Blood loss is the most concerning cause of iron deficiency, most commonly due to menstrual or gastrointestinal loss. One study found that healthy women lose an average of 30mL (10-110mL) of blood per menstrual cycle.

Poor iron intake is a common cause of deficiency, and less commonly deficiency can be caused by malabsorption. Iron deficiency may occur in late pregnancy, though the most common obstetric cause of anaemia is haemodilution.

The most specific marker of iron deficiency is serum ferritin, and as such a reduced serum ferritin makes iron deficiency likely. Ferritin can be elevated in the setting of an acute phase response and can appear normal, though a serum concentration above 100μg/L makes iron deficiency unlikely.

Iron deficiency will present with an elevated serum transferrin and elevated total iron binding capacity; these two measures are proportional to each other and relatively interchangeable. The transferrin saturation (TSat) is the percentage of iron that is bound to transferrin and is reduced in iron deficiency, though inflammation, infection and malignancy can also reduce the TSat.

Serum iron (Fe3+) concentration tends to fluctuate with iron intake, acute and chronic disease and in itself is a poor marker of iron status.

The anaemia of iron deficiency tends to be microcytic and hypochromic and the blood film may exhibit poikilocytic changes such as target cells or elliptocytes. Often in early iron deficiency the anaemia is normocytic, with anisocytosis (i.e. an elevated RDW) due to a mix of normocytic and microcytic cells.

If iron deficiency is suspected but not confirmed, improvement in haemoglobin following a trial of iron supplementation can clinch the diagnosis.

A priority in iron deficiency anaemia is to treat the underlying cause of deficiency. Heavy menstrual or intermenstrual blood loss should be investigated and treated. Referral to a gastroenterologist is often required to investigate GI bleeding, and in Helicobacter pylori-infected patients eradication therapy may be required.

Patients with poor iron intake should be advised to add iron-containing foods to their diet, such as beef, chicken, fish, legumes, leafy greens and iron-fortified grains.

Certain vitamin C-rich foods such as fruits, potatoes, cauliflower and cabbage enhance the absorption of iron and should also be encouraged.

Certain foods inhibit iron absorption, and these should be either consumed in moderation or timed to not coincide with meals in order to maximise absorption. Examples include phytates in cereals, nuts and seeds; tannins (iron binders) in tea, coffee an cocoa; and calcium found typically in dairy products.

Oral supplementation (usually with ferrous sulphate or ferrous fumarate) - this is often the first pharmacologic step. These are generally well tolerated but may cause nausea, vomiting, abdominal discomfort, diarrhoea or constipation. Patients on oral supplements should be aware that iron will cause their stools to become dark, which may mimic the appearance of malaena. 

Iron infusions are generally reserved for patients to do not respond to oral iron supplementation. Some common formulations are ferric carboxymaltose, iron polymaltose or iron sucrose. Infusions should be dosed based on the sestimated total body iron deficit, based on the patient's body weight and serum haemoglobin. Patients recieving iron infusions should be monitored closely as they can develop allergic reactions. Consult local guidelines for further information including dosing of iron infusions.

Iron may also be given intramuscularly, though it is painful and may cause staining of the skin.