Abstract
This report describes the case of a 52-year-old man with an obstructed para-oesophageal hiatus hernia who required a gastropexy, who postoperatively developed gastroparesis which inadequately responded to conventional prokinetics including erythromycin, metoclopramide, ondansetron, and domperidone. The patient’s symptoms were relieved rapidly with a trial of mirtazapine. A review of related literature is presented.
BACKGROUND
Gastroparesis is a recognised compilation of abdominal surgery. It is a poorly understood condition and is often difficult to manage. We present a case report of one patient who benefited from an uncommonly used therapy.
CASE PRESENTATION
A 52-year-old man presented as an outpatient with a large incarcerated hiatus hernia and iron deficiency anaemia. While awaiting surgical review the patient was suffering from progressive dysphagia and eventually was admitted as an emergency with a 5 day history of projectile vomiting.
Gastroscopy showed grade IV reflux oesophagitis and a para-oesophageal hiatus hernia. A barium swallow revealed a gastric volvulus with evidence of strangulation. An emergency gastropexy was performed; the volvulus was easily reduced into the intra-abdominal compartment and hiatal defect repaired with sutures.
Postoperatively, the patient suffered with severe nausea and vomiting, requiring a nasogastric tube. Despite treatment with prokinetics including erythromycin, metoclopramide, ondansetron and domperidone, the patient continued to have high gastric aspirate via his nasogastric tube. A repeat gastrograffin swallow test showed free flow of contrast into the stomach with no passage into the small bowel, leading to a diagnosis of postoperative gastroparesis. He was commenced on total parenteral nutrition; 4 weeks after the operation a feeding jejunostomy via a percutaneous gastrostomy was inserted in view of his non-resolving gastroparesis.
Despite percutaneous feeding and virtually no oral intake, the patient continued to have high gastric aspirates via the gastrostomy and poorly tolerated his jejunostomy feeds. He could not be discharged due to his continued bloated symptoms and he was in very low mood for a further 4 weeks. At this point a trial of mirtazapine 15 mg sublingually once daily was commenced. Within 12 h the patient was tolerating fluids and gastric aspirate had reduced significantly; by 48 h the patient was managing a soft diet and was discharged home.
On review 3 months after commencing mirtazapine the patient was continuing to tolerate a full diet and exhibited and apparent improvement in his affect.
DISCUSSION
Gastroparesis is delayed gastric emptying in the absence of mechanical obstruction. The various causes for gastroparesis include diabetes, idiopathic, post-surgery, malignancy, neurological disorders, metabolic and endocrine disorders, infections, collagen vascular disorders, and pharmacological agents.1
The pathogenesis of gastroparesis is not fully understood. Vittal et al2 in clinical studies found multifactorial mechanisms involving neurological and cellular elements that control gastric motility and sensation. Parischa3 postulated that gastroparesis may be caused by nausea rather than the inverse. The first approach to treating gastroparesis is to address any underlying cause. Many different medical treatments have been used to try and promote gastric emptying by aiding smooth muscle contraction within the stomach. Commonly used prokinetic drugs include antidopaminergic agents, serotonergic agents, and motilin receptor agonists. Other treatment options include gastric electrical stimulation and botulinum toxin injections, both used with varying success. None of the current treatments have a high efficacy rate and often are ineffective in controlling symptoms.
Mirtazapine is a novel antidepressant, being the first noradrenergic and specific serotonergic antidepressant. It blocks postsynaptic 5-HT2/3 receptors and presynaptic α2-autoreceptor by stimulating postsynaptic 5HT1 receptor,4 and by blocking 5HT3 receptor it has been shown to be a successful anti-emetic agent. One of its effects is weight gain, possibly due to increased appetite.
Published evidence on the efficacy of mirtazapine in gastric conditions is scarce. In the case of severe nausea and vomiting in psychiatric patients, an article by Pae4 discussed two case reports, and found low dose mirtazapine to be an effective treatment. Neither patient had any evidence of organic cause for their symptoms.
A case report by Kim et al showed a beneficial effect of mirtazapine in a patient with a 7 month history of resistant gastroparesis who had a history of depression. She had complete resolution of her gastric symptom and a significant improvement of her depression related symptoms.5 However, in a double blind, randomised, control trial involving healthy volunteers, there did not appear to be an increased rate in gastric emptying in patients on mirtazapine.6 This may be due to the fact that mirtazapine only has an effect on dysfunctional smooth muscle, and its potential benefits should not be dismissed solely on the grounds of this result.
In this case, routinely used prokinetic medications were trialled over an 8 week period with no improvement in symptoms. Although postoperative gastroparesis can resolve spontaneously over time, it is felt that the rapid change in gastric function of this patient once treated with mirtazapine was unlikely to be purely coincidental. Further use of mirtazapine in patients with postoperative gastroparesis will help to support this association.
LEARNING POINTS
This is the first time mirtazapine has been reported to have a benefit in the treatment of postoperative gastroparesis, managing both physical and psychiatric elements of this condition.
Further research needs to be done to assess the effects of mirtazapine in patients suffering from gastroparesis to identify whether it has a place in the routine management of this condition.
Footnotes
Competing interests: none.
Patient consent: Patient/guardian consent was obtained for publication
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