Clinical Pathology Homework #6 Key
Case 1. Boomer
Boomer has a normal CBC except for 1+ echinocytes, which are likely related to
electrolyte abnormalities or are artifactual.
Serum biochemical profile
Azotemia with hyperphosphatemia and hypermagnesemia: Boomer’s azotemia has a
pre-renal component due to the dehydration noted on physical examination. There is
also likely a post-renal component given the history of abdominal trauma and the
abdominal distension and fluid wave. The abdominal fluid analysis could be consistent
with a uroabdomen, however a fluid creatinine measurement is required for
confirmation. The less than optimally concentrated urine indicates a renal component to
the azotemia, however this may be due to medullary washout or other reversible factors
external to the kidney.
Panhyperproteinemia is due to dehydration without concurrent protein losses.
The hyponatremia (-21) and hypochloridemia (-25) are relatively proportional, although
the chloride is a bit lower which is attributed to vomiting. These electrolytes are primarily
low due to the retention of urine with a dilutional effect on serum Na and Cl. The
potassium is elevated due to failure of elimination of urine from the body in adequate
amounts. There are currently no acid base abnormalities noted on inspection of the
bicarbonate and anion gap, which support relatively equivalent changes in Na and Cl.
Decreased ALT is not significant
Hyperglycemia is due to stress.
Abdominal fluid is consistent with mild suppurative inflammation, which could be related
to the incident of trauma and the chemical irritation of uroabdoment. Abdominal fluid
creatinine is recommended.
Urinalysis: see azotemia section, there is some blood in the sample, likely related to
trauma or catheterization.
Summary:
Pre, renal, and post-renal azotemia
Dehydration
Electrolyte and abdominal fluid abnormalities consistent with uroabdomen
Diagnosis: Uroabdomen due to trauma
Additional tests
Abdominal fluid creatinine
Imaging or straight to abdominal explore
Serial chemistry and UA to establish resolution of renal azotemia
Case outcome and summary:
Boomer went to surgery and an abdominal exploratory revealed two small tears near
the apex of the bladder, which is why he was still able to pass some urine. The dead
tissue around the tears was removed and the bladder was repaired. No other
abnormalities were found. Boomer was monitored overnight in ICU and discharge to the
owner on severe activity restriction.
Case 2: Cheese
CBC
Cheese has a lymphocytosis with morphologic evidence of atypia. Consider monitoring
and testing for BLV
Cheese has a relative polycythemia associated with dehydration described on clinical
examination.
Hyperfibrinogenemia suggests inflammation despite the neutrophil and band numbers
that are within the reference intervals.
Serum biochemical profile
There is a mild azotemia that is likely pre-renal based on the dehydration, a urine
specific gravity is required for definitive classification.
Hypocalcemia is attributed to the anorexia and possibly compounded by milk
production, although the change is currently mild and it would be late in the lactation
cycle for milk fever.
There is very mild hyponatremia (-1) with a disproportional hypochloridemia (-23) and
hypokalemia. The significance of the hyponatremia is questionable (milk loss?),
however the change in chloride is interpreted to be associated with absomasal stasis or
blockage. The low potassium could be the result of anorexia, although the alkalosis
may result in intracellular translocation of potassium in exchange for hydrogen ions to
buffer the alkalosis.
The anion gap is low, which is often attributed to hypoalbuminia, however in this case
the albumin is normal.
Hyperglycemia is due to stress
Summary
Lymphocytosis, rule out BLV/lymphoma
Inflammation and dehydration
Pre-renal azotemia
Metabolic alkalosis due to abomasal stasis/blockage
Hypocalcemia (diet?)
Differential diagnosis:
Displaced abomasums/abomasal stasis +/- BLV lymphoma
Case summary and outcome
Exploratory laparotomy revealed mild intestinal thickening, a firm rumen, and a mildly
distended cecum. The cause of the clinical presentation was not determined. Clinical
pathology strongly recommended monitoring of CBCs and evaluation of the patient for
BLV/lymphoma.
Case 3: Did It
CBC
Leukopenia with neutropenia, a degenerative left shift and toxic change indicative of
acute/overwhelming inflammation and corticosteroid effects. (2 pts)
Relative polycythemia due to probable dehydration (1 pt)
Mild to moderate thrombocytopenia-rule out DIC given the history and leukogram (1 pt)
Serum biochemical profile
Azotemia and hyperphosphatemia. Pre-renal azotemia supported by leukokogram,
reddish mucous membranes, and relative polycythemia. Renal azotemia supported by
less than optimally concentrated urine. Horses with colic may be predisposed to renal
complications due to hypoperfusion +/- the use of potentially renotoxic medications
while dehydrated such as nonsteroidal anti-inflammatories and aminoglycoside
antibiotics. The history of fluid administration might cause concern for a cause of
reduced USG, however we are a few days away from that and it is unlikely to be a
significant factor at this time. (3 pts)
Hypocalcemia is attributed in part to the hypoalbuminemia and decreased protein bound
calcium, however colic is associated with hypocalcemia in some cases, possibly due to
anorexia/decreased intestinal absorption. (1 pt)
Hypokalemia is caused by anorexia in combination with gastrointestinal losses and
increased renal wastage if the patient is polyuric due to renal dysfunction (2 pts) .
The bicarbonate is within reference intervals, however the mildly increased anion gap in
this clinical context suggests a developing metabolic acidosis, likely uremic and/or lactic
(1 pt).
Hyperbilirubinemia is hepatic and associated with anorexia and sepsis (2 pts).
Increased ALP is associated with colic, possibly due to intestinal source of enzyme (1
pt).
Increased AST and CK with normal SDH and GGT suggest muscle damage, which is in
this case likely iatrogenic or associated with poor tissue perfusion (2 pts).
Summary (2 pts)
Inflammation/sepsis
Dehydration
Pre renal and renal azotemia
Mild uremic/lactic acidosis
Muscle damage
Hepatic cholestasis due to sepsis and anorexia
DDX (2 pts)
Colic complicated by sepsis and possible renal failure
Additional tests (1.5 pts)
Abdominal fluid analysis
Full UA
Full coagulation profile
Repeat CBC, profile, UA to monitor sepsis, coagulation, and renal function
Palpation +/- abdominal imaging (US)
Blood or abdominal fluid cultures could be considered
Case summary and outcome
Did It was treated with IV fluids, antibiotics, anti-inflammatory medications, hoof support
and icing. The horse was stable but then become more painful and refractory to
treatment after about 24 hours. Humane euthanasia was performed. Necropsy revealed
severe segmental hemorrhagic infarction of the left dorsal colon, multifocal moderate
infarction of the kidneys, and necrotizing laminitis with stratum epidermis-laminar corium
separation.