hypoalbuminemia

One of the main symptoms of hypoalbuminemia is edema , because albumin is the protein that contributes most to oncotic pressure, regulating the outflow of fluid from the bloodstream to the tissues. Colloid osmotic pressure is related to plasma albumin and protein levels. The level of this pressure determines whether the fluid remains outside the vessel. Albumin is a regulator of oncotic and colloidal osmotic pressure. It prevents blood from leaking from the vessels, that is, it is the force that keeps the fluids in the vessels. In the intravascular flow of blood, osmotically active particles (such as sodium urea and glucose) are usually small and can freely pass between the vascular and interstitial compartments. In contrast, albumin is too large to pass through the vascular endothelial wall and remains in the vessel. Oncotic pressure in the vessels due to the presence of albumin is the main force holding the fluid within the vascular compartments. However, other plasma proteins such as globulins also have an oncotic potency.

Albumin Normal Range:

Dogs 2.6 to 3.5 g/dl
Cats2.8 to 3.9 g/dl

hypoalbuminemia

Light

2.0 – 2.6 g/dl

Few clinical findings

moderate

1.5 – 2.0 g/dl

Few clinical findings

severe

<1.5 g/dl

Edema
acidity
pleural effusion

Clinical Signs of Hypoalbuminemia

Classical clinical manifestations of hypoalbuminemia peripheral edema, ascites, and pleural effusion . These clinical signs demonstrate the hypoalbuminemic patient’s ability to retain fluid in the vascular space and usually only occur when plasma albumin levels fall between 1.0 and 1.6 g/dl. Typically, the fluid leaking into the extravascular spaces is of a transudate nature.

Transudate:

clear and colorless
Protein
Specific weight
Few cells seen (if any)

Decreased oncotic pressure and intravascular fluid loss can also lead to hypovolemia, which can lead to problems such as poor peripheral perfusion and pre-renal azotemia.

Causes of Hypoalbuminemia

Liver failure (failure of albumin synthesis)
Digestive protein loss (protein-losing enteropathy) PLE
Renal protein loss (protein-losing nephropathies)PLN

Hemorrhages (rodenicide poisoning)
starvation/protein malnutrition
Chronic diseases, Viral diseases and conditions that cause vasculitis
hypoadrenocorticism
Age normal (young puppies and kittens)
lab errors

Despite these numerous potential etiologies, the diagnostic approach to patients with hypoalbuminemia is usually very simple.
Gastrointestinal and other non-renal diseases (such as third-degree burns, open pyometra or peritonitis) in which protein is lost, most of the causes are usually obvious. Hyperglobulinemia, starvation, protein deficiency and chronic diseases rarely cause mild hypoalbuminemia.
Due to its rarity in hypoadrenocorticism moderate to severe hypoalbuminemiacan usually be narrowed down to just three main potential causes:

1. Hepatic failure
2. Protein-losing enteropathy
3. Protein-losing nephropathy

Diagnostic Approach to Hypoalbuminemia

1. Initial diagnostic approach:

history

Hematology

physical examination

Biochemistry (including globulins)

urine analysis

Serum globulin levels can sometimes provide the clinician with guidance as to the potential cause of hypoalbuminemia. Serum globulins are usually normal in protein-losing enteropathies and protein-losing nephropathies. They tend to increase in hepatic failure.

2. Potential further diagnostic tests:

The standard investigations above will usually reveal the likely cause of an animal’s hypoalbuminemia. Other specific tests are performed based on the results of routine assays, but often specific investigations of urinary, gastrointestinal, and hepatic functions are required. Because precise detection of gastrointestinal protein loss can be difficult and may require invasive intervention, it is usually first potential urinary protein loss and hepatic failureis being investigated.

(a) Protein-Losing Nephropathy (PLN)

Urine protein level and concentrates are determined by laboratory assays. Normal animals have little or no protein in their urine, and such a finding in a hypoalbuminemic patient usually excludes PLN as a potential diagnosis.

When proteinuria is detected in the absence of an active urinary problem (pyuria or hematuria…), the magnitude of urinary protein loss can be more accurately measured using the urine protein:creatinine ratio.

Protein:creatinine ratio <1:Normal

Protein:creatinine ratio <2:Suspicious (‘grey’ area)

Protein:creatinine ratio > 2:protein-losing nephropathy

(b) Hepatic Failure

Hepatic failure can be evaluated by routine serum biochemistry and urinalysis results.

hypoalbuminemia
low serum urea
hyperglobulinemia
hypoglycemia
hyperbilirubinemia
Ammonium biurate crystalluria
Raised SAP and BOTTOM

However, not all patients with hepatic insufficiency will show the classic biochemical changes usually associated with liver dysfunction. Hypoalbuminemia can sometimes be the only real clue to hepatic failure. In such cases, although abdominal radiography and ultrasonography are helpful in determining hepatic size and structure, liver function testing is the primary way to determine the presence of liver failure:

Ammonia, fasting and postprandial bile acids should be evaluated.

Protein Losing Enteropathy (PLE)

A hypoalbuminemic patient with normal kidney and liver function is likely to have protein-losing enteropathy if GI findings, especially hypoglobulinemia, are also present. However, some patients with PLE may have severe hypoalbuminemia and no history of vomiting or diarrhea. In such patients, PLE can only be confirmed and ruled out by intestinal biopsies. PLN and hepatic failure should be ruled out first, as biopsy requires surgery. Non-invasive (non-surgical) tests such as fecal parasitology, culture, serum TLI, folate, and B12 can be performed for the possibility of PLE. Recently, a stool test that measures alpha levels, a protease inhibitor that shows fecal protein losses, has been developed.

Major Differential Diagnosis in Hypoalbuminemia

1. Protein-losing nephropathy

Renal amyloidosis Glomerulonephritis

Common causes of PLN, amyloidosis and glomerulonephritis, can be distinguished by kidney biopsy. It is controversial whether biopsies should always be performed, as these diseases do not always respond to treatment and renal biopsy is invasive.

2. Hepatic Insufficiency

Hepatic failure has many causes, and the most common causes include:

chronic hepatitis

hepatic lipidosis

cholangiohepatitis

hepatic neoplasia

Copper toxicity

FIP

Cirrhosis

Portosystemic shunt

Because of the multitude of causes of hepatic failure and many of the underlying etiologies that are specifically treatable, definitive diagnosis by fine-needle hepatic aspiration (limited diagnostic utility), ultrasound-guided liver biopsy, or exploratory laparotomy for excisional liver biopsies (or imaging techniques in Portosystemic shunts) is almost always always available.

3. Protein Losing Enteropathy (PLE)

Among the most common causes of PLE are:

inflammatory bowel disease (IBD)

lymphangiectasia

Neoplasia (lymphosarcoma)

Gastrointestinal parasites

histoplasmosis

pythiosis

Because the causes of PLE respond to numerous and different treatment regimens, gastrointestinal biopsy via endoscopy or laparotomy can usually be performed.

Treatment of Hypoalbuminemia

If a diagnosis cannot be made, the options for treating hypoalbuminemia are unfortunately somewhat limited.

The main treatment options are given below:

1. Specific Disease Process Treatment

As a general rule, most causes of PLE can be treated effectively, and many causes of hepatic failure can be managed or, in limited cases, cured.

On the other hand, causes of PLN rarely respond to specific treatment.

Examples of disease-specific therapy include:

immunosuppressive therapy

inflammatory bowel disease
chronic hepatitis
lymphocytic cholangiohepatitis
Glomerulonephritis (rarely responds to treatment)

Chemotherapy

lymphosarcoma

antibiotics

Suppurative cholangiopathy

Intensive nutritional support

hepatic lipidosis

Copper chelating agents

Copper-associated hepatopathy of Bedlingtons and other dog breeds

Ursodeoxycholic acid (UDCA)

Chronic hepatitis and cholangiopathy

DMSO and/or colchicine

Renal amyloidosis (very rarely effective)

It is best to make a definitive diagnosis before starting a specific treatment. However, in rare cases where a diagnosis cannot be reached, immunosuppressive doses glucocorticoidtreatment that includes it may be worth a try.

2. Drainage of fluid in the pleural and body cavities

accumulating liquid dyspnea(pleural effusion) or to abdominal discomfort It is recommended in cases where it causes (ascites). If the underlying cause is not treated, the fluid taken will tend to re-accumulate rapidly. Repeated fluid intake will put the patient in excessive fluid loss (dehydration) and hypovolemia. It will increase the risk of causing secondary pyloritis and peritonitis.

3. Treatment with Colloids

Crystalloids are aqueous solutions based on sodium, electrolyte and glucose. Colloids, on the other hand, contain larger molecules that do not easily leave the vascular space. Colloid solutions therefore do the same job as albumin, which retains water in the vascular space and increases blood volume.

PlasmaThe prototype is the colloidal solution. dextranand hydroxyethyl starch (Hetastarch)available in synthetic colloid solutions.

Colloid Solutions

liquid type

starting dose

Colloids (dextran, hetastarch)

5-10ml/kg in 10-20 minutes

Plasma

5-10ml/kg in 10-20 minutes

all blood

10-15ml/kg in 10-20 minutes

from liver failurein patients with insufficient albumin production due to plasma initially seems to be the preferred colloidal solution in hypoalbuminemic patients. In these patients, albumin given by transfusion is expected to circulate effectively in the body for several weeks. With this, PLNor with PLEIn patients, transferred plasma is almost always ineffective because exogenously administered albumin tends to leak extravasously too quickly, along with the animal’s own albumin.
In fact, in such patients, although plasma albumin is often measured immediately after transfusion, it is not significantly measurably increased due to leakage. Due to problems with the use and supply of plasma or albumin in patients with PLN or PLE, synthetic colloids is the preferred liquid in such animals. Because most commercial synthetic colloids contain larger molecules than albumin.
These molecules therefore remain in circulation rather than leaking out the same way as albumin.

But recent research in dogs with low oncotic pressure has shown that even synthetic colloids are rarely effective for longer than a day. Colloid transfusions should therefore be scheduled for the time they will be most effective (for example, before and during anesthesia and surgery) and are given two or three times a day to critically ill patients.

like normal saline crystalloid solutions, increases blood volume and hydrostatic pressure without increasing oncotic pressure. In fact, such solutions often dilute the patient’s remaining albumin concentration, reducing oncotic pressure. Indiscriminate use of crystalloids in patients with moderate to severe hypoalbuminemia (especially if there is edema, ascites, or pleural effusion) is therefore very dangerous and can cause acute pulmonary edema.

Crystalloid solutions are very dangerous in patients with moderate to severe hypoalbuminemia.

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