Precautions in the dental treatment of children with deficiency anemias – an overview

Introduction

The term anemia refers to a reduction in the blood’s ability to carry oxygen, which is characterized by a drop in hemoglobin, hematocrit, and red blood cell count. This reduction can be caused by blood loss (iron deficiency anemia), a decrease in red cell production (aplastic anemia), or an increase in red cell destruction (hemolytic anemia)⁽¹⁾.

Anemia is defined by the World Health Organization as a hemoglobin (Hb) level in adult males below 13 g/dL, in adult females not pregnant below 12 g/dL, and in pregnant women below 11 g/dL. Because hemoglobin levels might differ between races and ages, caution must be used, especially when interpreting borderline readings⁽²⁾.

Classification

I. Morphological classification based on erythrocyte indices (mean cell volume – MCV; mean cell hemoglobin – MCH; mean corpuscular hemoglobin concentration – MCHC), in:

A. Macrocytic anemias characterized by an increase in MCV (folate deficiency, vitamin B12 deficiency).

B. Normochromic, normocytic anemias with normal indices (posthemorrhagic, sickle cell anemia – SCA, some hemolytic anemias, glucose 6-phosphate dehydrogenase – G6PD deficiency).

C. Microcytic hypochromic anemias with a decrease in all indices (anemias due to deficiency of iron, thalassemia, inflammatory anemias).

D. Normochromic microcytic anemias in which only the MCV is low (spherocytosis hereditary).

II. Physiopathological classification according to the production mechanism, in:

A. Central anemias – due to insufficient marrow production with decreased production of erythrocytes.

B. Peripheral anemia – due to increased loss or destruction of erythrocytes.

III. Erythrokinetic classification according to the number of reticulocytes, in:

A. Regenerative anemia, when reticulocytes are 150,000/mm³, the cause being peripheral (hemolysis, hemorrhages).

B. Hypo- or aregenerative anemia, when the reticulocytes are <50,000/mm³, the cause being central (depression or medullary suffocation)⁽³⁾.

The diagnosis is established based on:

1. Clinical suspicion of anemia, in case of pallor of the skin and mucous membranes, cardiovascular changes (tachycardia, large pulse, “anemic” breath, etc.).

2. Anamnesis regarding child’s age, ethnicity, family history of hematological diseases, nutritional survey, presence of jaundice, recent infections, or blood loss.

3. Laboratory and paraclinical examinations:

a) confirmation of the suspicion of anemia by the decrease of Hb below 11 g% in infants and small children and below 11.6% in children over 5 years old⁽⁴⁾;

b) isolated damage to the erythrocyte line or global interest in hematopoiesis;

c) establishing the mechanism of anemia production by determining reticulocytes;

d) establishing the etiology.

• Morphological examination of peripheral blood

- hypochromic microcytes: iron deficiency anemia, thalassemic syndrome, anemias by disrupting HEM synthesis;

- macrocytes: folate deficiency, B12 vitamin deficiency;

- normochromic normocytes: acute posthemorrhagic anemias, anemias from infections or chronic inflammations, anemias due to infiltration of the bone marrow with neoplastic cells, aplastic anemias;

- specific morphological aspects: microspherocytes, ovalocytes, sickle cells, the presence of Heinz bodies.

• Bone marrow examination

e) specific examinations to confirm the etiological diagnosis of an anemia⁽⁵⁾.

• Iron deficiency anemias: serum iron concentration, ferritin, TIBC (total iron binding capacity), occult hemorrhages, sideroblasts in the bone marrow.
• Anemias due to folate or B12 vitamin deficiency: B12 serum level, serum or erythrocyte folates, B12 vitamin absorption tests, gastric tube, morphological examination of the bone marrow.
• Corpuscular hemolytic anemias: morphological examination of the peripheral blood smear, autohemolysis tests, osmotic fragility tests, thermal stability test, Hb electrophoresis, determination of erythrocyte enzyme activity, etc.
• Extracorpuscular hemolytic anemias: Coombs test, erythrocyte lysis test in acid medium, erythrocyte lysis test in the presence of dextrose, etc.
• Aplastic anemia: morphological examination of the bone marrow, cytogenetic studies.

Table 1 summarizes the necessary further tests and therapies for determining the cause of anemias, as suggested by Patton and Glick⁽⁶⁾.

Deficiency anemias

1. Iron-deficiency anemia

Iron-deficiency anemia – which is typically hypochromic and microcytic – afflicts approximately one-third of the global population. It is more common in women and increases in occurrence with age⁽⁷⁾. According to World Health Organization (WHO) data from 2001, in developing countries, 30% of children between the ages of 0 and 4 years old and 48% of children between the ages of 5 and 14 years old are anemic⁽⁸⁾. If it is minor or asymptomatic, it usually doesn’t need any therapy at all⁽⁷⁾. It can be brought on by inadequate iron intake associated with unhealthy eating patterns, severe blood loss, such as that seen in menorrhagia and some gastrointestinal ulcers, or an increased need for iron during pregnancy or as a result of some chronic illnesses, including Crohn’s disease, ulcerative colitis and hematological cancers^(6,9). A complete blood count (CBC) will typically show low serum ferritin, low iron levels, and increased total iron-binding capacity (TIBC), in addition to decreased red blood cell size (low mean cell volume, or MCV) and mean corpuscular hemoglobin concentration (MCHC) in cases of iron-deficiency anemia. Hypochromic RBC may be seen on a blood smear in a chronic condition. It is important to distinguish between anemia caused by chronic illnesses and iron-deficiency anemia, where the latter has low TIBC and normal ferritin levels along with low circulating iron⁽¹⁰⁾.

Oral manifestations of iron-deficiency anemia⁽¹¹⁾:

• Overall mucosal pallor.
• Tongue that hurts or burns (smooth tongue without papilla; frequently normal Hb).
• Moeller’s glossitis (red line pattern; similar to erythroplakia).
• Atrophic glossitis (red, shiny, smooth, and painful; severe anemia).
• Plummer-Vinson syndrome – mostly affecting women in northern Europe; it causes dysphagia and glossitis, and it increases the risk of oral and post-cricoid cancer.
• Candidiasis (in particular, persistent mucocutaneous; low iron).
• Angular cheilitis (typically linked to Candida albicans).
• Ulcers (particularly, late start; insufficient folate).
• Reduced capacity for healing.

2. Vitamin B12 and folate deficiency anemias

Anemias caused by deficiencies in vitamin B12 and folate are categorized as hypoproliferative and macrocytic. Additionally, both are classified as megaloblastic anemias, which are characterized by segmented neutrophils and abnormal DNA synthesis. They are caused by vitamin B12 and/or folate (previously known as vitamin B9) deficits⁽⁶⁾. Actually, erythropoiesis in the bone marrow depends on both of these vitamin B components^(6,12). Vitamin B12 deficiency anemia – also known as pernicious anemia – typically results from a shortage in intrinsic factor, which is secreted by the gastric mucosa, and has the function of binding to and transporting vitamin B12 down the gut to the terminal ileum, where it is absorbed^(13,14). Vitamin B12 insufficiency has been related to Crohn’s and celiac disease, as well as to some medications, including metformin⁽¹⁵⁾ and proton pump inhibitors (PPIs)⁽¹⁶⁾. Consequently, it might result from starvation, malabsorption, or other disorders; it usually develops gradually over a long period of time, and it is chronic in nature.

However, folate deficiency anemia is primarily a dietary condition, associated with diets low in fruits, vegetables and meat⁽¹⁷⁾ or with impaired folate absorption as a result of gastrointestinal disorders; chronic alcoholics and drug addicts are also at risk for this condition⁽¹⁸⁾. Deficits in folate and vitamin B12 are uncommon worldwide; nonetheless, research indicates that approximately 2% of adults over 60 years old exhibit them⁽⁶⁾.

Oral manifestations of vitamin B12 and folate deficiency anemia⁽¹¹⁾:

• Mucosal pallor.
• Emphasized incremental line.
• Developmental abnormalities brought on by hypomineralization of enamel and delayed tooth eruption.
• Pulpal pain caused by tissue infarction and thrombosis may be the cause of pulp stones or pulp calcification.
• Hypercementosis.
• Tooth decay.
• Hyperplasia of the marrow causing midfacial enlargement, skull thickening, and osteoporotic abnormalities in the mandible.
• Alveolar bone appears as a step ladder.
• Malocclusion, diastema in the midline.
• Coarse trabecular pattern between the root apices.

3. Glucose 6-phosphate dehydrogenase (G6PD) deficiency anemias

Hereditary normocytic hemolytic anemia of the G6PD deficient type is associated with a high rate of RBC destruction due to oxidative stress. It is the most common enzyme disorder, particularly affecting populations in the Mediterranean, Middle East, and Asia⁽¹⁹⁾. The hexose monophosphate shunt route is disturbed by G6PD deficiency, which causes hazardous oxidants to build up inside red blood cells and cause the development of Heinz-Ehrlich bodies; hemolysis removes these entities, which barely pass through the liver and spleen. When the bloodstream of the afflicted individual is subjected to oxidative agents, such as medications (aspirin, sulfonamides, vitamin K, etc.), fava beans and/or infections, hemolysis occurs⁽⁶⁾.

Oral manifestations of hemolytic anemia⁽¹¹⁾:

• Susceptibility to infection.
• Propensity to bleed.
• Issues pertaining to bone marrow transplants.
• Intense mucositis, parotitis or sinusitis (side effects of radiation therapy, cytotoxic treatments, and immunosuppression).
• Lichenoid reactions or xerostomia.
• Edema of the gingiva (from cyclosporine).

Therapeutic dental management
of children with deficiency anemias

As a general recommendation, patients should be sent to their primary care provider if they exhibit anemia-related signs and symptoms. Elective surgical operations may be avoided in many cases, depending on the severity, as there may be a higher risk of bleeding and inadequate wound healing in case of low Hgb levels.

In summary, the precautions in the dental management of children with deficiency anemia would be the following^(20-24):

1. Short dental visits are ideal to minimize potential patient stress.

2. It is impossible to overstate the significance of an intensive preventative program, which should aim to preserve optimal oral health and reduce the likelihood of oral infection.

3. It is not recommended to start dental treatment when a crisis is present. In an emergency, the only course of action that should be taken to improve the patient’s comfort should be offered.

4. Extra caution needs to be used to prevent tissue irritation, since it can cause bacteremia and compromise the suggested course of treatment.

5. It is better to restore teeth, including pulpotomies, rather than removing them.

6. If a pediatric dentist is reasonably convinced that a nonvital tooth can remain free of infection, then performing a polypectomy on it makes sense. If the tooth continues to be a source of infection, extraction is the best course of action.

7. In cooperation with the anesthesiologist and hematologist, general anesthesia should be used with caution during dental procedures.

8. The transfusion aims to lower the patient’s hemoglobin levels below 40% and increase the patient’s hemoglobin level to greater than 10 g/dL. Although transfusions cannot completely prevent venous problems, they can temporarily improve a patient’s condition and lessen the risks associated with surgery.

9. The current consensus is that transfusion hazards should be considered before inducing anesthesia.

10. There are recommended protocols for administering a prophylactic transfusion prior to general anesthesia. Individuals with hematocrit levels below 50% and hemoglobin levels below 7 g/dL more than 20% might need a transfusion.

11. Compared to adult patients, pediatric patients typically experience less posttransfusion problems. Patients with more severe anemia are more likely to be hospitalized frequently, and they may need a transfusion before surgery.

12. A transfusion might not be necessary for minor procedures.

13. According to Malamud, local anesthetic is the recommended anesthetic for those patients who fall under the ASA Ill categories. The application of a local anesthetic has no effect on the delivery of oxygen to the blood molecule.

14. Another use for oral sedation is as an anxiolytic.

15. The oxygenation of the blood molecule is unaffected by the administration of local anesthetics.

16. Use local anesthetic without epinephrine for routine dental care; for surgical procedures, use 1:100,000 epinephrine in local anesthetic.

17. Avoid liberal use of salicylates; control pain with acetaminophen and codeine.

18. Institute aggressive preventive dental care.

Cases to be evaluated while under general anesthesia^(25,26)

1. In order to prevent anemia crises, proper/adequate hemoglobin levels should be activated through transfusion 15 days before to the treatment.

2. A child’s optimal level should be maintained at 10-12 g/dL. Antibiotics will be administered prophylactically prior to the procedure to prevent infection.

3. Aplastic crises, splenic sequestration and other acute illness symptoms are treated with blood transfusions.

4. Use nitrous oxide-oxygen with higher than 50% oxygen, high-flow rate and good ventilation⁽²⁷⁾.

5. Use pulse oximeter, and maintain oxygen saturation above 95%.

Conclusions

Despite being highly prevalent, anemia may not always manifest as a preclinical condition with minimal bearing on dental practice. Children who suffer from anemia often show oral symptoms of the illness. In order to reduce morbidity and prevent a potential result, prevention, early detection and appropriate treatment of oral problems are crucial. Dental professionals should be aware of these symptoms in order to diagnose the condition in children at an early age, as oral lesions may be the initial sign of these anemias. As a result, they live better lives.   

Corresponding author: Diana Monica Preda E-mail: diana_monica_preda@yahoo.com

Conflict of interest: none declared.

Financial support: none declared.

This work is permanently accessible online free of charge and published under the CC-BY licence.