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Tag: Creatinine

  • Thoracentesis, part 2: sample work

    Thoracentesis, part 2: sample work

    Last week we gave some hints and tips about how to perform a thoracocentesis. This week we look at what to do with the sample you collected and where to go to next.

    Looking at the sample is not enough, there are several things you need to do to make sure you are getting the most information from the collected sample. This includes:

    • Fluid cell counts
    • Total protein assessment
    • Packed cell volume
    • Glucose
    • Lactate (if it is an exudate)
    • In-house cytology
    • Collect a sample for culture and sensitivity, and also external cytology assessment

    With this information you can narrow down your list of differentials; often enough it can give you a diagnosis.

    Here is the list I use. Note, it is not exhaustive and assumes you have taken three-view thoracic radiographs as part of the initial diagnosis.

    Transudate

    • Haemorrhagic effusion.
      Haemorrhagic effusion.

      Clear appearance – characterised by low protein and low cellularity

    • Transudates are caused by reduced oncotic pressure
    • Total nucleated cell counts = <0.5x10e9/L
    • Total protein = <25g/L

    Differentials to consider

    • Liver disease
    • Protein-losing nephropathy
    • Protein-losing enteropathy

    Additional diagnostics

    • Cytology and culture of fluid
    • Haematology and biochemistry
    • +/- dynamic liver testing
    • Urinalysis, urine protein/creatinine ratio, culture and sensitivity

    Modified transudate

    • Yellow/serosanguinous/cloudy appearance
    • Caused by increased hydrostatic pressure leading to passive leakage of proteins and fluid into the pleural space
    • Total nucleated cell counts = 3.5-5x10e9/L
    • Total protein = variable, ~25-50g/L

    Differentials to consider

    • Increased capillary hydrostatic pressure and pericardial disease
    • Diaphragmatic hernia
    • Neoplasia
    • Lymphatic obstruction, such as neoplasia, diaphragmatic hernia and abscess
    • Increased permeability of vessels (blood and lymphatics), such as FIP

    Additional diagnostics

    • Cytology and culture of fluid
    • Haematology and biochemistry
    • Cardiac auscultation and ultrasound
    • +/- CT

    Exudate

    • Turbid appearance – Very proteinaceous liquid, froths when shaken
    • Fluid is a mix of plasma and inflammatory mediators, and is caused by either septic or aseptic inflammation
    • Total nucleated cell counts = >3.0x10e9/L
    • Total protein = >30g/L

    Aseptic exudate

    • Non-degenerate neutrophils and activated mesothelial cells predominate
    • Non-infectious cause

    Differentials

    • Inflammation: FIP (can have high globulins), liver disease, lung torsion and hernia
    • Neoplasia

    Additional diagnostics

    • Haematology and biochemistry
    • Cytology and culture of fluid
    • +/- ultrasound/CT
    • Further testing for FIP

    Septic exudate

    • Degenerate neutrophils predominate: nuclear swelling and pale staining
    • Intracellular or extracelluar microorganisms
    • Culture and sensitivity: aerobic and anaerobic
    • Pleural fluid [glucose] < serum [glucose]
    • Pleural fluid [lactate] > serum [lactate]

    Differentials to consider

    • Ruptured abscess
    • Foreign body inhalation or penetrating injury
    • Fungal infection

    Additional diagnostics

    • Haematology and biochemistry
    • Cytology and culture of fluid
    • +/- ultrasound/CT

    Chyle

    Thoracocentesis-Chyle
    Chyle.

    Opaque (milky) to pink.

    Differentials to consider

    • Rupture or obstruction of lymphatic flow
    • Neoplasia, traumatic and idiopathic
    • Secondary to heart failure (especially in cats)
    • Pseudochyle (usually formed by lymphoma)

    Additional diagnostics

    • CBC and biochemistry
    • Cytology and culture of fluid
    • Fluid [TAG] > serum
    • Large number of lymphocytes and other inflammatory cells
    • +/- ultrasound/CT

    Haemorrhage

    • Red blood cells
    • True haemorrhagic; for example, not iatrogenic: should not see platelets or erythophagocytosis on smears and sample should not clot
    • Time frame
    • Assess history
    • Compare fluid PCV/total protein (TP) to peripheral PCV/TP:
    1. <1% – non-significant
    2. 1% to 20% – neoplasia, trauma, pneumonia
    3. >50% – haemothorax
    • Other tips:
    1. If PCV/TP is similar = recent bleed, if PCV is low and TP normal = chronic
    2. If PCV is increasing or is higher than peripheral then active bleeding
    3. Presence of erythrophagocytosis = chronic

    Differentials to Consider

    • Trauma
    • Neoplasia
    • Coagulopathies
    • Ruptured granuloma

    Diagnostics

    • Activated clotting time, activated partial thromboplastin time, prothrombin time, blood smear and other coagulation tests, see “coagulopathy”
    • Blood smear
    • CBC and biochemistry
    • +/- ultrasound/CT

    Good luck with your next thoracocentesis. I hope this information was useful.

  • Icteric serum

    Icteric serum

    The final discolouration of the serum we are going to cover is icteric serum.

    Icteric serum
    Icteric serum is caused by the presence of excess bilirubin in the blood stream.

    Icteric serum is caused by the presence of excess bilirubin in the blood stream as a result of increased production (pre-hepatic) or inappropriate excretion (hepatic and post-hepatic).

    The most common cause of pre-hepatic icterus is haemolytic anaemia, while hepatic disease and biliary tract obstruction are the most common causes for hepatic and post-hepatic icterus, respectively.

    Tips on where to start

    If icterus and concurrent anaemia exist, my first suspicion would be some kind of pre-hepatic cause. The most common causes are immune-mediated haemolytic anaemia and infectious haemolytic anaemia, such as haemotropic mycoplasma and babesiosis.

    Other causes can include snake envenomation and oxidative injury from heavy metal toxicity or onion ingestion.

    Regarding hepatic and post-hepatic causes, unfortunately it is not always clear-cut. Both are commonly associated with elevation in both alanine transaminase (ALT) and alkaline phosphatase (ALKP), and, although no specific changes are pathognomonic for hepatic or post-hepatic disease, the pattern of change may help identify the origin of the cause. ALT is released from the inside of hepatocytes, and in higher amounts when cell damage occurs.

    Hepatic hints

    Some pointers on what you can do to help differentiate:

    • Compare the ALT and ALKP elevation; if one is in order of magnitudes higher than the other then it can help point to an origin.
    • If the cause is of hepatic origin, one would expect the ALT to be significantly more elevated than the ALPK. Likewise, this is usually true in reverse for post-hepatic causes. However, it should be noted in chronic hepatic diseases, where active damage to hepatocytes is comparatively lower, a mild increase in ALT and marked increase in ALPK does not preclude disease of hepatic origin. Therefore, biopsies should always be used for definitive diagnosis.
    • If other biochemistry parameters such as albumin, glucose and cholesterol are low, or prolonged clotting times are present, the case for a hepatic origin is strengthened.
    • The gallbladder and bile duct can be assessed using abdominal ultrasonography. The presence of a dilated bile duct, or evidence supportive of pancreatitis, is highly suggestive of a post-hepatic cause.

    Finally, it is important to be aware of the impact on hyperbilirubinaemia on laboratory testing. Hyperbilirubinaemia generally causes decreased cholesterol, triglyceride, creatinine, lipase, total protein and gamma-glutamyltransferase levels.

  • Urinalysis: dipstick tips

    Urinalysis: dipstick tips

    Following on from July’s post entitled Urinalysis: the neglected test, let’s have a look at the dipstick – it’s a very easy part of a urinalysis and essential to perform.

    Here are some of my tips in regards to using dipsticks:

    Poli_dipstick
    Dipstick: despite the name, DON’T DIP!
    • It may sound obvious, but you should always use veterinary-specific dipsticks. Human-specific dipsticks include panels for urobilinogen, nitrates and leukocytes, which we often do not interpret in small animal patients, as they are neither sensitive nor specific.
    • DON’T DIP! Use a syringe and drop samples on to each square, leave for 10 seconds, then flick off the excess.
    • Any amount of protein in dilute urine should raise suspicion. A reasonably large amount of protein has to be present in the urine for it to be positive on a dipstick. A urine protein to creatinine ratio may be the only way to quantify the amount of protein present, but first you must rule out evidence of inflammation or haematuria via a sediment examination.
    • The ketone panel on the dipstick test is only for acetoacetate (and not beta-hydroxybutyrate), although it is extremely rare for diabetic ketoacidosis patients to not produce any acetoacetate.
    • Trace blood can be a common artefact finding, especially during a cystocentesis where needle trauma can contaminate the sample with blood.
    • In our feline patients, any hyperbilirubinuria is abnormal, but this may be normal in a dog depending on urine concentration.
  • Making sense of effusions (part 1): is your patient septic?

    Making sense of effusions (part 1): is your patient septic?

    Interpreting effusion samples can be confusing, so try to think of effusions as if you were collecting a blood sample.

    Septic effusion
    Septic effusion.

    Many of the in-clinic diagnostic tests that apply to blood samples also apply to effusions, such as:

    • PCV/total protein
    • smears
    • glucose
    • lactate
    • potassium
    • creatinine
    • bilirubin

    It’s not enough to only check the protein concentration of the effusion then classify it as either a transudate, modified transudate or exudate and leave it at that – there is more information left to extract from that sample.

    Challenging diagnosis

    Determining if an effusion is septic can be a challenge. Here are the steps I take.

    analysis
    Abdominal and peripheral blood gas analysis.
    1. Perform a cytological examination of your effusion in the smear and look for inflammatory cells and the presence of bacteria. Look inside the cells as well as outside. If you don’t see bacteria it does not mean it isn’t a septic effusion, and only a couple bacteria are needed for me to call it septic.
    2. Glucose and lactate: You need to compare the glucose levels in the effusion with blood glucose levels. If the effusion glucose level is less than serum glucose, it is more likely you have a septic exudate. This makes sense in that bacteria would metabolise glucose in the effusion, leading to lower glucose levels. A by-product of metabolism is, of course, lactate. Therefore, you next need to check the lactate levels in the effusion and compare it to the serum lactate level. If lactate level in the effusion is more than the serum lactate level, then again you have more evidence you are dealing with a septic exudate.

    Try to measure glucose and lactate from both blood and effusion samples at the same time on the same machine. Keep in mind glucose and lactate values are less accurate for monitoring for the presence of bacteria in post-surgical patients.