Solution for case 4


Tentative diagnosis: Azotemia due to chronic renal failure (CRF).


Further diagnostic tests:
* Abdominal radiography/ultrasound to demonstrate decreased size of kidneys.


* Urine creatinine:protein ratio.


* Renal biopsy (not commonly performed).


* Blood pressure to demonstrate hypertension.


Isosthenuria is a common finding in chronic renal failure when two thirds of the functioning nephrons are lost.


Azotemia is seen when at least three fourths of the functioning nephrons are lost. Azotemia presents with increased BUN, creatinine, GI, and neurological clinical signs. This patient’s presentation would suggest that she has lost at least three fourths of her functioning nephrons.


Predisposing factors for CRF are age, chronic obstruction, infection, heart failure, and tubular disease. A urine sample taken from this patient, via a cystocentesis, ruled out bacterial infection. Patient’s heart sounded normal on auscultation. The renal failure was attributed to her age.


Management of chronic renal failure is a multifactor process. Most importantly hydration and electrolytes must be maintained with in normal limits. An appropriate renal diet will be low in protein, phosphorous, and sodium. Some other factors which must be addressed in the management of chronic renal failure include anemia, proteinuria, and gastrointestinal processes.


Anemia is due to decreased production of erythropoietin by renal peritubular cells. The anemia could also be from blood loss via GI ulcers, or iatrogenic from blood draws. The anemia is non-regenerative normochromic normocytic.


Treatment of anemia with erythropoietin (EPO) is indicated when the PCV falls below 18% and the patient is showing clinical signs of anemia/hypoxia. Caution must be used with EPO since it is of human origin. Dogs can produce antibodies against it. In severe anemia requiring immediate relief of clinical signs a blood transfusion can be done.


Proteinurea is seen because glomeruli have been damaged enough to allow loss of protein and anti-thrombin III. This decreases oncotic pressure, leading to edema. The loss of anti-thrombin III causes coagulation issues. Many of these patients have pulmonary thromboembolism as a complication.


These patients can be treated with angiotensin converting enzyme inhibitors which decreases the pressure in the glomeruli by dilating the efferent renal artery. This decrease in pressure helps prevent loss of proteins into the urine. Canine patients with CRF and proteinuria tend to have a decreased survival.


GI ulcers and nausea and vomiting are the common clinical signs seen. Uremic toxins activate the chemoreceptor trigger zone which leads to the nausea and vomiting. These uremic toxins also increase gastrin production which increases hydrochloric acid production in the stomach, leading to GI ulcers.


These complications are treated by decreasing the uremic toxins via hydration; protecting the stomach by decreasing acid production, and controlling the nausea and vomiting by blocking the chemoreceptor trigger zone. Acid production can be decreased using histamine blockers or proton pump inhibitors. Sucralfate can be used to protect/coat ulcers. The nausea can be controlled with medication targeted at dopamine antagonism, serotonin, or neurokinin.


Treatment:
Hospitalize patient
– NPO
– Fluid diuresis to decrease azotemia
* * Maintenance: 60ml/kg/24 hours = 2100ml
* * Deficit (5%) = 1715ml
* * Total fluid/day = 3850ml (160ml/hr)
– Decrease gastric acid and control N/V
* * Famotidine 20mg Q12 hours
* * Anti-emetic - Cerenia (maropitant citrate)
– Re-evaluate
* * BUN, Creatinine, Phosphorus every 48 hours
* * PCV and TP daily

The patient remained azotemic.
– After 3 days, fluids increased to 250ml/hr during the day and 160ml/hr during the evening.
– NPO
– Continue H2 blocker and Cerenia
– Continue to monitor BUN, SCr, TP, PCV, Phosphorus
The patient did not improve and was euthanized on consultation with owner.


See following Links for more info on CRF:


http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/130603.htm


http://courses.vetmed.wsu.edu/vm552/urogenital/crf.htm


http://www.marvistavet.com/html/body_chronic_renal_failure.html


http://www.felinecrf.com/what0.htm
Posted by at No comments:
Labels:

Case 4

Presentation:
A 12 year old spayed female Labrador was presented to AcaseAweek Clinic with one week history of vomiting, decreased appetite and lethargy. Bad breath of the pet was also a complaint. The patient was brought to clinic 4 month back for ehrlichia and mild azotemia. She is currently on Hill’s k/d diet.
Physical exam:
  • Weight: 34.8 kg
  • Temperature: 100.7
  • Pulse: 136
  • Respiration rate: 28
  • Mucus membranes: pale
  • Capillary refill time: > 2 seconds.
  • Dehydration: ~5%
  • Abdomen was tender upon palpation.
Lab tests: (Reference Values)
  • BUN: 112 mg/dl
  • Creatinine: >13.6 mg/dl
  • Phosphorous: 16.1
  • PCV: 25%
  • USG: 1.011
  • TP: 6.4 mg/dl
  • Albumin: 2.7 mg/dl
  • Non-regenerative anemia was also noted.



What is your tentative diagnosis?
Give differentials for your diagnosis.
What further diagnostic test(s) will be performed to confirm the tentative diagnosis?
How will you treat and manage this case?

Solution for this case
Posted by at 1 comment:

Solution for case 3


Diagnosis:
A 4Dx snap test was performed and was positive for Anaplasma. Normal clinical signs seen with Anaplasma are fever, lymphadenopathy, splenomegaly, weight loss with a history of tick infestation. Lab finding are normally thrombocytopenia, non-regenerative anemia and decrease in white blood cells, hyperproteinemia, hyperglobulinemia, hypoalbuminemia, and increase ALT. Lymphadenopathy and polyarthritis is sometimes seen and petechial hemorrhages or epistaxis due to the thrombocytopenia.

The snap 4DX test identifies both IgM (acute exposure) and IgG (chronic exposure) antibody responses to Anaplasma platys (previously known as Ehrlichia platys) and it infects the platelets leading to thrombocytopenia.

Dogs become infected with Anaplasma spp. when a feeding tick inoculates the organisms. The rickettsia enters the granulocytes, platelets, or macrophages, where it survives and multiplies, and spreads throughout the body. Anaplasma is maintained in a tick vector/vertebrate reservoir host system. 

Other diagnostic tests:
Urinanalysis, bone marrow or lymph node biopsy, abdominal radiographs. We can also go for blood smear stained with Giemsa stain. PCR has also been developed for this condition. 

Differentials:
Rocky mountain spotted fever, multiple myeloma, chronic lymphocytic leukemia, lymphoma, ehrlichia and immune mediated thrombocytopenia. But, since this patient was positive for Anaplasma on the 4Dx snap test, the differentials can be ruled out.

Treatment:
Anaplasma species infections in dogs usually respond to treatment with doxycycline, a treatment regimen of 10mg/kg for 28 days is currently recommended. This patient was admitted to the clinic and IV LRS fluids were given at 180 ml/hr. He was also given doxycycline at 200 mg PO BID for 28 days. This will help clear the infection, but some side effects you must watch out for are nausea, diarrhea, vomiting, upset stomach, loss of appetite, dysphagia, and a possible hypersensitivity to the drug.

Protective immunity does not develop and re-infection may occur following treatment, which would require additional courses of therapy. Vaccines are not available to prevent infections. Therefore, control and prevention of ticks is the key.  Brown dog ticks transmit this infection.

Click here to see image of Anaplasma morula in a Neutrophil and diagnostics.

Click here for a case report of Anaplasma in young dog. 

Click here for more description about Anaplasma.
Posted by at 1 comment:
Labels:

Case 3

Presentation:
A 5 year old castrated male Rottweiler Labrador mix canine was presented at AcaseAweek Clinic for lethargy and inappetence for the past 4 days. He was still drinking water, and urinating normally. The diet consists of adult dry food, Alpo, of which he is eating less of. He has also lost a lot of weight recently.  Vaccinations were giving 12 days ago, and the dog is currently on ivermectin.
Physical Exam:
The patient weighed 20 kg (44 lbs) on physical exam, he was lethargic. His temperature was 103.2, pulse rate was 100 and respiration rate was 40. Mucus membranes were pink, and CRT was less than 2 seconds.  On physical exam there were enlarged pre-scapular and popliteal lymph nodes.  All other systems were within normal limits.
CBC and Blood Chemistry:
On general blood chemistry, all the values fell within normal limits except for ALT which was slightly increased, 166 (10-100).         The complete blood count revealed a hematocrit of 28.1 (37.0 – 55.0), hemoglobin of 10.2 (12.0 – 18.0), granulocytes of 3.1 (3.3 – 12.0), neutrophils of 1 (2.8 – 10.5), eosinophils of 2.1 (0.5 - 1.5) and platelets of 36 (175 – 500).

What is your tentative diagnosis?
Give differentials for your diagnosis.
What further diagnostic test(s) will be performed to confirm the tentative diagnosis?
How will you treat and manage this case?

Solution to this case
Posted by at 1 comment:

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:



Posted by at 3 comments:
Labels:

Case 2

A 13 year old, female spayed, mixed breed dog was presented to AcaseAweek Clinic with history of collapse, depression, lethargy and vomiting 3 times the night before presentation. The patient had been anorexic for the past 2 days and appeared healthy previously. The patient lives mostly inside and her owner reported no possibility of accidental ingestion of foreign body or chemicals. Her vaccination status is current and she is on heartworm preventative. She was treated for Ehrlichiosis with doxycycline two months back.

Physical Exam:
Remarkable weight loss and muscle atrophy.
T: 98
P: 88
R: 44
MM: pale pink
CRT> 2 sec

Cardiovascular: murmur, cardiac arrhythmia, pulse deficit.
Respiratory: lungs sound clear
Abdomen: distended, positive succession, moderately painful

CBC/Cytology:
PCV: 23% [37-55]
WBC: 28.9 x103/μL [6-16.9]
Mature Neutrophils: 26.3 x103/μL [3.3-12]
Band Neutrophils: 0.6 x103/μL
Lymphocytes: 0.3 x103/μL
NRBC: 0.9 x103/μL
Smear: Platelets: 1-4/hpf
RBC morph: marked polychromasia, moderate anisocytosis

Biochemistry:
ALKP: 267 U/L [23-212]
ALT: 164 U/L [10-100]
AMYL: 2490 U/L [500-1500]
BUN: 130 mg/dL [7-27]
CREA: 6.1 mg/dL [0.5-1.8]
PHOS: >16.1 mg/dL [2.5-6.8]
TBIL: 1.4 mg/dL [0-0.9]

Urinalysis:
Bilirubin: ++
SG: 1.013
Blood: +++
pH: 5.0
Protein: +

Abdominocentesis:10 mL fluid was withdrawn.
Abdominal Fluid Analysis/Cytology:
Color: red
Turbidity: 3+
Protein: 7.2 g/dL
PCV: 23%
Smear: many RBCs, neutrophils and macrophages, moderate lymphocytes, almost no platelets seen, few reactive mesothelial cells.
What will be your tentative and differential diagnosis?
What further diagnostic test(s) you will perform to confirm your diagnosis?
What will be your treatment plan(s)?


Solution to this case
Posted by at 5 comments:

Soluton for case 1


Diagnosis: Tentative diagnosis is hyperadrenocorticism (cushing disease) based on the typical presenting signs. Click here to see image of the case from merck vet manual site.

DDx: Hypothyroidism, diabetes mellitus, renal diseases and other causes of PU/PD.

Diagnostic tests:
Low Dose Dexamethasone Suppression Test (LDDS):
Basal cortisol: 5.1 µg/dL
4-hour post test: 2.2 µg/dL
8-hour post test: 6.5 µg/dL [<1.0>
These values indicate the hyperadrenocorticism, but to differentiate the adrenal tumor from pituitary dependent hyperadrenocorticism (PDH) we need to perform HDDS test.
High Dose Dexamethasone Suppression Test (HDDS):
Basal cortisol: 4.8 µg/dL
8-hours post test: 0.8 µg/dL [<1.0>
(The ACTH stimulation test is a screening test for diagnosis of hyperadrenocorticism, but was not done in this case.)


Definitive diagnosis: Pituitary dependent hypheradrenocorticism.


Treatment:
Mitotane is a commonly used drug in hyperadrenocorticism. Ketoconazole can be used in dogs which are unable to tolerate mitotane at the required dose.
This patient was started on 60 mg of Trilostane (Vetoryl®) once daily and his status will be monitored with an ACTH stimulation test in 1-2 weeks time. If he has still not achieved a hypoadrenal response at this time or has achieved a response but is still exhibiting clinical signs, we can consider increasing his dose or increasing to a BID regime. After achieving therapeutic stability, the patient should have an ACTH stimulation test every 3-4 months to monitor cortisol response to therapy.
Trilostane tends to be better tolerated by dogs. Trilostane is a competitive inhibitor of 3-β-hydroxysteroid dehydrogenase. This enzyme mediates the conversion of pregnenolone to progesterone in the adrenal gland, with the net effect being inhibition of cortisol production.
With PDH treatment, it is important to achieve a hypoadrenal response but avoid the complete adrenal suppression to a point that glucocorticoids and mineralocorticoids are deficient. Specifically, mineralocorticoid deficieny and hypoaldosteronism have the deleterious effects of cardiac disturbances (due to hyperkalemia and hyponatremia), hypovolemia and hypotension.



Posted by at No comments:
Labels: , ,

Case 1

A 9-year old neutured male Wirehaired Dachsund was presented to AcaseAweek Clinic with history of lethargy, generalized bilateral symmetrical alopecia of increasing severity, potbellied appearance and complaint of polyuria/polydipsia for one month duration. The patient is current on vaccinations, heartworm preventative, de-worming, and flea and tick control.

Physical Exam:
T: 102.8
P: 100
R: 32
MM: pink/moist
CRT <2

Bilateral symmetrical alopecia, rat-tail, comedones over ventrum, bruising on left lateral thorax. Potbellied abdomen, weakness, muscle wasting (esp. semitendinous, semimembranous muscles).

CBC and Biochemistry: all values within reference range

Urinalysis:
Color : pale yellow
pH : 8.0
SG (refractometer): 1.015, SG (dipstick): 1.010 [1.015-1.060]
Protein (dipstick): 2 + (100-300 mg/dL) [negative-trace]
Blood (Dip stick): Moderate
Sediment exam: small number of cocci


What will be your tentative and differential diagnosis?
What further diagnostic test(s) you will perform to confirm your diagnosis?
What will be your treatment plan(s)?

Post your answers in the comments section of this site.

Posted by at 6 comments:
Subscribe to: Posts (Atom)