corrected the haemodynamics. It was eventually weaned off over the next 12 h. Throughout, the serum lactate concentrations remained within normal limits; however, the serum sodium dropped to 131 mmol l−1 and so his maintenance fluid of sodium chloride 0.45% and glucose 5% was restricted to 36 ml h−1. His serum sodium normalized within the next few hours without any further measures, and he was transferred to the ward 36 h after admission to the intensive care area. He was discharged home on day 6.


Haemodynamic instability is a common occurrence during resection of a phaeochromocytoma. Tumour manipulation during dissection can lead to surges of circulating catecholamines and episodic hypertension, followed by a decrease in the secretion of vasoactive substances and hypotension after tumour ligation. Furthermore, any blood loss experienced during the procedure will compound any efforts for haemodynamic control.

The use of vasopressin for the perioperative management of a phaeochromocytoma resection is not a new discovery; there are case reports in the literature describing its use in adult cases. Our case report adds to the only other case described in the paediatric population.1

It is now standard practice to preoperatively achieve blood pressure control for patients awaiting a resection with catecholamine blockade whenever possible; such management has led to a decrease in mortality with this operation.2 The classic approach is with phenoxybenzamine, a noncompetitive and irreversible inhibitor of α1 and α2 adrenergic receptors, often along with a concomitant β-blocker. The prolonged duration of action of phenoxybenzamine, as well as other antihypertensives, has been implicated in the subsequent catecholamine-resistant hypotension.

In a recent review article by Jochberger et al.,3 vasopressin's vasoconstrictive potential was discussed in detail. Areas in which vasopressin has been successfully used include cardiopulmonary resuscitation; various states of shock: septic, anaphylactic and haemorrhagic; after bypass; with neuroaxial anaesthesia; with brain stem dead donors;3 as well as with refractory hypotension following reperfusion in a liver transplant.4

With its use in phaeochromocytoma resections, vasopressin may prove helpful in several ways. By providing vasoconstriction via a non-α-adrenergic mechanism (a route which would be hindered by phenoxybenzamine), it allows the blood pressure to be maintained. It is also hypothesized that vasopressin causes massive vasoconstriction of truncal and mesenteric arteries,5 which may well be beneficial in cases of intra-abdominal surgery and bleeding. Furthermore, it is thought that with the very high levels of circulating endogenous catecholamines, as found in most phaeochromocytomas, this downregulates the posterior pituitary's synthesis and release of vasopressin, so administration of this deficient vasoactive substance would help to counteract the hypotension encountered.6 Additionally, Boccara et al.7 described how some phaeochromocytomas are, in fact, vasopressin secreting, some without excess catecholamines. In these cases, the sudden reduction in circulating vasopressin after resection would lead to profound hypotension requiring exogenous replacement. It has also been stated that opioids and catecholamines, often administered simultaneously with phaeochromocytoma resections, inhibit the endogenous vasopressin release; therefore, an exogenous supply would again be beneficial.8 Finally, it has been shown that during neuroaxial blockade, such as epidurals and spinal anaesthesia, with the sympathetic outflow reduced, vasopressin acts as the body's natural compensatory system for haemodynamic control.9 This last point is of particular relevance to our case, as an epidural was sited and used intraoperatively for analgesia. Its sympathetic blockade would have further exaggerated the antiadrenergic effects of the preoperative blood pressure control.

It should also be noted that, in our case, vasopressin was commenced as an infusion only without an initial bolus dose, but that it still had a rapid and effective response.


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© 2010 European Society of Anaesthesiology