CASE ANALYSIS 45
MEMBERS OF THE GROUP
Gioliva Wido Septiarga – 20820128 Erfida Damayanti Suseno – 20820116 Oktavianus Fernando Kello – 202820115
Firman Supriadiansyah – 20820106
Mohammad Abel Junjunan Hidayat – 20820103
Case 45
A 3-year-old female Holstein cow presented
approximately 4 months following breeding with decreased
milk production and partial anorexia of 3 weeks’ duration.
EXAMINATION FINDINGS
A distended abdomen was observed, with ‘ping’ following
percussion and auscultation of the left abdomen. Thirty-five
litres of abomasal reflux were removed by orogastric tube.
HAEMATOLOGY
Measurand (units) Result Reference Interval RBC count (1012/l) 8.7 5.0–7.5
Haemoglobin (g/l) 13.7 85–132
Haematocrit (l/l) 0.41 0.24–0.36
MCV (fl) 49.0 37.8–56.0
MCH (pg) 16.1 14.2–20.1
MCHC (g/l) 330 317–404
Platelet count (109/l) 507 220–640
WBC count (109/l) 10 3.8–11.0
Neutrophils (109/l) 5.5 0.7–4.9 Lymphocytes (109/l) 4.2 1.0–5.8 Monocytes (109/l) 0.3 0.0–0.9 Eosinophils (109/l) 0 0.0–1.9
Basophils (109/l) 0 0.0–0.1
Fibrinogen (g/l) (heat precipitation
method)
0.8 0.2–0.6
RBC (normally at 5.0 - 7.5)
8.7 shows a higher than normal RBC (red blood cell count) result, caused by polycythemia vera (This disorder occurs due to malignant growth of blood cells when the bone marrow produces too many red blood cells.) Hemoglobin (normally at 85-132)
13.7 shows the results of the numbers which state that hemoglobin is lower than the normal number which will result in anemia
Hematocrit (normally at 0.24-0.36)
0.14 indicates that the hematocrit is lower than normal. There are several conditions characterized by: Iron deficiency anemia, B12 and folate deficiency anemia. Chronic inflammatory disease.
Neutrophils (normally at 0.7-4.9)
5.5 shows a neutrophil count higher than normal neutrophil count, a high increase is usually caused by ciclera infection (stress, leukemia, rheumatoid arthritis).
Fibrinogen (normally at 0.2-0.6)
0.8 indicates a higher fibrinogen yield than normal Cardiovascular
BIOCHEMISTRY
Analyte (units) Result Reference Interval Total protein (g/l) 78 65–76
Albumin (g/l) 42 23–39
Glucose (mmol/l) 3.9 2.6–3.9 Creatinine (μmol/l) 184.2 61–133 Sodium (mmol/l) 140 140–146 Potassium (mmol/l) 2.7 3.5–4.6 Chloride (mmol/l) 82 98–110
TCO2 (mmol/l) 40 22–34
BLOOD SMEAR EVALUATION
total protein (normally at 65 - 76)
78 is a result that shows higher than normal, increases in conditions of abnormally increased protein production (inflammation) dehydration, bone marrow disorders albumin (protein in blood plasma) (normally at 23 - 39)
42 is a result that shows higher than normal, which results in excess albumin.
kidney failure, kidney stones, urinary tract infections, blockage of blood flow creatinine (normally at 61 - 133)
184.5 is a result that shows higher than normal, which results in the kidneys not working properly (kidney disease including: kidney infection, kidney failure and chronic disease)
potassium (normally at 3.5 - 4.6)
2.7 is a result that shows lower than normal, which results, the body is exposed to hypokalemia
chloride (normally at 98-110)
82 is a result that shows lower than normal, which causes dehydration, loss of appetite, weight loss
TCO2 (normally at 22-34)
40 is a result that shows higher than normal, which causes carbon monoxide poisoning in some cases leading to death
What is your assessment of these findings and the physiological bases for them?
The ‘ping’ noted on auscultation with percussion and abdominal distension is consistent with abomasadisplacement resulting in partial anorexia and decreased milk production. The increase in RBCs, haemoglobin, haematocrit, total protein and albumin all support the presence of dehydration. Dehydration is suggested by partial anorexia and removal of the abomasal reflux. The neutrophilia and increased fibrinogen support the presence of inflammation. The increased creatinine may be due to pre-renal (dehydration), renal or post-renal conditions. Urinalysis and measurement of USG is recommended to help determine if conditions other than dehydration may be contributing.The hypokalaemia may be due to decreased intracellu-lar potassium because of partial anorexia, loss of K+-rich fluid in the abomasal reflux and/or metabolic alkalosis (see below).
What is your assessment of these findings and the physiological bases for them?
The hypochloraemia is likely due to chloride sequestration in the abomasum and loss of chloride with removal of the reflux fluid. It is likely to be further com- pounded by an alkalosis.The increased TCO2 is consistent with metabolic alka- losis. The abomasum normally secretes large amounts of HCl for digestion and this is neutralised by bicarbo-nate secretion in the duodenum stimulated by passage of a food bolus from the abomasum into the duodenum. With abomasal displacement, the abomasum is func-tionally obstructed, resulting in sequestration of H+, Cl−- and K+-containing fluids. K+ is further depleted by decreased food intake. Without ingesta passing into the intestine, bicarbonate is retained and metabolic alkalosis results.
What is your diagnosis?
Displaced abomasum with resulting metabolic alkalosis, hypokalaemia and hypochloraemia.
What might you expect to find in the urine, and why?
A paradoxical aciduria is expected in the urine. In response to dehydration, increased aldosterone secretion will stimulate Na+ resorption and retention of water in the kidney. Usually Cl− is absorbed with Na+, but with concurrent hypochloraemia, HCO3− is absorbed to maintain electroneutrality and the urine becomes more acidic.
Na+ can also be absorbed in exchange with K+ or H+. With hypokalaemia, H+ is exchanged for Na+, further contributing to the acidic urine.Urine chloride concentration is expected to be low (<10 mmol/l) owing to the hypochloraemia.
What treatment is needed?
Treatment is aimed at correction of the abomasal displacement and abomasopexy. Correction of serum Cl− and K+ levels with fluid therapy is needed to help resolve the dehydration, metabolic alkalosis and paradoxical aciduria.
