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Why is hematocrit low: Hematocrit Test: MedlinePlus Medical Test

all you need to know!

If fatigue has hit your doorstep, and you notice various symptoms such as pale complexion, decreased endurance, shortness of breath, tachycardia, difficulty in concentrating, or even tendency to faint, it may be time for some blood tests!

Surely your doctor will tell you which indicators to check, however it is easier when you yourself understand what it is about! After all, most of us today want to know exactly what is going on in our body and how we can deal with it.

Table of Contents

What is a hematocrit?

The hematocrit is a value that indicates the percentage of the volume occupied by red blood cells in our blood. These are the cells that contain hemoglobin, a protein that carries oxygen to the tissues and is responsible for the red color in the blood!

Red blood cells are produced in the bone marrow. To do this you need some nutrients such as iron, folic acid and Vitamin B12! When they are absent from the body due to poor nutrition or due to some disease, then there is difficulty in the production of red blood cells, their amount in the blood decreases and the result is a low hematocrit!

Symptoms of low hematocrit

But how does one understand that he has a low hematocrit? Some of the most common symptoms that should make us suspect that something is wrong are (1):

  • Pale or yellow skin complexion
  • Weakness, low energy
  • Fatigue
  • Breathing difficulty
  • Tachycardia or arrhythmia
  • Cold hands or feet
  • Difficulty in concentrating
  • Dizziness or fainting
  • Intense hair loss
  • Fragile nails
  • Pica syndrome: a tendency to consume inedible substances
  • Restless legs syndrome

Many of them also indicate the presence of anemia, a condition quite common in women, in which also low hemoglobin levels are observed.

Low hematocrit: When is it observed?

But how does the body get to the point of having a low hematocrit and what are the main causes? It is usually seen in the following cases:

1.Bleeding

There may be some obvious external bleeding, as is often the case with heavy menstruation or an accident. Sometimes, however, there may be internal bleeding that we have not noticed, such as e.g. occurs in peptic ulcers due to the bacterium H.pylori or chronic use of anti-inflammatory drugs (2).

2. Nutritional deficiency or malnutrition

Lack of iron, vitamin B12 or folic acid in the diet can be very important causes.

3. Inability to properly absorb iron from the body

It may be due to an illness, the wrong food combinations (see below) or an malabsorption syndrome.

4. Hormonal disorders

There may be disturbances in hormones that play an important role in erythropoiesis (eg erythropoietin), menstruation or thyroid function.

5.

Bone marrow diseases

Since red blood cells are produced in the bone marrow, some relative health issues have a direct effect on hematocrit levels.

6. Kidney disease

Kidney disease can reduce the production of red blood cells and consequently lead to low hematocrit levels (2).

7. Taking various medications

Some drugs can cause a drop in the hematocrit as a side effect. Your doctor will inform you about it and you will definitely find it on the package leaflet.

8. Pregnancy

There is an increased need for folic acid and iron, which is often not covered by the diet, which is why most gynecologists often recommend a specialized supplement.

9. Liquid overload

Since the hematocrit is an indicator that shows the percentage of volume occupied by red blood cells per blood unit volume, it is easy to see that an overload of fluid can disrupt its levels.

In addition, a small drop in hematocrit can be observed in viruses, body fatigue, intense stress, but also insomnia! When the hematocrit value is low, then oxygen has difficulty reaching body organs.

Foods that strengthen the hematocrit

If the low hematocrit is due to a lack of iron, then you should include in your diet foods rich in it, both from animal (heme iron) and plant (non-heme iron) sources. Very good options for increasing hematocrit are the following (3):

Good sources of heme iron

  • Oysters, mussels, clams (avoidance by pregnant women)
  • Beef or chicken liver (avoidance by pregnant women)
  • Meat, poultry
  • Sardines, tuna and other fish
  • Eggs

Good sources of non-heme iron

  • Dark green vegetables
  • Nuts and seeds (preferably raw and unsalted)
  • Legumes
  • Quinoa
  • Sweet potatoes
  • Whole grain foods
  • Dried fruits (prefer sugar free)
  • Molasses
  • Dark chocolate (at least 45% in cocoa)
  • Tofu
  • Soy

Animal vs Vegetable Iron

Depending on whether the iron is of animal or plant origin, ie whether it is heme or non-heme, there is a difference in its bioavailability, ie the percentage that is ultimately absorbed by the body. It is a fact that iron from animal foods has a much higher bioavailability compared to that of plant origin.

In order to improve the absorption of non-heme iron, combine it with fruits and vegetables rich in Vitamin C, β-carotene and malic acid! Some good combinations are the following:

  • Lentils and other legumes with red pepper, carrot, tomato or even vinegar
  • Dark green vegetables with lemon juice or good quality vinegar
  • Colorful salads (vegetables in green-red-orange)
  • Unsalted raw nuts with dried fruits (eg apricots, plums, dates, raisins, strawberries)
  • Whole grains with dried fruits, orange, kiwi etc.

Foods that reduce iron absorption

Beware of plant iron sources, so as not to combine with foods rich in calcium, tannins or phytates, as its absorption is reduced. Avoid combining e.g. beans or spinach with cheese, drink tea or coffee immediately after a meal, while be sure to soak legumes and whole grains in lukewarm water with a little lemon for several hours in order to reduce phytates.

Other causes of low hematocrit

If low hematocrit is due to a lack of Vitamin B12, then focus on foods of animal origin, while if folic acid or otherwise vitamin B9 is the problem, find it in whole grains, legumes, spinach, avocados, asparagus. etc.

What is ferritin?

Ferritin is a protein that stores iron and under normal conditions reflects the total iron stores in the body. It is a reliable indicator and disturbances in its levels can mean serious problems for our body. People with hypothyroidism often have low ferritin levels (4).

Low ferritin

Low ferritin levels indicate iron deficiency, which can lead to anemia, but is also associated with hypothyroidism, leg weakness, difficulty in breathing, even fainting. Low ferritin can result in skin, hair and nail lesions, and in severe cases, clefts in mouth corners , cavities or even a neurological syndrome (4).

High ferritin

When ferritin levels are high then it means that the body is overloaded with iron, a condition of particular concern as it may indicate a liver problem, the presence of inflammation, while some research shows an increased risk of atherosclerosis mainly in men (5).

Some of the symptoms that indicate high ferritin are fatigue, joint pain, decreased memory and mood disorders, or liver disorders (4).

Is there a special examination?

The hematocrit (Hct) measurement is part of the “General Blood Test“, and is prescribed by the treating physician. By further checking the hemoglobin levels, we can determine if someone has anemia.

Further tests that can show the causes of low hematocrit are the control of iron, B12, folic acid, but also ferritin! It is not uncommon to have normal hematocrit and iron, but low ferritin. That’s why it’s good to include the control of the latter, since as we said it shows the iron reserves in the body.

Iron supplements

The specialist who monitors you will give you specific instructions and if he deems it necessary will recommend a dietary supplement with iron, folic acid or B12 depending on the deficiencies that will be identified.

Side effects

Particular attention should be paid to the form in which these nutrients will be found, in order to avoid unpleasant side effects, but also to have better bioavailability in the body.

Specifically, in the case of iron, disorders are sometimes observed, such as constipation, nausea, stomach upset, abdominal pain, tendency to vomit, metallic taste, etc. (3). It is therefore very important to inform your doctor if you notice any discomfort, but also to read carefully the description of the preparation before taking it.

If constipation occurs for several days and is not treated or stopped, the poisoning can be caused, since the useless substances are not eliminated, but accumulate in the intestine. Now, there are specialized formulas of dietary supplements, which emphasize that they do not cause constipation and do not bother the stomach.

Instructions for Use

Also, read the instructions for use carefully about when to take the supplement (on an empty or full stomach), as this often varies by manufacturer. Usually, iron intake is recommended on an empty stomach or with the simultaneous consumption of a source of vitamin C (eg orange juice).

At Vita4you.gr you will find a great variety of supplements for anemia!

References

  1. How to get more iron from the diet
  2. What is a normal hematocrit level?
  3. The Nutrition Source – Iron
  4. Λεξικό διατροφής: Φερριτίνη
  5. Association Between High Serum Ferritin Levels and Carotid Atherosclerosis in the Study of Health in Pomerania (SHIP)

Anemia in the Elderly | AAFP

DOUGLAS L. SMITH, M.D.

Am Fam Physician. 2000;62(7):1565-1572

Anemia should not be accepted as an inevitable consequence of aging. A cause is found in approximately 80 percent of elderly patients. The most common causes of anemia in the elderly are chronic disease and iron deficiency. Vitamin B12 deficiency, folate deficiency, gastrointestinal bleeding and myelodysplastic syndrome are among other causes of anemia in the elderly. Serum ferritin is the most useful test to differentiate iron deficiency anemia from anemia of chronic disease. Not all cases of vitamin B12 deficiency can be identified by low serum levels. The serum methylmalonic acid level may be useful for diagnosis of vitamin B12 deficiency. Vitamin B12 deficiency is effectively treated with oral vitamin B12 supplementation. Folate deficiency is treated with 1 mg of folic acid daily.

Anemia is common in the elderly and its prevalence increases with age.1–4 Using World Health Organization criteria for anemia (hemoglobin of less than 12 g per dL [120 g per L] in women and less than 13 g per dL [130 g per L] in men), the prevalence of anemia in the elderly has been found to range from 8 to 44 percent, with the highest prevalence in men 85 years and older. 1–3

The increased incidence of anemia with aging has led to speculation that lower hemoglobin levels may be a normal consequence of aging. However, there are at least two reasons for considering anemia in the elderly as a sign of disease. First, most older people maintain a normal red cell count, hemoglobin and hematocrit. Second, in most elderly patients an underlying cause of anemia is found for hemoglobin levels of less than 12 g per dL.5

Clinical Presentation

Even though the high prevalence of anemia in the elderly makes it a condition that clinicians might expect to find frequently, several features of anemia make it easy to overlook. The onset of symptoms and signs is usually insidious, and many elderly patients adjust their activities as their bodies make physiologic adaptations for the condition. Typical symptoms of anemia, such as fatigue, weakness and dyspnea, are not specific and in elderly patients tend to be attributed to advancing age. Pallor can be a helpful diagnostic clue, but pallor can be hard to detect in the elderly. Conjunctival pallor is a reliable sign, and its presence should prompt the clinician to order blood tests for anemia.6

Aside from conjunctival pallor, few other signs are attributable specifically to anemia. Frequently, patients have signs of a disorder that is made worse by the anemia, such as worsening congestive heart failure, cognitive impairment, dizziness and apathy. Unless clinicians consider anemia as a possibility in the elderly, it can be easily overlooked.

Cohort studies2,5 of the elderly have found that the two most common causes of anemia in the elderly are chronic disease and iron deficiency (Table 15). In 15 to 25 percent of elderly patients with anemia, no cause is found; even when no cause is found the prognosis is good.

Cause of anemiaPercentage of cases
Anemia of chronic disease30 to 45
Iron deficiency15 to 30
Posthemorrhagic5 to 10
Vitamin B12 and folate deficiency5 to 10
Chronic leukemia or lymphoma5
Myelodysplastic syndrome5
No identifiable cause15 to 25

EVALUATION

Anemia in the elderly is evaluated in a manner similar to that in younger adults, including an assessment for signs of gastrointestinal blood loss, hemolysis, nutritional deficiencies, malignancy, chronic infection (such as subacute endocarditis), renal or hepatic disease, and other chronic disease. In patients without evidence of an underlying disease, the initial laboratory evaluation should include a complete blood count, red blood cell indices, a reticulocyte count and peripheral blood smear (Table 2).

TestFindingPossible etiology
Complete blood count
RBC indicesMCV < 80 μm3 per cell (80 fL)Iron deficiency anemia
Anemia of chronic disease
MCV > 100 μm3 per cell (100 fL)Vitamin B12 deficiency; folate deficiency
MCV normalRenal, liver and thyroid diseases as well as those above
WBC and platelet countsAbnormalPrimary marrow production problem
Peripheral smearBurr cellsChronic renal failure
Spherocytes, fragmentsHemolytic diseases
Dysplastic changesMyelodysplasia
Reticulocyte count< 1%Inadequate production in presence of anemia
≥1%Increased production but unclear whether it is of appropriate magnitude; reticulocyte index helpful for clarification
Reticulocyte index*≥2Reticulocyte release appropriate for anemia
< 2Inadequate response to anemia

Anemia algorithms used for evaluation of younger adults are based on the mean corpuscular volume. Such algorithms may be less helpful in the elderly because the classic changes in erythrocyte size do not often accompany anemia in this age group. In most elderly patients with anemia, red cell indices disclose normocytic, normochromic anemia.7,8 Clinicians therefore might begin the evaluation of anemia as they would in younger adults, but, if they do not find one of the classic causes of microcytosis or macrocytosis, the search for a cause might need to be enlarged (Figure 1). It also should be remembered that the cause of anemia is not always found.

Anemia of Chronic Disease

Anemia of chronic disease, also called anemia of chronic disorders, is the most common form of anemia in the elderly.9,10 Numerous diseases are associated with anemia of chronic disease (Table 39), but in many cases an underlying disease is not identified.

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The hematologic abnormality in anemia of chronic disease is an impaired ability to use the iron stored in the reticuloendothelial system. The reason the reticuloendothelial cells do not release iron is not known, but experts speculate that, similar to fever, this response aids the body’s defense mechanisms.11 Iron that is held in the reticuloendothelial system is not available for bacterial growth. Nor is the iron available for erythropoiesis, which is the similarity between anemia of chronic disease and iron deficiency anemia. The difference, however, is that the iron stores are normal or increased in anemia of chronic disease.

Patients with anemia of chronic disease have mild to moderate anemia that tends to correlate in severity with the underlying disease, although the anemia rarely progresses to a hemoglobin below 10 g per dL (100 g per L). In anemia of chronic disease, the erythrocytes are usually normochromic and normocytic, but about one third of patients with anemia of chronic disease have microcytosis. 8,12

DIFFERENTIATING ANEMIA OF CHRONIC DISEASE FROM IRON DEFICIENCY ANEMIA

Iron deficiency anemia is the main hematologic disorder to consider in the differential diagnosis of anemia of chronic disease (Table 49,13).14–16 Iron deficiency anemia and anemia of chronic disease are accompanied by a low serum iron level. Microcytosis may or may not be present in either disorder. The total iron-binding capacity (TIBC) tends to be increased when iron stores are diminished and decreased when they are elevated. In classic iron deficiency anemia, the TIBC is higher than 400 μg per dL (72 μmol per L). In anemia of chronic disease, the TIBC is usually below normal, not only because the iron stores are elevated but also because, as an acute-phase reactant, transferrin is reduced in the presence of acute and chronic stress.

Laboratory testRange for normal valuesIron deficiency anemiaAnemia of chronic disease
Serum iron, μg per dL (μmol per L)60 to 100 (11 to 18)< 60 (11)< 60 (11)
Total iron-binding capacity, μg per dL (μmol per L)250 to 400 (45 to 72)> 400 (72)< 250 (44)
Transferrin saturation, %20 to 60< 16< 20
Serum ferritin, ng per mL (μg per L)100 to 300 (100 to 300)< 100 (100)> 100 (100)

The serum ferritin level is the most useful test, differentiating anemia of chronic disease from iron deficiency anemia in 70 percent of patients. 17 Ferritin can also be an acute-phase reactant in liver injury and in some types of tumor, raising the serum ferritin to normal levels even in the presence of iron deficiency. For some cases in which both iron deficiency and anemia of chronic disease are possible, bone marrow aspiration is often the only means of identifying the true cause of the anemia (Table 49,13).

TREATMENT

There is no specific therapy for anemia of chronic disease except to manage or treat the underlying disorder. Iron therapy is of no benefit. Erythropoietin may be helpful in some patients with anemia of chronic disease. The dosage is 50 to 100 U per kg three times a week. The dosage can be increased to 150 U per kg per dose if the response to a lower dose is inadequate.

Iron Deficiency Anemia

Iron deficiency anemia, the second most common cause of anemia in the elderly, usually results from chronic gastrointestinal blood loss caused by nonsteroidal anti-inflammatory drug–induced gastritis, ulcer, colon cancer, diverticula or angiodysplasia. Chronic blood loss from genitourinary tract cancer, chronic hemoptysis and bleeding disorders may result in iron deficiency but are much less common causes. Older persons may become iron deficient because of inadequate intake or inadequate absorption of iron. Without blood loss, anemia takes several years to develop.

The serum ferritin level is the most effective way to diagnosis iron deficiency anemia. When the serum ferritin is less than 15 ng per mL (15 μg per L), iron deficiency is virtually certain (Table 514–17). Iron deficiency is unlikely if the serum ferritin level is greater than 100 ng mL (100 μg per L). Although ferritin levels between 15 and 100 ng per mL are moderately predictive of iron deficiency anemia, patients with levels in this range may have iron deficiency anemia, anemia of chronic disease, or both. If it is important to determine which is present or if the patient does not respond to iron therapy, a bone marrow biopsy might be necessary to measure iron stores directly.

Serum ferritin, ng per mL (μg per L)Sensitivity (%)Specificity (%)Likelihood ratio*
< 100 (100)94713.2
< 45 (45)859211.1
< 15 (15)599954.5

Iron deficiency anemia in the elderly almost always leads to an evaluation of the gastrointestinal tract as a possible source of bleeding. In 20 to 40 percent of patients, the source is in the upper gastrointestinal tract from peptic ulcer disease, gastritis, esophagitis or gastric cancer.18–20 The blood loss is in the colon in 15 to 30 percent of cases, most often caused by colon cancer, angiodysplasia, polyps or colitis. 18–20 A few patients (1 to 15 percent) have blood loss from disorders in the upper and lower gastrointestinal tract.18–20 The source is not found in the remaining 10 to 40 percent of elderly patients with gastrointestinal blood loss.18–20 Long-term follow-up of elderly patients in whom the gastrointestinal source is not identified indicates that most often the anemia resolves or remains stable with iron replacement.21

TREATMENT

In addition to treatment of the cause of bleeding, iron supplementation should be initiated for the treatment of iron deficiency anemia. The usual recommended dose of elemental iron is 50 to 100 mg three times a day; however, a smaller amount of elemental iron, such as a single 325-mg tablet of iron sulfate, may minimize side effects and improve compliance.22 This dose, equivalent to approximately 97.5 mg of elemental iron, is usually sufficient to replace iron stores, albeit at a slower rate.

Reticulocytosis usually starts within a week of initiation of oral iron supplementation. If the reticulocyte count increases but the anemia does not improve, continued blood loss or inadequate iron absorption must be considered. Intravenous iron replacement can be helpful in patients with iron deficiency that fails to respond to oral replacement.

Vitamin B12 Deficiency

While studies suggest that vitamin B12 (cobalamin) deficiency is the cause of anemia in 5 to 10 percent of elderly patients, the actual prevalence of vitamin B12 deficiency is likely to be much higher in the elderly.4,23 Vitamin B12 deficiency is difficult to detect in the elderly. First, the symptoms and signs of vitamin B12 deficiency are not reliably present in the elderly. Only about 60 percent of patients with vitamin B12 deficiency are anemic.20 In addition, neurologic symptoms of B12 deficiency can develop before the patient becomes anemic.24 Second, although anemia due to vitamin B12 deficiency is usually macrocytic and megaloblastic, it can be normocytic or even microcytic. Third, serum B12 levels do not reliably reflect tissue B12 deficiency. Up to 30 percent of patients with low-normal serum vitamin B12 levels have anemia and neurologic disease.23 This observation has prompted a search for more reliable ways of detecting vitamin B12 deficiency.

Studies have shown that serum methylmalonic acid and homocysteine levels are sensitive for detecting subclinical vitamin B12 deficiency, virtually excluding vitamin B12 deficiency when they are normal.25 These tests have become more widely available in recent years, but remain expensive, costing approximately $150 for each test. A less-expensive spot urinary methylmalonic acid assay has been purported to be an alternative to the serum assay.26 In addition to the advantage of reduced cost, the urinary assay can be normalized to creatinine levels, allowing correction for renal insufficiency and dehydration, both known to cause methylmalonic acid elevation. The disadvantage of the urinary assay is that it is not readily available.

A question that remains unanswered is which elderly patients with anemia should be further evaluated for vitamin B12 deficiency when the serum B12 level is normal. Some authorities recommend that serum B12 screening be initially performed in all elderly patients, with further testing in those with a B12 level of less than 350 pg per mL (260 pmol per L).4 Until the effectiveness of different screening strategies is evaluated, clinicians need to use their own judgment to decide how to identify vitamin B12 deficiency before it leads to anemia or neurologic disease.

CAUSES OF VITAMIN B12 DEFICIENCY

Vitamin B12 deficiency rarely is the result of inadequate intake, except in persons who are strict vegans. A common cause is reduced intestinal absorption of vitamin B12. Pernicious anemia is a classic example of a disorder that causes reduced intestinal absorption of vitamin B12. With pernicious anemia, the lack of intrinsic factor results from destruction of the gastric parietal cells by autoimmune antibodies. One study revealed that undiagnosed pernicious anemia was present in nearly 2 percent of otherwise healthy individuals 60 years or older.27 Inadequate absorption of vitamin B12 occurs in 10 to 30 percent of patients who have had a partial gastrectomy.28 It also may occur in patients with small bowel disorders and bacterial overgrowth. The prevalence of many of these conditions increases with age.

Previously, the Schilling test would have been used to identify the cause of inadequate vitamin B12 absorption. Recent studies, however, show that high-dose oral vitamin B12 effectively treats the deficiency regardless of the cause. Thus, there is less need to perform the Schilling test. (A review of the steps of the Schilling test can be found in a 1996 article in American Family Physician.29)

TREATMENT

Vitamin B12 deficiency is treated by vitamin B12 supplementation, parenterally or orally. The intramuscular dose is 1,000 μg, often given daily for one week to build up stores, then weekly for one month and then monthly thereafter. Oral therapy with 1,000 to 2,000 μg of vitamin B12 daily has been shown to be as effective as intramuscular injections and in some ways may be superior.26 A response to therapy, characterized by an increase in reticulocytosis, often occurs within a week of the initiation of vitamin B12 therapy.

Folate Deficiency

Unlike vitamin B12 deficiency, folate deficiency usually develops as a result of inadequate dietary intake. The body stores very little folate, only enough to last four to six months. Like vitamin B12 deficiency, folate deficiency classically causes macrocytic anemia, although a significant proportion (25 percent) of elderly patients with folate deficiency have normocytic anemia.8 The symptoms of folate deficiency are nearly indistinguishable from those of vitamin B12 deficiency.

Another similarity between folate deficiency and vitamin B12 deficiency is that the serum folate level can be misleading. The red cell folate concentration is more reliable than the serum level and should be considered. The serum homocysteine level is elevated in 90 percent of patients with folate deficiency25 and can be useful for detecting folate deficiency in patients with low-normal serum folate levels. If the methylmalonic acid level is also elevated, vitamin B12 deficiency must be considered.24 Identification of vitamin B12 deficiency is important: anemia secondary to vitamin B12 deficiency improves with folate therapy, but folate therapy does not reverse the neurologic damage caused by vitamin B12 deficiency. For this reason, it is important to ensure that vitamin B12 deficiency is not also present.

Folate deficiency is treated with oral folic acid, 1 mg daily.

Myelodysplastic Syndrome

Myelodysplastic syndrome is a relatively uncommon cause of anemia, but is a more common cause in the elderly than in younger patients. The syndrome, thought in the past to represent pre-leukemia, is characterized by a defect in the development of one of the marrow cell lines, limiting the release of functioning cells. Anemia results when the red cell lines are affected. Myelodysplastic syndrome should be a diagnostic consideration when white cell or platelet abnormalities accompany the anemia. The diagnosis of this syndrome is usually made by bone marrow biopsy (Table 64,22).

Myelodysplasia is treated supportively with transfusions.

Pancytopenia
Monoclonal gammopathy
Suspicion of myelodysplastic syndrome
Blood smear showing immature white cells or nucleated red cells
Indeterminate status of iron stores
Unexplained progressive or unresponsive anemia

Take an ESR (Erythrocyte Sedimentation Rate, ESR) test

Method of determination
See description.

Important! The results obtained by the Panchenkov and Westergren methods coincide in the region of normal values, in the zone of elevated values, the results obtained by the Westergren method are usually higher than those obtained by the Panchenkov method.

Test material
see description

Non-specific indicator reflecting changes in the protein composition of blood plasma. It is mainly used to diagnose inflammatory conditions and monitor their course.

The classical principle of measuring ESR is that when a certain volume of blood mixed with sodium citrate is placed in a vertically standing test tube or capillary, the erythrocytes will settle down under the influence of gravity, while the repulsive forces that occur between the negatively charged membranes erythrocytes, will prevent this settling. The ESR value is measured as the height of the plasma column above the formed elements, formed in 1 hour. Accordingly, the units of ESR are millimeters per hour (mm/h). With the appearance in the blood plasma of a large number of proteins of the acute phase of inflammation, which include fibrinogen, C-reactive protein, alpha and gamma globulins, etc., or paraproteins, the repulsive force between the erythrocytes decreases, and the erythrocytes settle faster. The erythrocyte sedimentation rate is also affected by their morphology (poikilocytosis of erythrocytes of the test sample leads to an underestimation of ESR, smoothing the shape of erythrocytes, on the contrary, can accelerate ESR), as well as the value of hematocrit (a decrease in hematocrit leads to an overestimation of ESR). In acute inflammatory diseases, ESR usually rises a day after the onset of the disease, while the normalization of this indicator after recovery is slower, and can take from several days to two or more weeks.

Also in modern laboratory practice, modified methods for measuring ESR are used to speed up and automate the performance of this test. With the help of a mathematical algorithm, the results obtained by these methods are reduced to the scales of classical methods (according to Westergren and Panchenkov), and are also given in the usual units, mm/hour.

In INVITRO, three methods are used to perform the ESR study:

ESR from venous blood in INVITRO is performed from test tubes with EDTA, using an automatic analyzer Ves-matis Cube 80 (Diesse Diagnostica senese S.p.A., Italy). In cases where this is not possible, the study can be performed by the micromethod (TEST1, Alifax, Italy)

Comparison of ESR methods used in INVITRO

Method name Principle Scale
ESR according to Westergren Measurement of the height of the plasma column above the shaped elements 0-200 mm/hour
TEST1, Alifax Measurement of the height of the plasma column above the shaped elements 0-100 mm/hour


In any case, the method by which the study was conducted is indicated when the result is issued.

Test material:

Venous blood – single tube with citrate / EDTA-stabilized whole blood.

Capillary blood is whole blood stabilized with EDTA.

Anemia in dogs – types of anemia, treatment and care in Moscow. Veterinary clinic “Zoostatus”

Anemia with blood loss

Hemolytic anemia

Immune-mediated (autoimmune) hemolytic anemia

Congenital hemolytic anemia

Anemia in dogs is a lack of red blood cells (erythrocytes) in the cardiovascular system. Adult dogs are anemic when the concentration of red blood cells (hematocrit) is less than 37%. The normal range for hematocrit is 39 – 60%.

Red blood cells are produced by the bone marrow and live an average of 110 – 120 days. Old red blood cells are filtered and destroyed by the spleen and removed from the circulation. The iron they contain is recycled to make new red blood cells.

The main task of red blood cells is to carry oxygen. Thus, the symptoms of anemia are caused by insufficient oxygen in the organs and muscles.

Signs of anemia are lack of appetite, general lethargy and weakness. The mucous membranes of the gums and tongue become pale pink or white. Dogs with severe anemia have elevated pulse and respiratory rates. On examination, heart murmurs are heard.

Anemia can be caused by blood loss, hemolysis, or insufficient production of red blood cells.

In adult dogs, the most common causes of blood loss are trauma, gastrointestinal bleeding associated with gastric and duodenal ulcers, parasites, and tumors in the gastrointestinal tract. Chronic blood loss can also occur with lesions in the urinary system. Hookworms and fleas are common causes of chronic blood loss in puppies.

Treatment should be directed to the underlying cause of the anemia. Gastrointestinal bleeding can be detected by examining the stool for microscopic traces of blood. A urinalysis will reveal traces of blood in the urine, which may not be visible to the naked eye. Other tests may also be used to determine the cause of occult (microscopic) bleeding.

Hemolysis is a greatly accelerated breakdown of red blood cells. Normally, erythrocytes are destroyed in the spleen, decay products are involved in the formation of bile and “new” hemoglobin for the construction of young erythrocyte cells. In severe hemolysis, these breakdown products accumulate in the body. Accordingly, a dog experiencing an acute hemolytic crisis may show jaundice and hemoglobinuria (dark brown urine containing hemoglobin). In addition, the dog appears weak, pale, and has a rapid pulse. The spleen, liver, and lymph nodes may be enlarged.

Causes of hemolysis include immune-mediated hemolytic anemia, congenital hemolytic anemia, infectious diseases (such as babesiosis and leptospirosis), drug reactions such as acetaminophen, and venomous snake bites. Many bacteria produce toxins that destroy red blood cells, so hemolysis can also occur in severe infections.

This is the most common cause of hemolysis in adult dogs. The destruction of a red blood cell is caused by autoantibodies that attack antigens present on the surface of cells, or by antigens from drugs or organisms that are attached to the walls of the red blood cell. Weakened cells are filtered in the spleen and destroyed.

Poodles, Bobtails, Irish Setters and Cocker Spaniels are particularly susceptible to immune-mediated hemolytic anemia, but the disease can occur in all dog breeds. Usually sick dogs aged 2 to 8 years, females are four times more likely than males.

In most cases, autoimmune hemolytic anemias are idiopathic, ie. the cause of the autoantibodies is unknown. Immune-mediated hemolytic anemia also occurs in systemic lupus erythematosus.

Diagnosis is made by microscopic examination of blood smears, which reveal certain changes in the appearance of red blood cells and other blood elements; and serological blood tests.

Treatment of idiopathic hemolytic anemia is aimed at preventing further destruction of red blood cells by blocking the antigen-antibody reaction with corticosteroids and immunosuppressants. Severe anemia is treated with blood transfusions. Splenectomy (removal of the spleen) may be helpful, but only when tests show that the spleen contributes to the hemolytic process.

The response to treatment depends on the rate of hemolysis and the ability to find and eliminate the underlying cause. Even with adequate treatment, the mortality rate for this disease is close to 40%.

Several hereditary pathologies in the structure of red blood cells can lead to their premature destruction. Phosphofructokinase deficiency is caused by an autosomal recessive gene found in English Springer and Cocker Spaniels. A lack of this enzyme leads to changes in the pH of red blood cells, causing the cells to periodically divide and cause bouts of hemoglobinuria. There is no effective treatment for this disease.

Pyruvic acid kinase deficiency is another enzyme deficiency in the erythrocyte caused by an autosomal recessive gene. This disease has been identified in several breeds, including Basenjis, Beagles, and West Highland White Terriers. Puppies usually develop hemolytic anemia between 2 and 12 months of age. Death occurs before the age of 3 years.

(с) Veterinary center for the treatment and rehabilitation of animals “Zoostatus”.