Menrath ulcer resulting in life-threatening anaemia in a cat

Introduction

Menrath ulcers are uncommon lesions of the rostral hard palate in cats, believed to arise from mechanical trauma associated with excessive grooming in individuals with pruritic skin disease. The abrasive nature of the feline tongue is thought to contribute to mucosal injury in predisposed patients. ¹ These lesions were first described in 1990 ² and are typically well demarcated, occurring either unilaterally or bilaterally.^3,4 The ulcer is most often located between the dental arcade and the midline of the rostral hard palate.^1,3

As a result of the superficial course of the major palatine arteries in this region, Menrath ulcers may result in significant arterial haemorrhage.^1,2,4,5 In some cases, the lesion may be small and difficult to visualise and haemorrhage may be intermittent. Furthermore, cats may swallow the blood, complicating clinical recognition of the bleeding episode by both owners and clinicians. Flea infestation and associated pruritus have been frequently reported as underlying causes in previously published case reports.^5–7

Given the potential for life-threatening haemorrhage, prompt intervention is often warranted when a Menrath ulcer is suspected. Surgical options described in the literature include unilateral or bilateral ligation of the major palatine artery, placement of horizontal mattress sutures and mucoperiosteal flap reconstruction.^1–3,5

Case description

An 11-year-old neutered male domestic shorthair cat was referred to the University Hospital for Companion Animals, Copenhagen, Denmark, owing to severe blood loss and the development of severe non-regenerative anaemia with a haematocrit (HCT) of 10.4%. Initial indicators of bone marrow response were present (reticulocyte count of 178.5 K/µl and reticulocyte percentage of 8.5%), suggesting that the anaemia was in a pre-regenerative phase. Before presentation, the cat sustained substantial haemorrhage at home. The owner reported suspected oral bleeding (Figure 1), along with melena and possible haematemesis noted the previous day.

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Figure 1

Large amount of blood observed on the floor at home by the owner before presentation at the hospital. The owner suspected the blood came from the oral cavity, which was later confirmed at the hospital

The cat was evaluated for marked pruritus 2 weeks before the bleeding episode. Despite clinical assessment, no aetiology was determined.

Before referral, the cat was treated with analgesia (methadone 0.1 mg/kg IV once), esomeprazole (1 mg/kg IV once) and Ringer’s acetate (RAC) (two boluses of 10 ml/kg over 10 mins each).

At presentation, the cat was quiet but alert and responsive. Abnormal clinical parameters included hypothermia (36.1°C), tachycardia (240 bpm) and a grade II/VI holosystolic murmur. The abdomen was non-painful on palpation, and no overt oral ulcerations were observed during the initial examination without sedation. Flea infestation was confirmed and considered a plausible cause of the owner-reported pruritus.

There was marked anaemia (HCT 8.2%) with moderate reticulocytosis (101.4 × 10⁹/l), indicating a regenerative response. Thrombocyte count was slightly outside the reference interval (177 × 10⁹/l), although the smear revealed small aggregates and macrothrombocytes. Morphological evaluation showed moderate polychromasia and mild anisocytosis, including microcytic and sporadic macrocytic erythrocytes.

Thromboelastography showed a hypercoagulable profile, with a marginally reduced K-value and increased alpha angle and maximum amplitude. Retroviral testing conducted by the referring clinician was negative. The biochemical profile demonstrated mild hypoalbuminemia, total hypocalcaemia and hyperglycaemia.

The patient received a feline packed red blood cell transfusion (25 ml diluted in 25 ml NaCl), resulting in improved mentation and a reduction in heart rate to approximately 160 bpm. Mild hypokalaemia, as noted in prior laboratory results, prompted initiation of intravenous potassium supplementation. The following day, a superficial erosion was identified on the right palatum durum (Figure 2), without evidence of active bleeding. HCT was 10.8% approximately 24 h after transfusion, after which the cat exhibited progressive icterus. Icterus had resolved completely 48 h after it was first confirmed.

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Figure 2

Erosion in the hard palate of a cat with severe bleeding from the oral cavity (arrow). This erosion was diagnosed as a Menrath ulcer

Three days after presentation, the patient underwent thoracic, abdominal and laryngeal radiography, as well as abdominal ultrasonography; HCT was 10.3%. Given the lack of access to additional packed red blood cells, anaesthesia was deemed highrisk, precluding comprehensive oral examination and endoscopic assessment of the upper gastrointestinal tract. Overnight, between days 4 and 5, the cat developed a new episode of profuse oral bleeding (Figure 3), with no identifiable source on inspection.

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Figure 3

Spontaneous extensive oral bleeding observed in a cat with a Menrath ulcer during hospitalisation

A whole blood transfusion (53 ml whole blood) was administered on day 5 after donor identification. Subsequent examination under anaesthesia included oral inspection and endoscopic assessment of the pharynx, oesophagus and stomach. No additional bleeding source was identified beyond a lesion on the hard palate. A biopsy was collected from the lesion, and the site was sutured to mitigate further haemorrhage. Dental radiography was performed to evaluate for maxillodental abnormalities indicating an underlying neoplastic lesion; the findings were unremarkable.

Therapeutic management included maropitant and mirtazapine for hyporexia, and a single dose of etamsilate (0.1 ml/kg IV) during an acute haemorrhagic episode. The patient received continuous intravenous fluid therapy (RAC) with potassium supplementation. Ectoparasite control was achieved using imidacloprid/moxidectin (Advocate). After endoscopy, dexamethasone (0.08 mg/kg IV) and mepyramine (1 mg/kg SC) were administered for extensive pruritus, and an Elizabethan collar was applied to prevent further mechanical irritation. Histopathological analysis of the palatal lesion demonstrated a focal, extensive ulceration characterised by fibrino-suppurative inflammation and granulation tissue proliferation, consistent with trauma-induced pathology. No histological evidence of neoplasia or eosinophilic granuloma was identified.

At 1 month after discharge, the patient remained clinically well. The palatal lesion had healed, although residual architectural changes (loss of palatine rugae) persisted. No further haemorrhagic episodes were reported. Dermatological evaluation revealed ongoing moderate pruritus with multiple ulcerative and crusted skin lesions. A hydrolysed diet and prednisolone (0.5 mg/kg PO q24h) were prescribed for suspected flea allergy. The clinical response was favourable, with resolution of pruritus. A tapering protocol over 6–8 weeks was communicated to the owner, with instructions to report any recurrence of pruritus or oral bleeding.

At 5 months after discharge, the patient exhibited a recurrence of pruritus. At that time, flea prophylaxis was ongoing; however, corticosteroid therapy had been discontinued. Prednisolone was reinitiated using the previously established tapering protocol, and the duration of flea treatment was extended to minimise the risk of reinfestation. No further episodes of oral haemorrhage were reported by the owner during this period.

The owner was also contacted 12 months after the initial presentation, and at that point the cat was doing well. He had not suffered any additional episodes of pruritus and was no longer on corticosteroid therapy. No oral haemorrhage was reported.

Discussion

This case report describes a feline patient that presented with a palatine ulceration accompanied by secondary, life-threatening oral haemorrhage. The lesion was suspected to represent a Menrath ulcer, resulting from mechanical abrasion after excessive grooming, triggered by flea infestation and pruritus. Menrath ulcers secondary to flea allergy dermatitis and pruritic skin disease have been previously documented in the veterinary literature, including isolated case reports^4,7 and, more recently, in a case series involving four feline patients. ⁵ These findings support the proposed association between flea-induced pruritus and the development of Menrath ulcers in affected cats.

Differential diagnoses for feline oral ulcerative lesions include eosinophilic granuloma complex, chronic gingivostomatitis, non-specific stomatitis, gingival hyperplasia and oral neoplasia such as squamous cell carcinoma. ⁸ In the present case, histopathological evaluation of a palatal biopsy revealed a focal, extensive ulceration with fibrino-suppurative inflammation and granulation tissue proliferation, consistent with a traumatic aetiology. No evidence of eosinophilic granuloma complex, neoplastic processes or other specific underlying pathology was identified. Based on the lesion’s anatomical location, the presence of severe flea infestation and the histopathological findings, a diagnosis of Menrath ulcer was established.

Menrath ulcers located in the hard palate are anatomically adjacent to the palatine artery, and haemorrhage from these lesions can be profound, occasionally resulting in marked anaemia. Clinical presentation may vary depending on whether the cat swallows the blood, and external bleeding is not always observed. In this case, the owner reported a sudden episode of profuse oral haemorrhage at home, which prompted immediate veterinary consultation.

Severe oral haemorrhage resulting in anaemia and necessitating blood transfusion, as observed in the present case, has been documented in previous reports of Menrath ulcers in cats.^5,9 However, the true incidence of life-threatening haemorrhage among affected individuals remains unknown. Several surgical techniques have been described in the literature for the management of Menrath ulcers, including appositional suturing of the ulcer margins, ¹⁰ ligation of the major palatine artery,^1,3 cauterisation of the lesion,^2,4 reconstruction using a bipedicle mucoperiosteal flap ⁶ and coblation therapy. ⁷ Although surgical intervention is often necessary to control active bleeding and prevent recurrence, addressing the underlying aetiology – typically pruritic skin disease such as flea allergy dermatitis – is essential for long-term resolution.

In the present case, surgical management included placement of sutures to close the palatal ulceration and mitigate further haemorrhage, after collection of a biopsy from the affected area. The underlying pruritic skin condition was addressed through a multimodal approach, including administration of anti-parasitic agents, oral prednisolone and antihistamines. In addition, the diet was shifted to a hydrolysed diet because food allergy was not ruled out. An Elizabethan collar was applied to prevent excessive licking, and the owner was instructed to maintain its use, with brief supervised removal periods to assess resolution of pruritus.

Persistent pruritus after anti-parasitic treatment raised suspicion of flea allergy dermatitis, prompting the implementation of a more comprehensive therapeutic plan.

Prognosis is generally favourable with appropriate treatment, underscoring the importance of accurate diagnosis.^4–6 In the present case, follow-up information for 1 year was available and no further episodes with oral haemorrhage were observed by the owner during this period.

Conclusions

Undetected Menrath ulcers in cats may result in significant blood loss, postponed treatment and unnecessary diagnostic interventions. The primary target of interest in feline patients presenting with oral haemorrhage, particularly in the context of concurrent pruritic skin disease, should be the oral cavity.