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Friday, November 14, 2008
Solution for case 2

Problem List:Hemoperitoneum
Cardiac arrhythmia and murmur
Poor peripheral perfusion
Mild anemia with marked regeneration
Moderate leukocytosis due to moderate neutrophilia
Mild lymphopenia
Mild thrombocytopenia
Mild↑ALKP, ALT
Mild↑amylase
Mild↑total bilirubin
Marked↑BUN and creatinine
Marked↑phosphate
Isosthenuria (single reading)
Moderate hematuria and bilirubinuria
Mild proteinuria
Anorexia, depression, lethargy
Vomiting
Marked weight loss and muscle atrophy


Primary problems on this patient are hemoperitoneum and acute renal failure.


Differentials for hemoperitoneumHemangiosarcoma (spleen/liver)
Coagulopathy (rodenticide)
Abdominal trauma


Differentials for acute renal failure
Ischemia due to hypovolemia, hypotension, shock or DIC
Nephrotoxicity (exogenous or endogenous toxins)
Immune mediated glomerulonephritis
Infectious (e.g. Leptospirosis, pyelonephritis)


Regarding the differentials for hemoperitoneum, hemangiosarcoma is the most likely. Hemangiosarcoma is most common in middle-aged to older dogs. Marked weight loss and muscle atrophy noted on physical exam may be suggestive of neoplasia.

The patient’s history and clinical signs are consistent with sudden rupture of splenic hemangiosarcoma causing hemorrhagic effusion into the abdominal cavity. Dogs with ruptured splenic hemangiosarcoma will commonly have abdominal enlargement due to hemoabdomen, pallor and hypotension. Poor peripheral perfusion and hypovolemia are evidenced by increased CRT and pulse deficit on physical exam. CBC with ruptured splenic hemangiosarcoma typically shows evidence of a recent bleed (marked regeneration with a mild decrease in PCV). Leukocytosis due to mature neutrophilia and thrombocytopenia are common CBC abnormalities noted in dogs with hemangiosarcoma of the spleen or liver. Mild lymphopenia may be a ‘stress’ response. High liver enzyme activity may be seen with hemangiosarcoma involving the liver. Mildly elevated liver enzymes are more likely pre-hepatic in origin; secondary to hypovolemia, hypotension and poor perfusion of hepatocytes. The icterus is most likely hepatic in origin, due to impaired uptake and conjugation by the underperfused liver. Mild pancreatic amylase increase is likely also secondary to decreased perfusion.

Regarding other differentials for hemoperitoneium, coagulopathy associated with rodenticide toxicity is less likely than hemangiosarcoma since there was not evidence of intrathoracic bleeding. With hemothorax, clinical signs of coughing, thoracic pain and/or dyspnea would be expected. There was also no history of possible ingestion. Abdominal trauma was ruled out on lack of history or any other evidence of a traumatic event.

This patient’s remaining problems are consistent with acute renal failure (ARF). The patient demonstrated a marked azotemia and hyperphosphatemia due to build up of nonprotein nitrogenous waste products and phosphate which are normally removed by the kidneys. Hypovolemia indicates that there is at least a partial pre-renal component to the azotemia. However if her azotemia was strictly pre-renal with tubular function intact, urine should be concentrated (SG >1.030) in the face of reduced renal perfusion. Patient’s urine SG of 1.013 is in the isosthenuric range, implying that kidneys are unable to adequately concentrate urine despite azotemia. Unlike pre-renal azotemia, renal azotemia is usually irreversible and is caused by extensive morphological or functional glomerular lesions with a loss of more than 75% of functional nephrons. On urinalysis, proteinuria and hematuria are supportive of glomerular damage.

Clinical signs of ARF are mostly caused by severe uremia and include lethargy, vomiting, anorexia and dehydration. The rapid build up of uremic toxins often causes the animal to become profoundly systemically unwell. Severe metabolic derangements are common, particularly hyperkalemia and metabolic acidosis. Electrolytes were not run on this patient, however hyperkalemia likely contributed to the arrhythmia noted on physical exam and being non-tachycardic despite being hypovolemic/hypotensive. Diagnosis of ARF relies on evidence of a sudden elevation in urea and creatinine, but definitive diagnosis would require renal biopsy or post mortem.

The cause of ARF is debatable. The most likely scenario is that this patient had a splenic hemangiosarcoma which ruptured 2-3 days before she was presented. Subsequent uncorrected hypovolemia and hypotension caused secondary insult to abdominal organs and renal failure due to prolonged ischemia. Multiple factors may have contributed to acute renal failure, and it is possible that patient had some degree of renal insufficiency prior to the ischemic insult which merely pushed her over the edge.


Emergency treatment:
IV catheter (20 G) – L cephalic vein
LRS @ 40 mL/hour (maintenance)
Urinary catheter – closed system


Owner did not want any other diagnostic tests performed and requested euthanasia and necropsy.


Further diagnostics (if patient was not euthanized):
Coagulation panel (OSPT to rule out rodenticide toxicity)
Abdominal ultrasound (hemangiosarcoma search)
Cardiac ultrasound (splenic HSA – often concurrent R atrium involvement)
Electrolyte panel (potassium level) → correct imbalances
Repeat urinalysis (confirm isosthenuria, monitor ARF)


Treatment of hemagiosarcoma is supportive and anti-neoplastic drugs. However, prognosis is Grave.


Necropsy findings:
About 500 ml of fluid was reported in abdominal cavity. Ruptured splenic mass of about 12 cm in size was also found and submitted for histopathology. Histopathology confirmed hemangiosarcoma.
Follow these two links for more information about the hemangiosarcomas:



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posted by Dr Banga's Websites @ 12:00 AM  
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