staging.vettimes.com

Tag: Potassium

  • Blood gas analysis, pt 5: metabolic acidosis and alkalosis

    Blood gas analysis, pt 5: metabolic acidosis and alkalosis

    Base excess (BE) and bicarbonate (HCO3-) represent the metabolic components of the acid base equation. In general, both components will change in the same direction.

    Decreased HCO3– and BE indicate either a primary metabolic acidosis or a metabolic compensation for a chronic respiratory alkalosis. Elevated HCO3– and BE indicate either a primary metabolic alkalosis or a metabolic compensation for a chronic respiratory acidosis.

    The exception to this rule arises when a patient hypoventilates or hyperventilates.

    Carbonic acid equation

    CO2 + H2O ↔ H2CO3 ↔ HCO3– + H+

    When a patient hypoventilates, CO2 will increase as a result of reduced expiration, so a shift to the right of the equilibrium will occur. The shift to the right will increase the bicarbonate levels proportional to the increase in CO2.

    The opposite occurs when a patient hyperventilates; the equilibrium shifts to the left, so a decrease in HCO3– is present.

    Since HCO3– is not independent to the patient’s respiratory status, it is an inaccurate way of measuring the metabolic component in patients with respiratory changes. For this reason, the BE value is the preferred.

    The BE represents the amount of acid, or base, needed to titrate 1L of the blood sample until the pH reaches exactly 7.4, with the assumption the blood sample is equilibrated to a partial pressure of CO2 of 40mmHg (the middle of the reference range) and the patient’s body temperature is normal.

    Possible causes

    The possible causes of the primary disease are:

    Metabolic acidosis

    • lactic acidosis – shock and poor perfusion
    • renal failure – reduced hydrogen ion (H+) excretion and increased loss of HCO3–
    • diabetic ketoacidosis – ketone acids
    • gastrointestinal (GI) losses – loss of HCO3– through vomiting and diarrhoea

    Metabolic alkalosis

    • GI outflow obstructions – loss of H+ and chloride via vomiting
    • reduced chloride levels and resultant poor perfusion – body attempts to reabsorb water and sodium to increase intravascular volume, but inadvertently also reabsorbs HCO3– in the process, despite existing alkalosis
    • refeeding syndrome
    • severe hypokalaemia:
      • transcellular shift – potassium ions leave and H+ ions enter the cell
      • transcellular shift in cells of proximal tubules → intracellular acidosis → promotes ammonium production and excretion
      • H+ excretion in the proximal and distal tubules increases → further reabsorption of HCO3– and net acid excretion
    • renal insufficiency
    • diuretic therapy (contraction alkalosis – loss of bodily fluids that do not contain HCO3-; this causes the extracellular volume to contract around a fixed quantity of HCO3-, resulting in a rise in the concentration of HCO3– without an actual increase in HCO3– levels)

    Next step

    After ruling out the differential causes of either respiratory or metabolic acidosis/alkalosis, the next step is to determine whether a compensatory response is present and, if so, if this is adequate or whether a true mixed acid-base disorder exists.

  • Blood gas analysis, pt 2: acid-base disturbances

    Blood gas analysis, pt 2: acid-base disturbances

    Acid-base disturbances are common in critical patients. These changes must be identified, as even minor deviations from the normal range can lead to significant abnormal body functions.

    Acidaemia and alkalaemia

    Acidaemia, which occurs when blood pH falls below 7.35, will lead to:

    • impedance of cardiac output
    • reduced cardiac contractility
    • a blunted response to catecholamine manifesting as hypotension
    • antagonism to insulin
    • a compensatory hyperkalaemia (extracellular movement of potassium in exchange for hydrogen ions [H+])

    Alkalaemia – blood pH above 7.45 – although less critical compared to acidosis, will result in:

    • muscle spasm
    • stuporous mentation
    • hypocalcaemia
    • hypokalaemia (intracellular movement of potassium in exchange for H+)

    As well as the aforementioned altered functions, H+ is essential for the normal function of enzymes and maintenance of normal cell structures. This is why the body maintains a very narrow pH range and uses multiple buffering mechanisms to achieve this.

    Buffering systems

    The two main buffering systems are the kidneys and lungs.

    Kidneys adjust the pH via the excretion of H+ and the uptake of bicarbonate (HCO3-), which is the primary extracellular buffer and has a linear relationship with pH.

    An increase in HCO3– concentration will result in a pH increase and vice versa. This mechanism can take hours or days from the time a shift in the pH is detected.

    The main respiratory buffer is CO2 – an acid. CO2 has an inverse relationship with pH, so an increase is equivalent to a lower pH level and vice versa. The effect of respiratory adjustments is immediate. This occurs by altering the respiratory rate to adjust CO2 levels.

    The first step towards interpretation of acid-base disturbances is identifying whether an alkalaemia or acidaemia is present. The next blog will discuss determining what is causing it – identifying the primary disorder and the compensatory mechanism employed to balance it out.

  • Lipaemia – the bane of biochemistry

    Lipaemia – the bane of biochemistry

    Last week we covered haemolysed samples – this week we’re looking at lipaemic samples.

    Lipaemic samples are caused by an excess of lipoproteins in the blood, creating a milky/turbid appearance that interferes with multiple biochemical tests and can even cause haemolysis of red blood cells.

    lipaemic sample
    A severely lipaemic sample (red arrow). IMAGE: eClinPath.com (CC BY-NC-SA 4.0).

    Lipaemia can follow recent ingestion of a meal – especially one high in fat. Although not pathognomonic for any diseases, its presence can help increase the suspicion of certain diseases, including:

    • pancreatitis
    • diabetes mellitus
    • hypothyroidism
    • hyperadrenocorticism
    • primary hyperlipidaemia (in some specific breeds, such as the miniature schnauzer)

    It warrants further investigation in patients that have been ill and inappetent.

    Irksome interpretations

    Lipaemia can dramatically impact laboratory testing and is often troublesome in critically ill patients, making interpretation of biochemistry particularly difficult, if not impossible.

    Lipaemia can affect different analysers in different ways, most commonly causing:

    • Falsely increased calcium, phosphorus, bilirubin, glucose and total protein (via refractometer) and some liver parameters such as alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, haemoglobin concentration, and mean corpuscular haemoglobin concentration.
    • Falsely decreased sodium, potassium, chloride, albumin and bicarbonate.

    Tube tips

    Assessment of a centrifuged haematocrit tube before running a biochemistry panel can help reduce wasted biochemistry consumables.

    If the sample is lipaemic in the haematocrit tube then maybe try some of the following tips.

    • If blood tests are planned in advance, try fasting the patient beforehand for 12 to 24 hours.
    • Repeat sampling a couple of hours later may yield a less lipaemic sample.
    • Collecting and centrifuging a larger amount of blood (3ml to 5ml, for example) can sometimes yield enough clear sample between the lipid layer and red blood cells.
    • Refrigeration of the sample can help the separation.
    • Extract lipids using polar solvents, such as polyethylene glycol.
    • Centrifugation at higher than normal speeds (if possible) can also assist in clearing the layer.
  • PCV/total solids interpretation: serum colour

    PCV/total solids interpretation: serum colour

    When interpreting the often misinterpreted and underused PCV and total solids test, it is important to take note of the serum colour as this may give clues into the diagnosis.

    PCV tubes
    Normal serum colour (left) compared to a patient with immune-mediated haemolytic anaemia. The serum is haemolysed and anaemia is present.

    The most common abnormalities seen in clinic are icteric, haemolysed and lipaemic serum.

    Clear serum can also be of importance – especially when you interpret it with blood counts and urine colour.

    Haemolysis

    The most common abnormality of serum colour changes is haemolysis. In my experience, the most common cause is suboptimal collection technique. To confirm this, simply collect another sample and repeat.

    If it is repeatable, and concurrent anaemia or pigmenturia is present, it warrants further investigation.

    Intravascular haemolysis can be caused by:

    • immune-mediated haemolytic anaemia
    • blood transfusion reactions
    • infectious diseases such as Mycoplasma haemofelis, Babesia canis, Ehrlichia canis, FeLV and others
    • Heinz bodies from the ingestion of heavy metal, onions or paracetamol
    • hypophosphataemia
    • macroangiopathic disease (neoplasia, for example)
    • envenomation – typically, snake bites

    Testing issues

    Haemolysis can also affect other laboratory testing. It can lead to an artefactual increase in glucose, phosphorus, bilirubin, total protein, fructosamine and triglycerides, and a decrease in sodium (pseudohyponatraemia), cholesterol, calcium, potassium and albumin.

    Extravascular haemolysis often does not cause haemolysed serum as it is generally slower and the body is able to clear the haemoglobin before it can lead to discolouration of the serum.

  • Focus on GDV, part 4: the recovery

    Focus on GDV, part 4: the recovery

    Postoperatively, gastric dilatation-volvulus (GDV) patients remain in our intensive care unit for at least two to three days.

    Monitoring includes standard general physical examination parameters, invasive arterial blood pressures, ECG, urine output via urinary catheter and pain scoring.

    I repeat PCV/total protein, lactate, blood gas and activated clotting times (ACT) immediately postoperatively and then every 8-12 hours, depending on abnormalities and patient progress.

    GDV recovery
    Patient recovering in the pet intensive care unit. As well as standard monitoring parameters, GDV patients have constant ECG, arterial blood pressure and urine output monitoring to enable the early detection and correction of abnormalities.

    I always repeat these blood tests postoperatively, as IV fluids given during the resuscitation and intraoperative period often cause derangements. I use the results to guide my fluid therapy, but also take it with a grain of salt.

    IV fluids

    I generally continue a balanced and buffered crystalloid. The rate depends on blood pressures, urine output and assessment of general physical examination parameters for perfusion and hydration, but I try to avoid fluid overload and reduce the IV fluids postoperatively as soon as possible.

    Coagulopathy

    Prolonged clotting times are frequently seen as a result of consumption in a dog with GDV. However, one should note it can also occur as the result of haemodilution.

    As the underlying disease process has been corrected, and haemostasis achieved during surgery, I usually monitor ACTs, but may not necessarily treat with blood products as prolonged ACTs do not always translate to clinical bleeding. Unless clinical evidence of bleeding exists, I generally hold off treatment and monitor.

    Hypoproteinaemia

    Low total protein is also common. This is generally due to haemodilution from fluid resuscitation. However, a low total protein does not mean oedema will develop, or that it requires management. I generally track the protein levels, use conservative fluid therapy and try to correct it by instituting enteral nutrition as soon as possible.

    Electrolyte imbalances

    Hypokalaemia is a common complication of fluid therapy. This can be rectified with potassium supplementation in the IV fluids.

    Hyperlactataemia

    If present post-surgery, this is usually corrected with a fluid bolus. However, I always assess for other things that may affect oxygen delivery to the tissues, such as poor cardiac output (arrthymias), hypoxaemia (respiratory disease) and anaemia (from surgical blood loss).

    Arrhythmias

    Ventricular arrhythmias are common post-surgery. Accelerated idioventricular rhythms are the most common cause, especially if a splenectomy was performed.

    arrhythmia
    Ventricular premature contractions are common postoperative arrhythmia.

    Before reaching for anti-arrythmia medications, first check and correct:

    • electrolyte abnormalities
    • hypoxaemia
    • pain control
    • hypovolaemia or hypotension

    If they are still present, despite correction of the above, consider treating the rhythm if:

    • multifocal beats (ventricular premature contractions of various sizes)
    • overall rate greater than 190 beats per minute
    • R-on-T phenomenon
    • low blood pressure during a run of ventricular premature contractions

    I start with a bolus 2mg/kg lidocaine IV and start a constant-rate infusion of 50ug/kg/min to 75ug/kg/min.

    Anaemia

    It is common to have a mild anaemia post-surgery, due to a combination of blood loss and haemodilution. In the absence of transfusion triggers – such as increased heart rate, increased respiratory rate or hyperlactataemia – it does not require treatment.

    Vomiting

    Anti-emetics are the first line of medication. Non-prokinetic anti-emetics, such as maropitant and ondansetron, can be used immediately; otherwise, after 12 hours, metoclopramide can also be used postoperatively. If the patient remains nauseous despite these medications, the placement of a nasogastric tube can ease nausea by removing static gastric fluid.

    Excessive pain relief may also contribute to the nauseous state.

    Pain relief

    I mostly rely on potent-pure opioid agonists, such as fentanyl constant-rate infusions and patches. This is generally sufficient for most patients. Ketamine is occasionally used.

    • Some drugs listed in this article are used under the cascade.
  • Maintenance fluids

    Maintenance fluids

    A while ago we discussed the components of a fluid therapy plan and talked about hydration deficits. This week I want to touch on maintenance fluids.

    Gerardo_IVF
    IV fluids

    Maintenance rates are typically calculated using the following formulae:

    ml/day = 80 × bodyweight (kg)0.75 (cats)
    ml/day = 132 × bodyweight (kg)0.75 (dogs)
    or
    ml/day = 30 × bodyweight (kg) + 70

    These formulae better estimate the needs of smaller and larger patients. The flat 3ml/kg/hr underestimates for small patients and overestimates for larger patients.

    This maintenance rate is in addition to rehydration rates.

    So what sort of fluid should you use for maintenance?

    True “maintenance” crystalloids:

    • used to replace ongoing fluid and electrolyte loss from normal metabolism, not to replace perfusion and hydration deficits or ongoing losses from diarrhoea, for example
    • sodium concentration less than plasma
    • potassium concentrations higher than plasma
    • glucose sometimes added to bring solute concentrations similar to extracellular fluid

    Do you have to use maintenance crystalloids or can you use replacement crystalloids?

    Replacement crystalloids are more frequently used for maintenance fluid therapy rather than maintenance crystalloids. This is because they are more readily available, we are more familiar with their use and effect, and patients are generally continued on these after perfusion and hydration deficits have been corrected.

    In reality, most of the time it doesn’t really matter if we are using replacement crystalloids for maintenance therapy as the patient can manage the excess sodium, but some patients – especially cats – may require potassium supplementation. The key point is regular assessment of the patient’s hydration status and electrolytes – for example, every 12 to 24 hours for patients on IV fluids and not eating.

  • 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.

  • SNAP cortisol test

    SNAP cortisol test

    While hyperadrenocorticism is not an uncommon incidental finding in patients presenting to our emergency clinic, hypoadrenocorticism is a lot less common. Or, possibly, more frequently underdiagnosed.

    Textbook clinical presentations combined with haematology and biochemicial changes can make diagnosis straightforward, but not all patients will present with all the classic signs.

    SNAP cortisol test
    The SNAP cortisol test is a quantitative ELISA test that measures the level of serum cortisol in dogs.

    To complicate things further, hypoadrenocorticism is the great mimicker of diseases; it is often impossible to arrive at a definitive diagnosis without knowing the cortisol levels.

    The SNAP cortisol test allows clinicians to determine cortisol levels in-house – a blessing to those of us who work out-of-hours – but is not without its limitations.

    Suspicious signs

    Patients with hypoadrenocorticism often present with vague and non-specific clinical signs, but certain clinicopathological changes help raise the suspicion:

    • a decrease in sodium-to-potassium ratio (below 1:27)
    • azotaemia
    • an inappropriately low urinary specific gravity, despite evidence of dehydration or hypovolaemia
    • a leukogram unfitting to the degree of illness of the patient (a “reverse stress leukogram”- neutropenia, lymphocytosis, eosinophilia)
    • anaemia
    • hypoglycaemia
    • hypercalcaemia

    Although most Addisonian patients will not present with all these signs – especially those in the early stages of disease or those with atypical Addisonian disease (glucocorticoid insufficiency only) – any patients showing any of these haematology and biochemicial changes should have hypoadrenocorticism ruled out as part of the diagnostic plan.

    Imperfect ELISA

    The SNAP cortisol test has been advertised as an in-house assay to aid the diagnosis, treatment and management of both hyperadrenocorticism and hypoadrenocorticism, although the quality of the result is not perfect. This quantitative ELISA test measures the level of serum cortisol in dogs.

    In one study1, the SNAP cortisol test appears to have a good correlation with an external laboratory chemiluminescent assay test; however, in 12.8% of cases (5 of 39 patients), the SNAP test result could have led to a different clinical decision regarding the management of the patient.

    Since long-term Cushing’s management relies on reliable, repeatable cortisol level detection, this high level of discrepancy is unacceptable, especially when more accurate alternatives are available at external laboratories.

    Still useful

    Despite this, it is still very useful helping to assess for the presence or absence of hypoadrenocorticism, especially in an emergency setting.

    I use the SNAP cortisol to measure the resting cortisol level. If it is below 2ug/dL or in inconclusive range (between 2ug/L and 6ug/L), but the clinical picture suggests hypoadrenocorticism, I would perform an adrenocorticotropic hormone (ACTH) stimulation test and send samples to an external laboratory. If it is well above the inconclusive range, I would not perform an ACTH stimulation test.

    In summary, I think the SNAP cortisol test can be useful in helping assess for hypoadrenocorticism, but would still recommend performing an ACTH stimulation test and running the samples externally.

    However, use it with caution for hyperadrenocorticism diagnosis and its long-term management – especially when more accurate and economical alternatives are available.