scott@vtx-cpd.com

Replying to Neus E. 28/04/2025 - 10:31

Hi Neus,

Thanks so much for jumping in, completely agree with all of this. Diagnosis and targeted treatment are absolutely the priority, and I also tend to reserve specific albumin supplementation for cases where the clinical signs (rather than the number) really demand it. I think your point about using plasma more for oncotic support and to reduce crystalloid volume in SIRS-type patients is key. And yes, nasogastric tubes are such a practical way to get early nutrition in without needing full anaesthesia—great option while stabilising before considering anything more invasive.

Really helpful summary.

Scott 🙂

Replying to Christina Frigast 28/04/2025 - 10:16

Hi Christina,

Great questions.

For aggressive enteral nutrition, I usually aim to introduce a complete and balanced recovery diet as early as possible. Hill’s a/d, Royal Canin Recovery, or Clinicare are all good options depending on tolerance. If a feeding tube is in place, I really like the Royal Canin GI High Energy Liquid as it is specifically formulated for tube feeding, energy dense, and generally very well tolerated. In patients without a tube, Oralade is a useful starting point to support hydration and provide glutamate, but it is not nutritionally complete, so I try to transition to a more complete diet quickly. Placing a nasogastric tube allows for gentle, consistent nutritional support and can help avoid the stress of syringe feeding. It also enables trickle feeding, which is often better tolerated in fragile patients and may reduce the risk of reflux or vomiting. In some cases, a syringe driver can be used to provide a constant rate infusion of liquid diet over several hours, which works especially well for patients with poor appetite or gastrointestinal sensitivity.

Here’s the full link to the Royal Canin GI High Energy Liquid for dogs in case it’s helpful:

https://www.royalcanin.com/uk/dogs/products/vet-products/gi-high-energy-liquid-dog-4913

For fluid support, I usually start at 1 to 2 mL/kg/hr in stable hypoalbuminemic patients. That provides volume support without risking overload. I adjust based on perfusion parameters, urine output, respiratory rate, and any evidence of effusions or peripheral oedema. If there are signs of third spacing, I tend to reduce the rate further and reassess frequently.

Hope that helps.

Scott 🙂

Hi Christina,

Thanks so much for your really thoughtful question. It is a great one, and not an easy area to manage, especially when no clear underlying cause for the hypoalbuminemia can be found.

In general, my approach would be to start by trying to identify or exclude common causes if possible. Even if no obvious GI, liver, or renal disease is evident, I usually revisit the possibilities carefully. For GI losses, I look for more subtle signs such as hypocobalaminemia, low cholesterol, or changes on ultrasound. For liver function, I check synthetic markers including glucose, cholesterol, BUN, and coagulation times. For renal causes, I always recommend checking a UPC ratio even if azotaemia is not present. I also keep in mind that systemic inflammation, sepsis, neoplasia, heatstroke, or endocrine diseases such as Addison’s can contribute to significant hypoalbuminemia through vascular leakage and altered hepatic synthesis. If no clear cause is found, I often categorize it as critical illness-related hypoalbuminemia secondary to systemic inflammation and endothelial dysfunction.

When peripheral edema or ascites is present, if it is mild to moderate, I tend to focus first on treating the underlying disease, optimizing nutrition, and providing cautious fluid therapy. If edema or ascites is severe or causing respiratory compromise, I would typically intervene, often with therapeutic abdominocentesis to relieve pressure and, if possible, plasma or albumin support.

In terms of plasma transfusions, plasma is generally much more useful for addressing clotting factor deficiencies than for meaningfully replacing albumin. Very large volumes, around 20 to 25 mL/kg, are needed to make any meaningful increase in albumin levels, and even then, studies show plasma can sometimes dilute albumin rather than improve it in critically ill patients.

When considering albumin therapy, ideally I would use canine-specific albumin where available. It is safe, effective, and carries a much lower risk of hypersensitivity reactions compared to human albumin products. If canine albumin is not available, human serum albumin can be considered, but it carries significant risk of both immediate type I hypersensitivity reactions and delayed type III hypersensitivity reactions, including serious complications such as vasculitis, glomerulonephritis, and in some cases death. Critically ill dogs do seem somewhat protected against acute reactions compared to healthy dogs, but they still develop antibodies against human albumin weeks after exposure. It is critical that clients are informed about these risks before human serum albumin is administered. Diluting it to a 5 percent solution and giving it as a slow infusion appears safer than rapid 25 percent infusions, but it does not eliminate the risk entirely.

If plasma or albumin products are not available, alternative strategies include early aggressive enteral nutrition to provide the building blocks needed for hepatic albumin synthesis and judicious use of isotonic fluids to maintain perfusion while avoiding overload. If ascites is causing respiratory compromise, therapeutic abdominocentesis can be very helpful.

For dosing guidance, to estimate the albumin deficit, the following formula is useful: Dose of albumin in grams equals ten multiplied by the difference between two and the patient’s albumin in grams per deciliter, multiplied by bodyweight in kilograms, multiplied by 0.3. The general goal is to raise albumin to at least two grams per deciliter where possible. Any albumin administered will initially replenish the interstitial albumin pool before serum albumin levels rise, which makes targeting specific goals a bit challenging and highlights the importance of clinical monitoring.

In summary, I would consider albumin supplementation particularly if the albumin concentration is less than 1.5 grams per deciliter with clinical signs of oedema or effusion. I focus on treating any underlying disease, prefer using species-specific albumin if available, use human serum albumin cautiously only when necessary, and understand that plasma alone is not an efficient method for albumin replacement unless there are concurrent coagulation abnormalities. Supportive care, close monitoring, and clear communication with the owner are key parts of managing these complex cases.

All the best,

Scott :