A 4-year-old female Rottweiler named Twice is admitted on an emergency basis to your hospital with an owner's complaint of
substantial depression, anorexia and vomiting of three days' duration.
The dog is "dominant" and has a history of trying to eat anything containing food, including the food containers and wrappings.
The owner stated that the dog had previous episodes of gastrointestinal episodes (vomiting and sometimes diarrhea) over the
past several months, but seemed to be "OK" prior to the current illness. The owners do not know anything about the volume
of urine voided when "Twice" is allowed outside to "do her business." She has not had any "urination accidents" in the house.
The owners suspect that their dog may have been poisoned with adulterated food placed in their yard by an elderly irate neighbor
who has complained about "Twice" going "number 2" in his flower garden.
Physical exam reveals the dog is depressed and dehydrated (10 percent loss of body weight). Her body condition is normal.
Respiratory rate is normal; heart rate is 95 per minute. The quality of the femoral pulse is difficult to evaluate. The mucous
membranes are tacky; the capillary refill time is 2.0 seconds. Rectal temperature is 102??F. Palpation of the left kidney
revealed that it is normal in size and shape. The right kidney cannot be palpated. The urinary bladder is partially filled
with urine, fluctuant and nonpainful.
You immediately begin aggressive intravenous therapy with lactated Ringer's solution to correct the fluid deficit. You also
administer antibiotics and glucocorticoids parenterally. About 15 minutes after initiating symptomatic therapy, samples of
urine and blood are collected for immediate (STAT) analysis at a nearby laboratory.
Ultrasonography of the abdomen reveals no obvious abnormalities; however, you do not consider yourself as an expert in interpreting
The best interpretation of these observations is:
a. The dog probably has hypoadrenocorticism associated with vomiting, impaired renal conservation of sodium and water and prerenal
b. The dog has primary GI disease due to eating foreign material which in turn is causing vomiting. The azotemia is of prerenal
origin; the specific gravity is <1.030 as a result of fluid therapy.
c. The dog probably has acute pancreatitis that at first caused prerenal azotemia. However, persistent fluid loss from vomiting
resulted in ischemia-induced primary renal failure.
d. The dog has some form of acute primary renal failure associated with vomiting, dehydration, an impaired ability to concentrate
urine, azotemia and hyperamylasemia. At least a component of the azotemia is prerenal in origin.
e. The dog has a disease characterized by vomiting, dehydration, anorexia, depression, neutrophilia, azotemia, hyperamylasemia
and hyponatremia. It is not possible to localize the vomiting as a primary or secondary gastrointestinal abnormality. Although
it is not possible to determine if the azotemia is prerenal or primary renal, at least part of the azotemia is prerenal in
origin. There is evidence of hemoconcentration (increased PCV and increased serum protein concentration).
Why do you think the owners named the dog "Twice"?
Comments about answers:
Answer a-The dog has hypoadrenocorticism.
This diagnosis is over-stated, but hypoadrenocorticism cannot be ruled out. Why? This dog has several findings commonly associated
with hypoadrenocorticism including depression (~ 90% of cases), anorexia (~90%), vomiting (~75%), dehydration (~90%), azotemia
(~90%), hyponatremia (~80%), acidemia (~75%), apparent impaired urine concentrating capacity associated with dehydration (~50
%), and a previous history of intermittent gastointestinal signs. However, most dogs with symptomatic hypoadrenocorticism
are hyperkalemic (~95%), and their Na+/K+ ratio is less than 27 to 1 (~90%). Unfortunately, it is not possible to determine
the magnitude of change in serum potassium and sodium concentrations that occurred as a result of administration of intravenous
fluids and glucocorticoids to this dog.
Other laboratory findings (not detected in this dog) which may be associated with hypoadrenocorticism include polyuria and
polydipsia (~40% of cases), diarrhea (~40%), melena (~15%), hypothermia (~35%), bradycardia (~20%), hypochloremia ~50%), hypercalcemia
(~25%), hypoglycemia (~20%), nonregenerative anemia (~25%), eosinophilia (~20%), and lymphocytosis (~10%).
Hyponatremia associated with hypoadrenocorticism occurs when the magnitude of impaired adrenal secretion of mineralocorticoids
and/or glucocorticoids interferes with tubular reabsorption of sodium. The magnitude of hyponatremia may be exacerbated by
vomiting and diarrhea. Likewise, hyperkalemia and acidosis associated with hypoadrenocorticism occurs when the magnitude of
impaired adrenal secretion of mineralocorticoids and/or glucocorticoids interferes with tubular secretion of excess potassium
and hydrogen ions. The severity of the hyperkalemia may be exacerbated by extracellular movement of intracellular potassium
as a result of acidemia. The magnitude of acidemia may be exacerbated by poor tissue perfusion. Reduction in the magnitude
of hyperkalemia, hyponatremia and metabolic acidosis following appropriate fluid and glucocorticoid therapy is often dramatic.
Differentiation of primary acute oliguric renal failure from hypoadrenocorticisma
The azotemia associated with hypoadrenocorticism is typically prerenal in origin and occurs primarily as a result of hypovolemia
associated with hyponatremia. Unlike most disorders associated with prerenal azotemia, the urine specific gravity values of
dogs with hypoadrenocorticism is often (~50%) below 1.030. It is probable that this paradox is associated, at least in part,
with reduction in renal medullary sodium concentration that in turn interferes with the counter-current mechanism of urine
concentration. It may also be associated with solute diuresis induced by natriuresis. A high index of suspicion is required
to prevent confusion of hypoadrenocorticism and prerenal azotemia with oliguric renal failure (see comment to answer d) since
the clinical manifestations of these two disorders mimic each other.
A diagnosis of primary hypoadrenocorticism can be confirmed by detection of reduced serum cortisol concentration, and subnormal
response to administration of ACTH.
Caution: Treatment with most forms of glucocorticoids (except dexamathasone) will interfere with laboratory tests for cortisol
resulting in false increases in serum cortisol concentrations. Therefore, try to complete the ACTH stimulation test prior
to treatment with glucocorticoids.
Answer b- The dog has primary gastrointestinal disease
This conclusion is overstated; however, primary GI disease cannot be ruled out at this time. Why? Because of the unmeasured
effect of therapy on laboratory data. For example, it is possible that the azotemia occurred as a result of prerenal volume
depletion secondary to vomiting caused by a primary gastrointestinal disorder, and that the pretreatment specific gravity
value was >1.030. However, failure to collect a urine sample prior to administration of intravenous fluids precludes assessment
of whether the current urine specific value of 1.025 was the result of fluid therapy or the underlying disease(s). In addition,
the possibility of alteration of results of the CBC and serum biochemistry profile data by therapy precludes ruling out other
diseases (see comment for answers a, d and e).
Answer c- The dog has acute pancreatitis.
This conclusion is over-stated; however, acute cannot be ruled out at this time. The clinical signs could be consistent with
acute pancreatitis; however, azotemia associated with pancreatitis is usually associated prerenal in origin and therefore
would be expected to be associated with appropriately concentrated urine (SG = >1.030). Increases in serum amylase activity
are typical of acute pancreatitis in dogs; however, mild to moderate hyperamylasemia may also be associated with other diseases
including primary renal dysfunction and primary GI disease.
Alterations in laboratory test results that may occur in dogs following treatment with glucocorticoids.
One might expect to encounter a greater magnitude of hyperamylasemia if the three-day course of illness of this dog was associated
with acute pancreatitis. Exogenous glucocorticoids have been reported to decrease serum amylase activity. They may also exacerbate
lesions associated with pancreatitis. Evaluation of serum lipase concentration, serum trypsin-like immunoreactivity and/or
serial measurement of serum amylase values over the next few days would likely be of value.
Results of abdominal ultrasonography that may be associated with pancreatitis include peritoneal effusion in the region of
the pancreas and ileus of the proximal duodenum (these changes were not detected in this case).
Answer d- The dog has primary renal failure.
This conclusion is over-stated; however, primary renal failure cannot be ruled out. Since the dog is clinically dehydrated,
at least a component of the azotemia is prerenal in origin. However, it is not possible to determine if the inappropriately
low urine specific gravity was associated with impaired urine concentration and/or fluid therapy induced diuresis.
A high index of suspicion is required to prevent confusion of primary oliguric renal failure with hypoadrenocorticism since
the clinical manifestations of these two disorders mimic each other (Table 1; see comment to answer a).
Unlike the prerenal azotemia associated with hypoadrenocorticism that rapidly resolves following adequate fluid replacement,
the intrarenal component of primary renal failure will persist following restoration of fluid balance.
Answer e - The dog has a disease characterized by vomiting, dehydration, anorexia, depression, neutrophilia, azotemia, hyperamylasemia
This is the best interpretation. Why? Because recent treatment with intravenous fluids often induces substantial changes in
results of urinalysis (especially specific gravity values), CBCs and serum chemical profiles. Likewise, glucocorticoids can
have a profound effect on laboratory test results (Table 2). As a result, it is difficult to depend on the results of the
post-treatment laboratory data to help localize the vomiting in this dog as a primary GI disorder or a secondary GI disorder.
Likewise, it is difficult to localize the underlying cause(s) of azotemia.
Since the dog is clinically dehydrated, at least a portion of the azotemia is prerenal. However, it is not possible to determine
if the inappropriately low urine specific gravity was associated with impaired urine concentration and/or fluid therapy-induced
Key point: obtain pretreatment urine and blood samples for diagnostic tests whenever possible.
Why do you think the owners named the dog "Twice"? Answer: Because she wouldn't come when she was called once.