A lot of clinicians continue to believe that impaired tissue oxygenation is the main cause of increased blood lactate, and lactate itself results in metabolic acidosis. This biochemical understanding has persisted for long time, but there are some good reasons to challenge these traditional views on the ‘bad’ lactate.
After its production by anaerobic glycolysis lactate is re-used in the liver and the kidneys, and it may be converted back to glucose. The important point though is that lactate is also produced via aerobic glycolysis as a response to catecholamine release and stress. This may happen in septic patients, albuterol toxicity, trauma and other critical illnesses. In these clinical scenarios, the trigger for lactate production is adrenergic stimulation and not lack of oxygen.
If you want to learn more about lactate metabolism, watch this short video below:
An 8-year-old neutered male dachshund was presented to the emergency department for evaluation of respiratory distress. The dog was previously diagnosed with a heartworm disease and was currently undergoing treatment with a “slow kill” method. Physical examination revealed tachycardia at 160/min, right-sided pulmonary crackles, and tachypnea with increased respiratory effort. The point-of-care blood work showed hyperlactatemia at 4.5 mmol/L, PCV/TS of 53%/7.8 g/dl, mild metabolic acidosis, normal electrolytes and renal values. The arterial blood pressure (Doppler) was at 130 mm Hg.
As the dog was getting flow-by oxygen, an abbreviated thoracic point-of-care ultrasound (T-POCUS) was performed (see below).
“Shock” is one of the most frequently used words in a small animal emergency room and ICU. Despite this fact, a lot of veterinary students and new graduates have only superficial understanding of this term. This lack of understanding may lead to inaccurate diagnosis and mismanagement of patients in shock.
Those of you who have ever participated in canine blood donation might have encountered a situation when the blood flow through a sampling line has significantly slowed down or even completely stopped, and despite your best efforts, you had to abort the mission. As a result, the blood bag may end up being half full and contain only 200-250 ml of blood. Since the majority of commercially available donor bags contain 63-70 ml of citrate-based anticoagulant, they are designed to be filled up with 400-450 ml of donor blood to maintain a 1:7 – 1:9 citrate-to-blood ratio. If not, the citrate-to-blood ratio goes up, which creates a risk for citrate toxicity during a blood transfusion. In this situation, a clinician or technician may elect to waste this blood product and send this donor home since collecting another full bag of blood will not be safe for the donor animal. On the other hand, there is an extreme shortage of blood products in veterinary medicine, and, if possible, any waste should be avoided. In this blog post, I will give you a tool that may help you decide on whether a blood product with a high citrate-to-blood ratio should be discarded or safely given to a prospective recipient.
A 2-year-old spayed female standard poodle was referred to a specialty private practice for evaluation of a suspected small intestinal mechanical obstruction. Two weeks prior, the dog started vomiting and stopped eating. The initial diagnostic work-up performed by her primary veterinarian showed normal bloodwork, and the dog received regular supportive care on an outpatient basis. Due to the presence of persistent vomiting and inappetence, the abdominal survey radiographs were performed, and they were consistent with the gastrointestinal obstruction as it was interpreted by a board-certified radiologist.