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Tag: Lactate

  • Focus on GDV, part 1: resuscitation

    Focus on GDV, part 1: resuscitation

    Last month we covered a bit of pathophysiology, presenting pathophysiology, presenting clinical signs and the radiographic diagnosis of gastric dilatation-volvulus (GDV).

    Now we cover the three things you need to do as soon as a suspected case is presented:

    1. IV fluid resuscitation
    2. decompression of the stomach
    3. pain relief

    Depending on the number of staff you have, all of these can be performed simultaneously. If not, follow the above order as shock is the most imminent problem.

    Catheter placement

    Fluid resuscitation is relatively straightforward. Most GDV patients will be in some degree of shock, varying from mild to severe. Regardless of the actual degree, all patients will require IV fluids.

    The placement of IV catheters is particularly important; their numbers and diameter will influence the rate of response to treatment. Large-bore catheters allow faster flow of fluids compared to smaller ones, while multiple catheters allow concurrent delivery of two bags of fluids as opposed to one – particularly important in large dogs. Therefore, always try to place the largest catheter possible (for example, 18G or larger for large-breed dogs) into the cephalic veins.

    Once the catheters have been placed, collect 2ml to 3ml of blood for baseline measurements. These can be collected directly from the catheters and should include:

    • PCV/total protein
    • blood gas analysis
    • lactate
    • activated clotting time
    • electrolytes
    • later, full haematological and biochemical analysis

    Once the baseline bloods have been collected, fluid resuscitation should start immediately.

    How much, how fast?

    fluid
    Fluid resuscitation is relatively straightforward, says vet Gerardo Poli.

    How much fluid should you deliver, and how fast? My “go to” fluid is crystalloids and I generally start with a 20ml/kg bolus of an alkalinising crystalloid.

    I perform bolus therapy, so 10ml/kg to 20ml/kg fluid doses rather than shock rates 90ml/kg/hr, as I feel it allows me to better titrate my fluid therapy to effect. It also helps minimise excessive fluid administration and the problems with haemodilution – such as anaemia, hypoproteinaemia and prolonged coagulation times.

    As fluids are being delivered, I administer pain relief and start gastric decompression (covered next week).

    The decision to administer more fluids depends on whether I have achieved some end point resuscitation variables, such as:

    • a reduction in heart rate
    • a reduction in capillary refill time
    • an improvement of mucus membrane colour
    • improvement in pulse pressures

    Improvement in mentation is not often reliable as the sedative effect of analgesia, which I generally give during fluid resuscitation, often confounds this effect.

    Shock therapy

    If evidence of shock still exists, despite the initial fluid boluses and gastric decompression, I will consider more fluids. This can include hypertonic saline or colloids.

    In my experience, a repeat of a smaller dose of crystalloid fluid bolus is often adequate (10ml/kg). The transition on to hypertonic saline (7% solution) or colloids is influenced by the results of the aforementioned baseline diagnostics.

    A reduction in PCV/total protein suggests blood loss. In this case, I will consider either hypertonic saline (3ml/kg to 5ml/kg of 7% solution), a dose of colloids or even blood products, such as whole blood or packed red blood cells.

    If significant prolongation in activated clotting time occurs, likely from consumption, then I may incorporate fresh frozen plasma into my fluid therapy. This is in anticipation of possible surgery, where prolonged coagulation times can not only be troublesome, but life-threatening.

    Lactate

    A quick note on lactate – I don’t use the baseline reading as a prognostic indicator or an indicator of gastric necrosis. This is supported by recent findings claiming it is not the level of lactate that is predictive, but the degree of improvement in response to fluid resuscitation and gastric decompression.

    I have seen unreadable lactate levels – greater than 15mmol/L – in patients who returned to reasonably normal levels within an hour of stabilising. These patients also went on to survive surgery.

    Pain relief

    After starting IV fluid resuscitation, I generally administer pain relief while the team is preparing for gastric decompression. To keep things simple, I stick to an easily accessible pure opioid agonist at 0.2mg/kg IV. I avoid subcutaneous or even intramuscular administration as the patient is often in shock; the peripheral blood is shunted centrally to the heart and the brain and absorption can be variable.

    I find this offers a reliable and great degree of pain relief that helps reduce anxiety levels and, consequently, reduces oxygen demand. It has minimal cardiovascular effects and the mild sedative effect also helps with the process of decompression.

    >>> Read Focus on GDV, part 2: Releasing the pressure (gastric decompression)

  • 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.

  • Linear foreign bodies, part 3: should YOU take it to surgery?

    Linear foreign bodies, part 3: should YOU take it to surgery?

    In the previous post we covered what to look out for on ultrasound when assessing for a linear foreign body. Now we discuss the things you should consider before deciding to take the patient to surgery.

    Read the following statements and answer the questions – either yes or no…

    • Linear foreign body surgeries can be technically difficult and can take a prolonged period of time to perform. The longer the surgery, the higher the rate of complications. Are you (or do you have access to) an experienced surgeon who has performed a linear foreign body surgery before, and do you have an additional pair of hands for surgery to help reduce surgery time?
    • Were bacteria visualised or is their presence likely based on the comparison of the abdominal fluid glucose and lactate to peripheral blood (see previous post)? If yes, then septic peritonitis is present. Approximately 40% of dogs with linear foreign bodies will have septic peritonitis. This means you need to be prepared to perform a resection and anastomosis; sometimes two. Have you performed a resection and anastomosis before?
    • Often a combination of gastrotomy, enterotomy, and resection and anastomosis are required. Are you prepared to perform a combination of these surgeries?
    • Linear foreign body surgeries can often require a significant number of surgical instruments and consumables. Do you have Balfour retractors, forceps, clamps, additional kit for closure, supply of lap sponges, as well as substantial amounts of lavage and access to suction?
    • Linear foreign body patients are often critically ill due to septic peritonitis. They can present in shock and have biochemical derangements such as hypoalbuminaemia, which indicates the need for perioperative critical care. Do you have experience stabilising, performing anaesthesia and postoperatively managing a critically ill patient?
    • Hypotension can be caused by hypovolaemia; however, if the hypotension has not responded to reasonable volumes of a balanced isotonic crystalloid fluid – for example, 30ml/kg to 40ml/kg – then the hypotension could be caused by vasodilation from septic shock. This means vasopressor agents will be required in addition to crystalloids. Do you have access and experience with vasopressor therapy?
    Image: Gerardo Poli.

    Conclusion

    This list of questions is not meant to be conclusive or definitive, but merely a list of considerations before taking a linear foreign body patient to surgery.

    If you answered no to many of these questions, then consider referral to a facility that is prepared and equipped for the challenges that often accompany linear foreign body patients. However, if referral is not an option, consider the list above as a way to be as prepared as possible for tackling those situations.

  • The beginning of the end of vet school

    The beginning of the end of vet school

    Hospital
    Exams passed, Jordan can walk the halls of Glasgow’s small animal hospital without feeling like an imposter.

    As regular readers of this blog may have noticed, I was a little apprehensive about starting my final year at veterinary school…

    Having already been in the small animal hospital for two days, we finally received our results – confirming I and many of my fellow classmates had passed our exams and could now wear our final year jackets without guilt and walk around the hospital without feeling like imposters.

    However, despite now knowing we had qualified to be in the hospital, it still felt like we had been thrown in the deep end.

    In at the deep end

    My first rotation was emergency and critical care, with the first part being internal medicine. The first couple of days were spent frantically researching the background of patients coming in for appointments, bumbling through clinical exams and brushing up on my rusty practical skills.

    It was my first time taking consults alone and, after missing out key questions the first few times, I eventually got into the swing of things and made fewer mistakes.

    cat scratch quote
    Image: seregraff / Fotolia.

    Despite feeling like I didn’t know anything to begin with, I at least managed to scrape together a few sensible ideas when clinicians tried to worm differentials out of us. It has been a steep learning curve, changing the way of thinking entirely to apply things to a real patient in front of you, which usually has not read the textbook.

    OOH my goodness

    Just as I was beginning to feel comfortable with medicine, we swapped to out of hours – which, against my presumptions, turned out to be a really enjoyable week.

    I adjusted to nights far easier than I expected and was powering through until one particularly long night when a bulldog came in with a suspected gastric dilatation volvulus (GDV).

    This was the first genuine emergency we’d been involved in and stress levels were running high. Having rapidly set up fluid boluses, taken radiographs to confirm our suspicions, checked lactate levels and run in-house bloods, we went through to theatre. After a very long night of surgery and having warned the owner of an extremely grave prognosis, we were delighted to see said bulldog looking bright and happy the following evening, eating and pulling us down the corridors to the runs outside.

    Not all GDVs end with such a happy ending, as we had learned earlier in the week – a dog that underwent the surgery at its own vets came to us for overnight care in ICU and, after a rocky night of a supraventricular tachycardia that we struggled to keep under control, crashed the following morning, was resuscitated successfully once, but could not be saved when it crashed again minutes later.

    Hearts, not brains

    Coming from nights straight back into days, however, was much harder and I felt like a zombie for the first day of my cardiology week.

    On the subsequent days, when my brain was working again, I was able to make a bit more sense of echocardiography and gain a better understanding of some conditions and the tray menu options available.

    I also learned a bit more about the genetics of Bengal cats and found trying to heart scan a cat that’s only two generations away from a leopard cat can be quite challenging (and may involve chasing said cat around the ultrasound room for some time, following an artful escape act).

    This year isn’t going to be a picnic, but, although I already feel exhausted, if last month is anything to go by, it will be an enjoyable one.