Chronic laminitis in a 10‐month‐old Arabian filly

The case report presented here describes in detail the treatment and clinical progression of a case of severe chronic laminitis in a 10‐month‐old Arabian filly. Starting from the acute onset of clinical signs through the severe, debilitating progression of the disease, the report describes the medical, surgical and farriery treatment over a period of 8 months. The combination of deep digital flexor tendon tenotomy, hoof wall resection, corrective trimming and shoeing was successful in halting progression of the disease. The successful treatment resulted in new healthy hoof wall growth, re‐establishment of normal third phalanx‐hoof wall alignment and reversal of the degenerative modelling changes that occurred in the third phalanx. To the best of our knowledge, this is the first study describing treatment of severe chronic laminitis in such a young filly.     

Mesh repair of a large traumatic lateral abdominal wall hernia in an 8‐day‐old foal

An 8‐day‐old French trotter colt was admitted with a traumatic lateral abdominal wall hernia with reducible intestinal content. A 15 cm long full thickness tear was identified in both the internal abdominal oblique and transverse abdominal muscles. This case report describes the surgical repair of the hernia using a polypropylene mesh.     

Reversed patent ductus arteriosus and multiple congenital malformations in an 8‐day‐old Arabo‐Friesian foal

An 8‐day‐old Arabo‐Friesian filly was presented with signs of severe dyspnoea, tachypnoea, coughing and cyanotic mucous membranes. On auscultation, a bilateral grade V/VI continuous heart murmur and heart rate of 155 beats/min (sinus tachycardia) were detected. Lung ultrasonography revealed pronounced comet tail artefacts indicating lung oedema. Echocardiography showed right ventricular hypertrophy, a 1.2 cm muscular ventricular septal defect with a left‐to‐right shunt, a stenotic bicuspid pulmonary valve and severe mitral and tricuspid valve regurgitation. Tricuspid regurgitation peak velocity indicated a right ventricular systolic pressure of 119 mmHg. The pulmonary artery was severely dilated and a 1 cm diameter patent ductus arteriosus was found. Colour flow Doppler showed systolic ductal flow reversal with right‐to‐left shunting through the ductus. Arterial partial oxygen pressure and saturation were lower in the metatarsal artery (25 mmHg, saturation 52.6%) than in the carotid artery (31 mmHg, saturation 64.3%). Due to the poor prognosis, the foal was subjected to euthanasia and necropsy confirmed the ultrasonographic findings. Patent ductus arteriosus is a rare condition and occurs most frequently in combination with tetralogy and pentalogy of Fallot. A genetic basis for congenital cardiac disease, especially for ventricular septal defects, in Arabians and for aortic rupture and aorto‐pulmonary fistulation in Friesians has been reported. Whether cross‐breeding leads to an increased prevalence is unknown. This is the first case report with echocardiographic visualisation of reversed ductal flow in a neonatal Arabo‐Friesian foal.     

Resolution of hypertrophic osteopathy in a 2‐year‐old filly

This article reports the successful management of a 2‐year‐old Thoroughbred filly that presented with clinical signs of hypertrophic osteopathy, diffuse granulomatous dermatitis, lethargy and inappetence. An infectious primary focus was suspected due to an elevated white blood cell count (WBC), marked neutrophilia and dramatically increased serum amyloid A (SAA) and plasma fibrinogen levels. After failure to respond to a range of antimicrobial treatments, an actinomycetes bacterial infection, such as Mycobacterium avium or Rhodococcus equi, was suspected and the horse was started on rifampicin and clarithromycin treatment, which resulted in a rapid and pronounced improvement in clinical signs. After 10 weeks of treatment the skeletal manifestations had regressed, both clinically and radiographically, in addition to normalisation of the WBC count, SAA and fibrinogen levels.     

Black locust (Robinia pseudoacacia) intoxication as a suspected cause of transient hyperammonaemia and enteral encephalopathy in a pony

Two ponies presented with mild abdominal pain and mild diarrhoea one hour after ingestion of roots of a black locust tree. On admission, symptoms had progressed to depression, weakness and the passing of dark, firm faeces. Treatment was symptomatic and supportive, aiming at the evacuation of the toxin from the gastrointestinal tract. One pony developed severe, reversible neurological signs associated with transient hyperammonaemia in the absence of liver disease. After 24 h the ammonia level returned to normal and central nervous signs disappeared. Both ponies recovered completely. This report describes the ingestion of black locust closely followed by the development of central nervous signs and hyperammonaemia. Increased ammonia absorption due to the intestinal wall inflammation caused by the toxins of the black locust tree, as well as increased ammonia production by enteric bacteria is therefore considered a plausible pathophysiological mechanism of the neurological signs displayed in black locust intoxication.     

Intestinal hyperammonaemia in horses

Intestinal hyperammonaemia in horses is a syndrome putatively caused by increased intestinal production and/or absorption of ammonia that clinically manifests as severe neurological abnormalities often in conjunction with signs of gastrointestinal dysfunction but without evidence of hepatic compromise. Ingestion of Black Locust (Robinia pseudoacacia) is a novel primary condition that may predispose to development of the syndrome as described in this issue. Treatment of the condition is symptomatic and aimed at decreasing blood ammonium concentrations by reducing further production and absorption, reducing brain oedema and preventing self‐inflicted trauma. Prognosis for survival is guarded, particularly in cases with severe gastrointestinal lesions, and is influenced by the ability to control clinical signs.     

Aortic rupture causing cardiac tamponade in a 24‐day‐old Friesian colt with concurrent colonic Chlamydiosis and Balantidiasis

A 24‐day‐old Friesian colt died suddenly and a physical examination the morning the foal died showed no abnormalities and serum IgG levels >8.0 g/l. Necropsy examination revealed haemopericardium and a 2 cm transverse tear at the root of the aorta. The foal was also found to have Chlamydophila spp. in the epithelium and Balantidium coli on the mucosal surface of the large colon. An aortic rupture is a novel finding in a foal, colonic Chlamydiosis has not been previously reported in horses and Balantidium coli has not been reported in equids in North America.     

Intra‐abdominal cystic lymphangiomatosis in a Thoroughbred foal

Cystic lymphangiomas are rare malformations of the lymphatics that result in the formation of a cystic mass. Where multiple cysts are seen, the condition is termed cystic lymphangiomatosis. This case describes the diagnosis and unique management of cystic lymphangiomatosis in a 10‐day‐old Thoroughbred foal. Ultrasonography, histopathology and laparoscopy were essential for diagnosis and appreciation of the extent of disease. Ultimately, the cystic lymphangiomatosis was so extensive in this foal that complete surgical excision was considered impossible and the presence of adhesions within the abdomen indicated a very poor long‐term prognosis; the owners elected for euthanasia at age 14 weeks. Although rare, lymphangioma and lymphangiomatosis should be considered as a differential diagnosis for an intra‐abdominal mass in a young horse.     

Urinothorax in a Quarter Horse filly

An 18 h old Quarter Horse filly, while being treated for diarrhoea, was evaluated for a distended abdomen and electrolyte abnormalities. Peritoneal and pleural fluid was detected by ultrasound and a presumptive diagnosis of a ruptured bladder was made. Intravenous fluid therapy was instituted to correct the electrolyte abnormalities prior to surgical repair of the bladder tear. Anaesthetic complications included hypoxaemia and decreased compliance secondary to the pleural effusion; therefore, a thoracocentesis was performed. Analysis of the pleural fluid revealed a pleural fluid to serum creatinine ratio of >1.0, indicative of urinothorax. The filly recovered from anaesthesia and was discharged on systemic antimicrobials. Urinothorax should be considered in cases of uroperitoneum with concurrent pleural effusion. Early detection may decrease patient morbidity and anaesthetic complications.     

Ataxia and weakness as uncommon primary manifestations of hepatic encephalopathy in a 15‐year‐old trotter gelding

A 15‐year‐old trotter gelding was evaluated because of an acute onset of ataxia in all 4 limbs. There was no known history of trauma. The gelding showed grade 2/5 ataxia in all 4 limbs, which was localised after clinical neurological examination to the cervical vertebral spinal cord. Initial therapy consisted of oral anti‐inflammatory doses of prednisolone and antimicrobial treatment with potentiated sulphonamides. The ataxia progressed to grade 3/5 at Day 10 of hospitalisation. Additionally, the horse was slightly depressed and showed spontaneous yawning during examination. Facial sensation was blunted. Blood chemistry revealed a marked elevation of liver specific enzymes and blood ammonia levels. Transcutaneous abdominal ultrasonography revealed hepatomegaly. Due to a guarded prognosis, the horse was subjected to euthanasia. At necropsy the left lateral liver lobe was markedly enlarged and showed a firm texture, whereas the cranial part and the right and quadratic liver lobe displayed a severe and diffuse atrophy. Histopathologically, the left lateral liver lobe revealed a moderate to severe cirrhosis with a severe, diffuse hepatocellular iron‐accumulation. Increased numbers of Alzheimer type II astrocytes in the cerebral cortex and cerebral white matter vacuolisation were indicative for encephalopathy. These findings were interpreted as haemosiderosis and cirrhosis of the liver with consecutive hepatic encephalopathy. Aetiologically, haemosiderosis should be considered as a cause of liver cirrhosis with consecutive hepatic encephalopathy. Although hepatic encephalopathy in horses usually presents with predominating cerebral signs, it has to be taken into account as a differential diagnosis in cases of acute onset generalised ataxia.     

Successful treatment of infectious (Salmonella type III: 44) polyarthritis and osteomyelitis in a 4‐week‐old foal

This article describes the acute onset of infectious polyarthritis and osteomyelitis in a 4‐week‐old foal. Analysis of synovial fluid obtained from the left femoropatellar and right tarsocrural joints combined with clinical signs consisting of joint effusion and lameness yielded a diagnosis of septic arthritis. Bacterial culture of synovial fluid from the left stifle revealed Salmonella type III: 44. Rapid, sustained clinical improvement was noted following discontinuation of empirical antimicrobial therapy (potassium penicillin and amikacin sulphate) and initiation of treatment with ceftiofur and ampicillin. The importance of combining knowledge of veterinary pharmacology and microbiology so that appropriate antimicrobials may be selected with regard to the local environment in which they are to eradicate infection is emphasised. Despite frequent reference to amikacin sulphate as an effective antimicrobial for treating infections in foals caused by Salmonella, factors are discussed that explain why amikacin may not be clinically effective for treating infectious arthritis caused by Salmonella.     

Femoral head excision after coxofemoral luxation in an Arab filly: Four years follow‐up

A foal with a cranio‐dorsal coxofemoral luxation was treated with a prosthetic capsulorraphy technique after open reduction. After reluxation a femoral head ostectomy was performed for salvage purposes. The filly was discharged with minimal lameness and was using the limb properly after 51 days of hospitalisation. Four years later the filly is still doing well as a breeding mare, with an acceptable quality of life despite angular deformities in the contralateral limb.     

Caecal duplication in a 13‐year‐old Thoroughbred

A 13‐year‐old Thoroughbred gelding was presented for evaluation of recurrent colic of 4 weeks duration. These colic episodes were mild and responsive to medical therapy. Episodes of colic became more frequent and more painful. Exploratory laparotomy revealed a large intestine duplication with a cystic structure located at the caecocolic junction that was unable to be exteriorized and therefore not amenable to surgical correction. Thirty‐six hours following surgery, the horse became acutely painful, sweaty, and febrile suggesting gastrointestinal rupture. Post mortem examination showed a 0.6 × 1 m duplication and a 0.5 × 0.6 m cystic dilation that was probably associated with the caecum. There was a 10 × 30 cm area of rupture located within the duplication. Histological evaluation confirmed the presence of a true duplication.     

Cerebellar abiotrophy in a 6‐year‐old Arabian mare

Cerebellar abiotrophy (CA) is an uncommon neurological disease that most commonly affects Arabian horses. Affected horses are typically identified within the first 6 months of life. Intention tremor, wide based stance and ataxia are common clinical signs observed in affected individuals. No treatment is available for resolution of clinical signs. Definitive diagnosis is based on histopathological examination of cerebellar tissue, which is characterised by loss of Purkinje cell layer. This report describes a case of cerebellar abiotrophy that had a delayed diagnosis until 6 years of age.     

Minimally‐invasive plate osteosynthesis of a Salter‐Harris type 2 fracture of the proximal phalanx in a filly

A 7‐month‐old Warmblood filly was referred to the equine hospital because of a Salter‐Harris type 2 fracture of the proximal physis of the right hind P1. On admission, the filly had acute grade 3/5 lameness at the walk and diffuse swelling in the area of the right hind proximal phalanx. Radiographs were taken to assess the fracture and plan treatment. Surgical treatment using two 4.5 mm narrow locking compression plates (PIP‐LCPs) resulted in fracture stabilisation and rapid healing. This case report suggests that internal fixation using PIP‐LCPs is useful for the treatment of Salter‐Harris type 2 fractures of the proximal physis of P1 in large foals.     

Intra‐uterine Infection with Babesia bovis in a 2‐day‐old Calf

Infection with Babesia bovis was diagnosed in a 2‐day‐old female calf apparently transmitted in utero. The calf was born as the second calving to a cross‐bred beef cow permanently on pasture. Diagnosis was based upon identification of B. bovis in peripheral blood smears and clinical signs which included fever, jaundice, pale mucous membranes and convulsions. Anaemia, leucocytosis, thrombocytopenia and lymphocytosis were noted at the febrile acute stage of the disease. The blood smears revealed evidence of regeneration of toxic neutrophils with a left shift, severe spherocytosis and high degree of basophilic stippling. Elevated concentration of aspartate aminotransferase, lactate dehydrogenase, and creatine kinase were also noted, and were probably the result of haemolysis, dehydration and muscle damage because of recumbancy. Elevated total bilirubin concentration following haemolysis resulted in jaundice. The neurological symptoms observed were probably caused by sludging of parasitized erythrocytes in the brain capillaries. The calf recovered following treatment with diminazene aceturate and the recovery was followed up clinically, haematologically and biochemically.     

Surgical management of an extrahepatic portosystemic shunt in a foal: A multidisciplinary problem

A 5‐week‐old American Miniature filly was referred due to intermittent neurological signs of 4 weeks' duration. Clinicopathological findings showed increased ammonia and bile acids in venous blood samples. Abdominal ultrasonography detailed a portosystemic shunt (PSS). The foal underwent laparotomy and operative mesenteric portovenography, which further defined the PSS as extrahepatic portocaval in configuration. The PSS was occluded and intraoperative portovenography confirmed successful shunt occlusion. The foal made a good recovery from surgery and had a successful showing career until she succumbed to colic just over 3 years after surgery.     

Successful cardiopulmonary cerebral resuscitation incorporating defibrillation in a filly with neonatal maladjustment syndrome following a routine anaesthetic procedure

A 10-h-old 56-kg Thoroughbred filly was presented for treatment of partial failure of passive transfer of immunity and presumed neonatal maladjustment syndrome (NMS). The filly was hospitalised, and supportive care initiated. On Day 5 of hospitalisation, seizures were observed and were controlled with IV administration of diazepam. Due to progression of clinical signs of NMS, magnetic resonance imaging of the filly's brain was performed. During the early anaesthetic recovery period, the filly exhibited cardiopulmonary arrest (CPA) at which point cardiopulmonary cerebral resuscitation (CPCR) was performed for a total of 48 min. During this time, ventricular fibrillation (VF) was observed on ECG and the filly was defibrillated three times at 1–2-min intervals using 2–4 J/kg of monophasic electrical defibrillation. The filly successfully recovered from CPCR, was discharged 5 days later and was reported healthy 12 months post-discharge.