04/10/2023
This is a bit of a hard post to put out there and I’ve sat on it for quite sometime. However the support I have gotten since July has been amazing and I’m super thankful for it and helping me get to where I am today and beyond 💕
Stuart’s findings…
GROSS PATHOLOGY:
Nutritional state: 3/5 BCS, with ample subcutaneous, intraabdominal and retroperitoneal adipose tissue and adequate muscling.
Preservation state: Good with minimally increased visceral tissue friability, carcass discolouration and odour.
Hydration state: Euhydrated as evidenced by moist mucous membranes and subcutaneous tissues. Mucous membranes: The gingival and conjunctival mucous membranes are pink and moist.
Spine: The proximal aspect of the left T3 and T4 spinal nerves are dark red (postmortem artefact). The spinal column is grossly unremarkable.
Stomach: Focally the glandular gastric mucosa adjacent the margo plicatus contains a single 1.5cm diameter, red, depression with irregular edges (erosion). The stomach is filled with a large volume of green fibrous organic material admixed with organic, bright orange, granular material.
Lungs: The lungs are discoloured dark red, incompletely collapsed with dense, rubbery parenchyma and a glistening pleural surface (pulmonary congestion and oedema). The tracheal lumen is completely filled with white stable foam (pulmonary oedema).
Heart: The left free ventricular wall width measures 35mm while the right free ventricular wall width measures 17mm, equating to a L:R free wall ratio of 2:1.
Gross morphological diagnosis:
Brain: Intraventricular cholesterol granuloma
Stomach: Minimal, focal, acute glandular mucosal erosion
Lungs: Moderate, regionally extensive, acute congestion and oedema
HISTOPATHOLOGY:
Spinal cord, cranial cervicothoracic (Block D): Multifocally up to 15% of axons in the dorsolateral funiculi are expanded up to 3-fold by clear spaces and occasionally filled with granular eosinophilic cellular debris (axonal degeneration).
Small intestine (Block C): Segmentally expanding the lamina propria of the small intestine are large, dense aggregates of eosinophils, lymphocytes and plasma cells (enteritis).
Lungs (Block A): Regionally up to 80% of alveolar spaces are filled with pale eosinophilic, homogenous fluid (pulmonary oedema). Diffusely the pulmonary vasculature is expanded by densely accumulated intraluminal erythrocytes (congestion). Multifocally up to 10% of alveolar spaces are partially filled with small aggregates of extravasated erythrocytes (haemorrhage).
Liver (Block A): The centrilobular sinusoids are generally markedly congested.
Kidneys (Block B): Multifocally the Bowman’s spaces of glomeruli contain homogenous eosinophilic
proteinaceous fluid. Diffusely the renal vasculature is moderately congested.
Spleen (Block A): The spleen is markedly congested.
Stomach (Block C): Focally the peripheral glandular mucosa is lost (erosion).
Cerebrum (Block F), Cerebellum (Block G): All tissues are histologically normal at the level of examination performed.
Histological morphological diagnosis:
Spinal cord: Moderate, segmental, subacute axonal degeneration
Small intestine: Marked, segmental, chronic eosinophilic and lymphoplasmacytic enteritis
Lungs: Marked, regionally extensive, acute pulmonary congestion, oedema and alveolar haemorrhage
Liver: Marked, generalised, acute centrilobular congestion
Kidneys: Moderate, diffuse, acute, congestion
Spleen: Marked, diffuse, acute congestion
Stomach: Mild, focal, acute erosion
FINAL DIAGNOSIS: Caudal cervical spinal cord axonopathy, enteritis and gastric erosions
Comments: The findings of axonal degeneration in the cranial cervicothoracic spinal cord are suggestive of central axonopathy. The absence of these findings in the caudal cervicothoracic spinal cord and lack of cerebral/cerebellar lesions suggests a focal insult to the axons at the level of the caudal cervical spinal cord. Differentials for these changes could include cervical vertebral stenotic myelopathy (Wobbler’s), focal trauma or intervertebral disc disease. The lack of gross lesions makes Wobbler’s the most likely differential in this case given the propensity for “dynamic” type Wobblers which are only evident at some stages of cervical vertebral column flexion/extension and may be missed at postmortem examination. Wobblers syndrome may cause pain, paresis and ataxia and could be an explanation as to the horse’s reluctance to ride in this case although it cannot be confirmed without corroborating clinical signs and/or grossly evident stenosis of the spinal canal.
The findings of marked segmental enteritis and mild gastric glandular erosions in this case are nonspecific and their clinical significance is unclear. Gastric ulcers are common in horses arising from stress, strenuous exercise or high energy diets and frequently cause an unwillingness to perform or be ridden. In this case gastric erosions are mild, and it is unclear if these have caused the unwillingness to ride indicated in the history. The enteritis identified was unexpectedly severe and could have led to clinical lethargy, hyporexia or colic signs however enteritis is not commonly considered a cause of unwillingness to ride. The large proportion of eosinophils in the inflammatory exudate of enteritis in this case could suggest parasitic or allergic aetiology, however no parasites were identified gross or histologically, making allergic causes more likely.