Signalment and history : 11y male cat, Lethargy and polydipsia. 1 month ago PCV was 38%
CBC::
PCV:13 (25-45)
RBC 1.55 (5-11)
Hb 4 (8-15)
MCV:84 (39-50)
MCHC 31 (33-37)
REtic 155,000 (0-60,000)
NCC : 20.6 (5.5-19.5)
Metas:0.4 (0)
Bands 0.8 (0-0.3)
Segs 9.9 (2.5-12.5)
Lymphs: 1.4 (1.5-7)
Monos 3.1 (0-0.8)
Eos:0.2 (0-1.5)
nRBC: 4.8 (0)
plt : Adequate
TP 8.9 (6-8.5)
biochem
Glu:249 (67-124)
BUN 96 (17-32)
Creat 6.6 (0.9-2.1)
Ca 10.2 (8.5-11)
Phos 7.9 (3.3-7.8)
TP 8.4 (5.9-8.1)
Alb:3.3 (2.3-3.9)
Glob: 5.1 (2.9-4.4)
T. bili 0.3 (0-0.3)
Chol 386 (60-220)
ALT 53 (30-100)
ALP 19 (6-106)
Na 150 (146-160)
K 4.9 (3.7-5.4)
CL 127 (112-129)
tCO2 10 (14-23)
AG ?? (10-27)
Calculte Osmolality ??? (290-310)
UA
color : yellow/cloudy
SG: 1.020
Pt : neg
Glu:2+
bili, blood, ketones are all neg
PH 5
WBC 6-8
RBC 1-2
Epi 1-3 tranitional
No casts, crystals bacteira
other : fat
這應該也算簡單的
I will be away from sat to next sunday. SEe you guys later : )
13 則留言:
Dear Cindy, yes, this is not a very challenging case. But it's quite interesting to collaborate the clinical findings and assumption into the laboratory interpretation.
I'll divide my findings and impression to three parts.
1. Calculation of AG and Osmolality
Anion Gap = (Sodium + Potassium) - (Chloride + Total Carbon Dioxide)
= 150 + 4.9 - (127 + 10)
= 17.9
Osmolality = 1.86(150 + 4.9) + 249/18 + 96/2.8 + 9
= 288.14 + 13.83 + 34.29 + 9
= 345.26
2. Summarising the laboratory findings.
CBC result
a. Severe macrocytic hypochromic / normochromic anaemia
b. Mild leucocytosis - mild left shift & monocytosis.
c. Increased nucleated RBC
d. Marked reticulocytosis (Retic % = 10)
Total reticulocyte counts could not be interpreted as its canine counterpart. No aggregate and punctate retic counts are provided in this case. However, in sight of marked reticulocytosis, macrocytosis and increased nRBC both presenting, I'd like to classify this should be regenerative anaemia.
Biochemistry
a. Severe azotaemia
b. mild to moderate hyperglycaemia
c. Increased osmolality
d. Hypercholestrolaemia
e. Mild hyperproteinaemia and hyperglobulinaemia
f. Decreased total carbon dioxide
Urinalysis
a. Mild hyperglycaemia
b. Isothenuric urine
3. Discussion
a. The most common differential diagnosis of polydipsia in cats are chronic renal diseases, DM, hyperthyroidism and pyometra. You may find other less common causes like DI, cushingnoids, etc in any internal medicine text. This is a male cat, and lethargy plus anaemia is not the common findings of hyperthyroidism. Interestingly, hyperthyroidism is NOT COMMON here but it should be one of the most common geriatric feline diseases in Western countries. I still recommend routine total T4 test for any senior cats.
b. It should be no doubts that chronic renal insufficiency and diabetes are the major differentials. Stress hyperglycaemia can not be ruled out and I ever saw blood glucose 350 something in stressed kittens!
Hypercholesterolaemia should be interpreted cautiously and personally I don't give a damn on a non-fasting sample. So elevated cholesterol level in this case DO NOT SUPPORT diabetes. I'd recommend urinalysis on specimen from home collection. Fructosamine can be used to differentiate stress glycaemia and DM as well.
c. For any cases with azotaemia plus urine SG < 1.035, it's surely abnormal and indicate renal problem. Amazingly urine protein is normal! One may wonder normally CRF cats have non-regenerated anaemia rather than regenerative. It's not absolutely true - uraemic gastritis can cause gastric bleeding and so haemorrhagic anaemia result. PCV was declining from normal range to severe anaemia within a month. A combination of decreased erythropoietin production, shortened red cell survival, gastrointestinal blood loss, and the effects of uraemic toxins such as parathyroid hormone on erythropoiesis cause this dramatically worsen anaemia.
e. Mild leucocytosis - mild left shift & monocytosis can be found in any haemorrhagic, chronic inflammatory and granulomatous diseases. I generally don't stuff around with these perimeters at this scale.
f. BEWARE OF diabetic nephropathy! This complication can mimic renal azotaemia and these two problems can not be differentiated without renal biopsy. Even under histopathology, there are many overlapping features and drive us crazy for diagnosis confirmation.
So, I don't recommend renal biopsy in these patients. And the affected cats are treated as renal insufficiency ones.
Oh... you should give some time for our junior "veterinaries". You are so experienced already.
To studuents: However, I think all the students can also do your own practice tho. ALso, you can also critic the findings Cornwell made. hahah....
Questions for students:
1. what is the different when we count cat vs dog retic? And, what is the difference between aggregates vs punctates in cats?
2. what is the differents between NCC and WBC?
3. What is the specific gravity we use to qualify as "isostheuria"?
4. What is other tests you will like to run, according to CBC findings??
Big hint: acute anemia, strong regenerative response and active inflammatory leukogram.
有點問題想要請問cornwell學長/姐
就是講到貧血的部分 為什麼會覺得CRF可能是再生性貧血?我知道CRF會造成貧血的原因一是產生EPO的細胞被破壞 二是尿毒症使RBC壽命減短和抑制紅血球生成 三是GI出血
我在想如果有CRF 就算只有GI出血造成貧血誘使骨髓反應 但身體儲存的反應能力足夠到產生這麼多的reticulocyte嗎?而且出血性的貧血 很多東西都流失掉不是更不利於再生嘛??
還是說因為是一個月內快速的進展 所以骨髓內之前留著的reticulocyte然後現在放出來這樣嗎?
I am 學長. Sorry I can't type Chinese freely in the office..sucks in Changjei input..
The statement "CRF可能是再生性貧血" is not true. The major findings of this case are regenerative anaemia, azotaemia and hyperglycaemia. From the RBC indices and reticulocytes, you know it's regenerative. Regenerative anaemia in cats can be caused by chronic blood loss like GI ulcer or any neoplasia or haemolysis, like immune mediated haemolytic anaemia, mycoplasmosis or heinz body anaemia. Without detailed history and further tests we just estimate the regenerative anaemia MAY BE due to uraemic gastritis.
Gastric ulcer may also due to DM related chronic pancreatitis. Diagnosing feline pancreatitis can be very challenging. fPL and ultrasonography by experienced sonographer are RELATIVELY reliable tests apart from biopsy.
You have to note that GI blood loss is an example of INTERNAL BLEEDING. The characteristics of internal bleedings are:
1. Iron supplies are conserved
2. Plasma protein resorption from the site of haemorrhage
So this statement "出血性的貧血 很多東西都流失掉不是更不利於再生嘛" should be further evaluated.
Moreover, if no further history or specific findings provided, I won't suspect AIHA in cats. First of all, no haemolysis were seen. Second, it's extremely rare for us practitioner to think of. I remember one case of feline AIHA throughout 7 years of practice.
我懂了!!!謝謝學長
1. GI bleeding supposed to be considered as external blood loss --> Iron def, low pt (so both did not fit our case)
2. Here we just use absolute retic number to evaluate regenerative, but not %. 155,000 in cat is consider as slight to moderate regenerative resposne. (I assumed this is aggregate retic count)
3. NCC is the count for all nucleated cells including nRBC. AFter correcting nRBC count, no leukocytosis is noted. However, this is acutally considered as a nice left shieft, since 0.4 meta was counted, which is even immature than bands.
4. MCV is really high for just regenerative response, I would worry about aggultination. Saline dispersion test or coomb's test is recommended. There is a unwritten rule in our clinic, any severe anemic cats, M. hemofelis cannot be ruled out. (plus, this case have acute hemolysis, regenerative response and a LS as well as monocytosis. Hemolysis is a big concern (intravascular or extravascular).
5. For isostheuria, I use 1.008-1.012 . In this case, in the face of mild dehydration, I think it still retains mild concentrating ability.
Okay, a lot of things need to be discussed. I will write more after heading back to columbus. Have fun, guys
1. Oh yeah I am wrong. Checked the text, GL blood loss is not an example of internal bleeding. So the assumption made was not accurate, too.
2. According to the table provided in Willard et al "Small Animal Clinical Diagnosis by Laboratory Method", there's a rough relationship between degree of erythroid regeneration in anaemia and % of aggregate reticulocytes in cats - >5% = marked degree. MacWilliams P et al "Red Cell Responses in Disease I" Proc Western Veterinary Conference 2003, there's a table about "Aggregate Reticulocyte Responses to Anemia" - 100,000/ul - moderate response and >200,000/ul - marked response.
3. I'd prefer saline dispersion test. It's less labour consuming and less expensive for most owners. Mycoplasmosis is surely one of the differentials for haemolytic anaemia. And it's far more common than AIHA in cats as well.
4. I expect some hyperbiliruinaemia and bilirubinuria for marked haemolytic response. And yes, haemolysis cause neutrophilia with left shift, monocytosis and regenerative anaemia. Also, TP is normal or high in this case and many blood loss anaemia lead to hypoproteinaemia. For this reason, I've a hard time to differentiate between two actually.
5. Yes, USG = 1.008 to 1.012 should be considered as isosthenuric. A dehydrated animal typically has a plasma osmolality greater than normal due to loss of water and abnormal retention of solutes. In this case, USG = 1.013 to 1.020 may be isosthenuric, in spite of being greater than the above reference value. I don't think it's normal response in face of dehydration.
My clin path sucks. Haha. But I'd rather buy one more - M.felis. Don't bet on AIHA though.
阿 來晚了..不過終於把報告都交出去了!順利希望明天就可拿到畢業證書啦!!
學長已經分析的超詳細,我就列我的dDX好了!
1 renal failure-
chronic or acute可能需要再用超音波,X-ray看看腎臟大小和質地,或是從更詳細的history去判讀,pre-renal 或是 renal我覺得都有可能,pre-renal的原因可能是Hyperosmolar DM造成的,osmolality345比我查到的正常值高(308-335 mOsm/kg from Small Animal Clinical Diagnosis by Laboratory Method),但從isostheuria來看比較像是renal azotemia)
2DM-
因為hyperglycemia+glucosuria+ polyphagia,雖然glu只有249可能是stress induced,但是因為有glucosuria所以應該可以rule out stress induced的原因,只是我覺得比較不合的是,若是假設它的腎臟衰竭是DM造成的,但是未何麼又沒有看到臨床上PUPD的症狀,兩個的機制都是hyperosmolarity造成的傷害. 想問學姊,在這個case我可以用以上的資訊就下DM的診斷媽(我覺得應該可以)? 還是需要再觀察是否有持續的高血糖或是做fructosamine?
3hemolytic anemia-
regenerative macrocytic hypochromic anemia,再生性貧血原因分兩大類失血或是溶血,這個case沒有體外出血的現象或是歷史,有可能在腸道有uremic ulcer造成出血,這有可能會有再生性反應,也可能造成鐵質不斷流失出現缺鐵小球性的貧血
,這可能要看內視鏡才能確診或排除.溶血性貧血可分血管內和血管外,血管內溶血通常有hemoglobinemia和hemoglobinuria上面的資訊並沒有講是否有hemoglobinemia,但是沒有hemoglobinuria,bilirubinema在血管內溶血較明顯,血管外因為RBC在脾臟直接被Macrophage吃掉了,溶血速度較慢,血中bilirubin通常不會超過肝臟可代謝的量,不過書上也說,通常血管內外溶血同時發生,只是有一個比較主要,在這個case看起來很可能是血管外的溶血為主. 從目前的資訊沒有明顯造成溶血的原因,所以可能要rule out貓常見的可能原因,H. felis FeLV, A/G ratio=0.64 FIP suspected,若是這些都是negative,也可能是idiopathic IMHA!不知道學長說很少見的是不是指的是這種idiopathic IMHA?
阿還有!
學姊,你說NCC校正就適用NCC去檢nRBC的數目,20.6-4.8=15,8媽?
我上面說的怪怪的!早上剛起來頭腦昏昏!
算法在書上找到了.因為nRBC的直是指100個WBC中看到幾個nRBC,所以校正公式為:
WBC X 100/(100+nRBC),所以這個case是20.6x100/104.8=19.65!!
今天拿到之前學姊推薦的foundamentals of veterinary clinical pathology,內容還真的蠻完整的!
我回來了
這個case其實我有一個很重要的finding沒有給,可是給了就不好玩了咩...反正這個finding遇到這個case的時候也不一定可以找到,但是只是要提醒大家要注意阿!!!
這個finding就是M. Hemofelis infection (這個是新的名字阿,H. Felis是舊的) 要知道,這東西是RBC外寄生,所以你抽血放一振子在EDTA上面就會掉下來,所以有時候你有stain precipitate救回搞不清楚到底是哪一個,所以最好的方法就是取血之後馬上做片子也不用放到凝血管,如果還是沒有看到,就測抗體...或者PCR
以下是解釋:
1. CBC: 明顯貧血不需要贅述,如同我之前提的, 84真的有點太大(reticulocytes), 所以agglutination要考慮, 這時候就做saline dispersion test or coomb's (記得一件事情, high protetin的時候血球也會看起來一團團的)
2. 大球低色再生性貧血: 沒有問題,我用的標準用D&P 貓aggregate reticulocytes 100,000/ul moderate; >200,000/ul marked. 所以應該是mod to marked response (我之前血的時候應該完全記去狗的....) 在這裡,想要在次提醒大家貓punctate 比較少人在用,因為這些可能都是代表過去幾個禮拜釋出的,而aggregate才是比較近期的,比較能代表BM狀況:
3. 忘記寫unit : nRBC這裡已經是absolute了,不過那個公式是正確的,需要注意這的原因是,有些機器可以做出NCC有些可以做出WBC, 所以得想一下
4. mixed Inflammatory and stress leukogram --> 有LS, monocytosis, lymphopenia
5. Renal azotemia: BUN, Creat up and decreased urine SG
6. Hyperphosphoremia --> down GFR
7. 高血糖血尿可能是因為DM or stress,需繼續觀察 (stress is supported by leukogram)
8. Hyperproteinemia --> increased globulin --> 建議做SPE 看是poly or mono
9. cholesterol is up--> metabolic disorder (可能跟DM有關)
10. CO2 is down --> metabolic acidosis
11. cal OSM increased --> due to hyperglycemia and increased BUN.
所以總結
這隻貓其實之前就被診斷出DM,只是沒有控制好,M. haemofelis 常會出現在免疫抑制的貓身上.....另外SPE結果是poly,support antigenic stimulation
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