Clinical, laboratory and ultrasonographic findings in 87 cows with type-4 abomasal ulcer

Abomasal ulcer disease is of great importance in cattle. Abomasal lesions are divided into erosions and ulcers [1]; erosions are superficial lesions of the mucous membrane and ulcers are deep defects that penetrate the basement membrane of the abomasal mucosa [2]. Abomasal ulcers vary in number and size and can heal spontaneously, but this is associated with the formation of a permanent scar [1]. Abomasal ulcers were previously divided into four types [1, 3], but a new system that has been used for a number of years classifies ulcers into five types [4]. Classification is based on the depth of penetration, the degree of haemorrhage and the degree of peritonitis caused by the ulcer. Type 1 denotes erosions and/or non-perforated ulcers with minimal haemorrhage; type 2 is associated with severe intraluminal haemorrhage because of erosion of a large blood vessel; type 3 is a perforated ulcer located close to neighbouring organs or the peritoneum resulting in acute local peritonitis and adhesions and sometimes the formation of abscesses; and type 4 is a perforated ulcer accompanied by diffuse peritonitis because of contamination of the abdominal cavity with ingesta from the abomasum. Abomasal perforation into the omental bursa associated with localised omental bursitis was previously considered a subset of type-3 ulcer [5] but has since been designated type 5 [4]. Individual cows may have multiple ulcers from more than one classification [2].

The clinical signs vary widely depending on the type of abomasal ulcer; generalised peritonitis is common in cows with type-4 ulcer and is often fatal within 24 to 48 h [3]. The clinical signs in cows with type-4 ulcer resemble those of septic shock and include tachycardia, tachypnoea, fever, congested scleral vessels, pale and muddy mucous membranes, decreased skin surface temperature, spontaneous grunting and abdominal guarding [6, 7]. Abdominal pain was observed in five of seven (71%) [1] and ten of 22 cows (45%) with a perforated ulcer [6], respectively. Transrectal palpation reveals absence of or a reduction in the normally negative intraabdominal pressure and the serosal surfaces may have a sandpaper-like texture. Almost all cows have diarrhoea [6, 7]. Increased haematocrit (> 35%) accompanied by a decrease in total protein (< 60 g/l) and leukocytosis attributable to neutrophilia, often with a left shift, are common [6, 7]. Metabolic acidosis has also been reported in cows with type-4 abomasal ulcer [7].

Ultrasound examination can be helpful in assessing the position, size, wall and content of the abomasum and possible inflammatory lesions that involve neighbouring organs [8]. However, mucosal erosions and type-1 ulcers that were diagnosed at postmortem in 16 of 50 (32%) clinically healthy cows were missed ultrasonographically [9]. When blood is aspirated during abomasocentesis, the likelihood of abomasal ulcer is high [10]. Ultrasonography was identified as the most important diagnostic procedure in a cow with abomasal lymphosarcoma [11]; a thickened abomasal wall and prominent abomasal leaves accompanied by enlarged lymph nodes were considered diagnostic. Ultrasonographic findings in cows with peritonitis vary widely [8]. Fibrinous peritonitis is characterised by echogenic deposits on the peritoneum and organ surfaces in the absence of effusion, but fibrin may have fluid inclusions. Anechoic to hypoechoic fluid accumulation (inflammatory ascites) interspersed with fibrin strands between organs may be seen in generalised peritonitis. With a perforated ulcer, ingesta can be seen as an echogenic coating on various abdominal organs.

Because the clinical diagnosis of type-4 abomasal ulcer is not straightforward, and detailed investigations of large numbers of cows with this ulcer type are lacking, the purpose of this study was to describe the clinical, laboratory and ultrasonographic findings of cows with type-4 abomasal ulcer to facilitate the diagnosis of this disease.

Forty-nine percent of all cases of type-4 abomasal ulcer occurred during the first four weeks of lactation, which had the highest incidence of all lactational stages. This was in general agreement with other reports [1, 6, 19–21]. Stressors affecting cows in the periparturient period, in addition to parturition, include the movement from the dry cow pen to the milking herd [22, 23] and the transition to a carbohydrate-rich ration [24], onset of lactation and a variety of typical early-lactation disorders [25]. These stressors are responsible for enhanced secretion of cortisol, hydrochloric acid and pepsin and also result in reduced secretion of prostaglandin E [25, 26]. Comorbidity was common in the present study and one third of all cows had one or more additional disorders. In an earlier study, 39 of 43 cows with perforated abomasal ulcer had one or more additional disorders [6]. Advanced pregnancy and early lactation in dairy cows is associated with increased stress, which was evidenced by increased hair cortisol concentrations in periparturient cows [27, 28] and in cows three weeks after parturition [27] compared with cows at other reproductive stages. Some of the cows had received NSAIDs and/or corticosteroids before referral; however, we were not able to determine when these drugs were given or the dosages used. It cannot be ruled out that these treatments were involved in the pathogenesis of the ulcers or in the perforation of a pre-existing type-1 or − 2 ulcer. Anti-inflammatory drugs such as corticosteroids and salicylic acid have been implicated in the pathogenesis of abomasal ulcer [7] and their use should be limited to 3 days. The clinical signs in cows with type-4 abomasal ulcer are associated with generalised peritonitis and have been described in many text books [7, 29–31], although details regarding the frequency of signs are sparse. The present study examined the clinical signs associated with a perforated ulcer in detail and identified compromised health status and anorexia (100%), abdominal guarding (81%), congested scleral vessels (77%), ruminal atony (73%), tachycardia (68%), tachypnoea (65%), positive foreign body tests (58%), decreased skin surface temperature (53%) and fever (49%) as the predominant clinical signs. However, with the exception of abdominal guarding and positive foreign body tests, these clinical signs may occur with many other disorders. Abdominal guarding and positive foreign body tests are pathognomonic for peritonitis, which is most often caused by traumatic reticuloperitonitis in cattle [32]. However, the same or similar signs of abdominal pain may also occur in disorders of the liver, omasum, lungs or, as shown here, the abomasum [32]. In the present study, 58% of the cows had one or more positive foreign body tests; the pole test was positive in 46% and the back grip in 40%. Of note, these frequencies were similar to those observed in 503 cows with traumatic reticuloperitonitis, in which the pole test was positive in 43% and the back grip in 39% of cows [14]. Taken together, these findings show that foreign body tests are not suitable for the differentiation of type-4 ulcer and traumatic reticuloperitonitis. Reduced or absent negative abdominal pressure detected during transrectal examination is an important clinical finding that suggests peritonitis [29] and occurred in 39% of the cows in the present study. Intraabdominal manoeuvrability with the examining arm is conspicuously increased compared with healthy cows [33]. Thus, type-4 abomasal ulcer is the most likely diagnosis when typical signs of peritonitis such as abdominal guarding, positive foreign body tests and fever are accompanied by a severely compromised health status, tachycardia, tachypnoea and other signs of shock. Of 503 cows with traumatic reticuloperitonitis, only 26% had tachycardia and 8% had tachypnoea [14] compared with 68 and 65% of the cows with type-4 ulcer. Tachycardia in cows with type-4 ulcer is attributable to shock and tachypnoea indicates pain.

Haematocrit and plasma protein are important laboratory variables in cows with type-4 ulcer. Increased haematocrit in 69% of cows indicated shock-induced haemoconcentration, but interestingly, this was accompanied by hyperproteinaemia in only 11% of cases. Usually an increase in haematocrit goes hand in hand with an increase in plasma protein concentration, but in the present study, 60% of cows had normal plasma protein concentrations and in 29% the concentration was even lower than normal. An increased haematocrit accompanied by normal or decreased plasma protein concentration is indicative of loss or active secretion of protein-rich fluid into the peritoneal cavity [34]. It constitutes an important diagnostic sign in cattle with clinical signs typical of peritonitis and reflects the enormous loss of fluid and protein into the peritoneal cavity as a result of generalised peritonitis associated with type-4 abomasal ulcer [6]. Hypoproteinaemia associated with haemoconcentration may also occur with protein-losing enteropathy. In contrast, an increased haematocrit was seen in only 12% and decreased protein concentration in only 1% of 503 cows with traumatic reticuloperitonitis [14]. Hyperfibrinogenaemia occurred in 45% of the cows in the present study. Fibrinogen is an acute-phase protein that may increase within two to three days of onset of an inflammatory disease [35]. Interestingly the glutaraldehyde coagulation test time was increased significantly (16 to 60 min) in 9% of the cows. In these cows, the secretion of protein-rich fluid into the peritoneal cavity led to inadequate concentrations of inflammatory proteins in blood and thus delayed coagulation. A lack of or a severe delay in coagulation with the glutaraldehyde test in cows with clinical signs typical of peritonitis should alert the clinician to hypoproteinaemia and to the likely diagnosis of generalised peritonitis associated with effusion into the peritoneal cavity. Similar to other infectious bovine diseases, the white blood cell count was difficult to interpret in cows with type-4 ulcer. Only 19% of the cows had leukocytosis and 35% had leukopenia. By comparison, in cows with traumatic reticuloperitonitis, 42% had leukocytosis and only 4% had leukopenia [14]. Leukocyte numbers vary with species and depend on the relationship between leukopoiesis and peripheral consumption, and can vary from severely decreased to severely increased in animals with an infectious disease [36]. Leukopenia in cows with type-4 ulcer is attributable to consumption of leukocytes that exceeds the compensatory capacity of the bone marrow, which is less efficient in cattle than in other species [37]. Massive consumption of leukocytes was also seen in cattle with toxic mastitis [38]. Stress-induced secretion of corticosteroids in cows with type-4 ulcer may have contributed to leukopenia. The metabolic acidosis that was diagnosed in 49% of the cows with type-4 ulcer was likely the result of severe dehydration and anaerobic metabolism associated with shock [1]. The determination of l-lactate is useful for the characterisation of shock but unfortunately this was not done. Likewise, azotaemia in 56% of the cows was caused by shock and thus was prerenal. Aciduria was likely due to catabolic metabolism of protein as a result of chronic anorexia.

All but one of 47 peritoneal fluid samples had abnormalities typical of peritonitis including increased specific gravity and/or increased protein concentration, green discolouration suggesting contamination with ingesta or a putrid odour. However, it should be remembered that the standard classification of transudate and exudate do not always apply in sick cattle [39–42]. In contrast, the glucose concentration of peritoneal fluid has been shown to be a very sensitive and specific diagnostic parameter for septic peritonitis. The glucose concentrations of blood and peritoneal fluid are usually similar but because of glucose metabolism by microbes, the concentration is lower in peritoneal fluid than in blood in cows with septic peritonitis [43]. D-dimer concentration is considered the best criterion for the diagnosis of peritonitis [43] and is < 0.60 mg/l in healthy cattle [44]. This is a fibrin degradation product and plays an important role in the diagnosis of coagulation disorders. Peritonitis in cattle is associated with massive synthesis of fibrin immediately accompanied by fibrinolysis, which results in an increase in d-dimer concentration. It has a diagnostic sensitivity of 96% and a specificity of 98% [43]. This implies that the determination of glucose and d-dimer concentrations in peritoneal fluid should be part of the diagnostic workup in a cow suspected of suffering from peritonitis. D-dimer determination was not part of the standard examination protocol used in the present study because most cases occurred before the relationship between peritoneal d-dimer concentration and peritonitis in cattle was described [43].

Ultrasonography was useful for visualising and assessing generalised peritonitis in 47 cows. The proximity of the abomasum to the reticulum showed reticular lesions in many cows with careful scanning of both sides. This underlines the importance of a thorough examination of the entire abdomen even in cases where lesions that support the tentative diagnosis are readily detected. For instance, when ultrasonographic examination is limited to the reticulum in cows with a history or clinical signs typical of traumatic reticuloperitonitis, the examiner runs the risk of missing changes associated with generalised peritonitis. Widespread peritonitic changes were seen in 26% of 503 cows with traumatic reticuloperitonitis [45]. Fibrinous changes of the abomasal serosa, which provide direct evidence of a type-4 ulcer, were seen in only seven cows; however, more extensive inflammatory lesions in the abomasal region also strongly suggest a perforated ulcer. Type-4 abomasal ulcers have not been visualised ultrasonographically, presumably because the ulcer itself is obscured by inflammatory lesions soon after perforation. On the other hand, the resolution of 3.5 to 5.0 MHz transducers that are routinely used may be insufficient to visualise small ulcers, and higher frequencies are associated with insufficient penetration depth of sound waves.

Cows with diffuse peritonitis attributable to a perforated abomasal ulcer respond poorly to treatment [4] and reports of successful treatment are scarce [46]. An ulcer can be resected but peritonitis is usually advanced and resistant to therapy [6]. All cows of the present study were euthanased or died peracutely; treatment was discontinued once diffuse peritonitis was confirmed.

The diagnosis of type-4 abomasal ulcer based on clinical signs alone is difficult and therefore requires additional diagnostic procedures including the determination of the haematocrit and plasma protein concentration, abdominal ultrasonography and analysis of peritoneal fluid. In most cases, these steps lead to a correct diagnosis and allow timely euthanasia of the cow to prevent further suffering and unnecessary treatment costs. The dilemma faced by clinicians is that even though a correct diagnosis is usually possible, effective treatment of type-4 abomasal ulcer is not feasible. Efforts should therefore be made to minimise or eliminate ulcerogenic factors in cattle in later pregnancy and early lactation.