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Correspondence

Midodrine, an alternative to intravenous vasopressor therapy after spinal surgery

O'Donnell, B.; Synnott, A.

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European Journal of Anaesthesiology (EJA): November 2002 - Volume 19 - Issue 11 - p 841-842
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EDITOR:

We report the novel use of midodrine in a patient with haemodynamic derangement due to spinal cord pathology. Midodrine is an orally available α1-agonist that produces an increase in vascular tone and an elevation of blood pressure [1]. It has been licensed for use in the treatment of orthostatic hypotension; however, there have been reports of its beneficial use in other conditions, namely neurocardiogenic syncope [2], intradialytic hypotension [3], chronic hypotension in dialysis patients [4] and hypotension in spinal cord-injured patients [5,6].

A 44-yr-old male was referred to this hospital with acute spinal cord compression. He underwent an emergency multilevel laminectomy. The compressive lesion transpired to be a leukaemic deposit extending from C7 to T6.

Anaesthesia was induced with fentanyl, thiopental - with rocuronium for muscle relaxation - and was maintained with oxygen, nitrous oxide and isoflurane. Arterial and central venous pressures were invasively monitored by means of a radial artery catheter and a long peripheral catheter in the cephalic vein of the left arm. Following induction of anaesthesia, blood pressure fell from 110/80 to 70/40 mmHg, and heart rate increased from 100 to 125 beats min−1. Hypotension was treated with intravenous (i.v.) fluids and frequent boluses of methoxamine. To maintain normotension peroperatively, the patient received an i.v. infusion of norepinephrine via the long peripheral catheter, which was continued on return to intensive care unit (ICU).

Four hours after return to the ICU, the patient was alert and orientated, and haemodynamically stable with the norepinephrine infusion. He had a dense paraplegia and a T6 sensory level. As vasopressor requirements had remained unchanged since his return from the operating room, midodrine 10 mg three times a day was instituted. One hour after administration of the initial dose, his blood pressure rose to 150/100 mmHg and heart rate fell to between 65 and 70 beats min−1. This observed response is in keeping with the pharmacokinetic and pharmacodynamic properties of the drug [1]. The patient was discharged from the ICU to the neurosurgical high-dependency unit on the first postoperative day, and to the neurosurgical ward 2 days later. At follow-up 7 days after surgery, he remained well, his blood pressure had stabilized at 110/70 mmHg and his heart rate was 65 beats min−1. He showed no adverse effects of treatment with midodrine.

Midodrine is a prodrug, being metabolized by deglycination to its active metabolite desglymidodrine. It is readily absorbed orally and reaches peak plasma concentrations after 60 min. Peak concentrations of desglymidodrine are achieved 60-120 min after ingestion of the prodrug, and its half-life is 3-4 h [1]. The response to midodrine in the case illustrated is in accordance with the pharmacokinetics described above.

The absolute bioavailability of midodrine is 93% [1]. Midodrine and desglymidodrine are metabolized to some extent by the liver. Midodrine has almost no renal elimination. Desglymidodrine, however, is extensively excreted by the kidney via active tubular secretion.

Midodrine is prescribed in a dose of 10 mg twice or three times daily [7]. Patients who have proven refractory to monotherapy with midodrine have benefited from the addition of octreotide to their treatment regimen. It is contraindicated in severe heart disease, acute renal failure, urinary retention, phaeochromocytoma and thyrotoxicosis. It should be used with caution in those with hepatic or renal insufficiency. Reported adverse reactions include supine hypertension, paraesthesia, pruritis, piloerection, urinary retention and facial flushing. These tend to be mild, and the medication is generally well-tolerated [7].

Our patient was admitted to the ICU postoperatively to control hypotension. In this case, the observed hypotension may be, at least in part, attributed to loss of sympathetic outflow from the thoracolumbar spine. Central venous administration of a vasopressor such as norepinephrine is routinely used at this hospital in such cases. By substituting midodrine for norepinephrine, i.v. vasopressor therapy could be quickly and safely discontinued. Midodrine was well-tolerated and permitted speedy discharge from the ICU. Central i.v. catheter insertion was not required, bed days in the ICU were saved and the risk of nosocomial infection with multiresistant organisms was reduced. While we accept that further evaluation of this therapy is required, this case illustrates the potential usefulness of midodrine in similar situations.

B. O'Donnell

A. Synnott

Department of Anaesthesia and Intensive Care Medicine; Beaumont Hospital; Dublin, Ireland

References

1. Mosby's GenRx, 10th edn. St Louis, USA: Mosby, 2000.
2. Ward CR. Midodrine: a role in the management of neurocardiogenic syncope. Heart 1998; 79: 45-49.
3. Cruz DN. Intradialytic hypotension: is midodrine beneficial in symptomatic haemodialysis patients? Am J Kidney Dis 1997; 30: 772-772.
4. Fang JT. Midodrine hydrochloride in patients on haemodialysis with chronic hypotension. Renal Failure 1996; 18: 253-260.
5. Blackmer J. Orthostatic hypotension in spinal cord injured patients. J Spinal Cord Med 1997; 20: 212-217.
6. Barber DB. Midodrine hydrochloride and the treatment of orthostatic hypotension in tetraplegia: two cases and a review of the literature. Spinal Cord 2000; 38: 109-111.
7. Wright RA, Kaufmann HC, Perera R, et al. A double blind, dose response study of midodrine in neurogenic orthostatic hypotension. Neurology 1998; 51: 120-124.
© 2002 European Academy of Anaesthesiology