Bandemia refers to an excess of band cells (immature white blood cells) released by the bone marrow into the blood. The ICD diagnosis code for bandemia is 288.66.

It is a signifier of infection (or sepsis) or inflammation.

Measurement of it can play a role in the approach to appendicitis.

Generally, the treatment for SIRS is directed towards the underlying problem or inciting cause (i.e. adequate fluid replacement for hypovolemia, IVF/NPO for pancreatitis, epinephrine/steroids/diphenhydramine for anaphylaxis).

Selenium, glutamine, and eicosapentaenoic acid have shown effectiveness in improving symptoms in clinical trials. Other antioxidants such as vitamin E may be helpful as well.

Septic treatment protocol and diagnostic tools have been created due to the potentially severe outcome septic shock. For example, the SIRS criteria were created as mentioned above to be extremely sensitive in suggesting which patients may have sepsis. However, these rules lack specificity, i.e. not a true diagnosis of the condition, but rather a suggestion to take necessary precautions. The SIRS criteria are guidelines set in place to ensure septic patients receive care as early as possible.

In cases caused by an implanted mesh, removal (explantation) of the polypropylene surgical mesh implant may be indicated.

The International Pediatric Sepsis Consensus has proposed some changes to adapt these criteria to the pediatric population.

In children, the SIRS criteria are modified in the following fashion:

- Heart rate is greater than 2 standard deviations above normal for age in the absence of stimuli such as pain and drug administration, or unexplained persistent elevation for greater than 30 minutes to 4 hours. In infants, also includes heart rate less than 10th percentile for age in the absence of vagal stimuli, beta-blockers, or congenital heart disease or unexplained persistent depression for greater than 30 minutes.

- Body temperature obtained orally, rectally, from Foley catheter probe, or from central venous catheter probe less than 36 °C or greater than 38.5 °C. Temperature must be abnormal to qualify as SIRS in pediatric patients.

- Respiratory rate greater than 2 standard deviations above normal for age or the requirement for mechanical ventilation not related to neuromuscular disease or the administration of anesthesia.

- White blood cell count elevated or depressed for age not related to chemotherapy, or greater than 10% bands plus other immature forms.

Anomalies resembling Pelger–Huët anomaly that are acquired rather than congenital have been described as pseudo Pelger–Huët anomaly. These can develop in the course of acute myelogenous leukemia or chronic myelogenous leukemia and in myelodysplastic syndrome. It has also been described in Filovirus disease.

In patients with these conditions, the pseudo–Pelger–Huët cells tend to appear late in the disease and often appear after considerable chemotherapy has been administered. The morphologic changes have also been described in myxedema associated with panhypopituitarism, vitamin B12 and folate deficiency, multiple myeloma, enteroviral infections, malaria, muscular dystrophy, leukemoid reaction secondary to metastases to the bone marrow, and drug sensitivity, sulfa and valproate toxicities are examples. In some of these conditions, especially the drug-induced cases, identifying the change as Pelger–Huët anomaly is important because it obviates the need for further unnecessary testing for cancer.

Peripheral blood smear shows a predominance of neutrophils with bilobed nuclei which are composed of two nuclear masses connected with a thin filament of chromatin. It resembles the pince-nez glasses, so it is often referred to as pince-nez appearance. Usually the congenital form is not associated with thrombocytopenia and leukopenia, so if these features are present more detailed search for myelodysplasia is warranted, as pseudo-Pelger–Huët anomaly can be an early feature of myelodysplasia.

Is a benign dominantly inherited defect of terminal neutrophil differentiation as a result of mutations in the lamin B receptor gene. The characteristic leukocyte appearance was first reported in 1928 by Karel Pelger (1885-1931), a Dutch Hematologist, who described leukocytes with dumbbell-shaped bilobed nuclei, a reduced number of nuclear segments, and coarse clumping of the nuclear chromatin. In 1931, Gauthier Jean Huet (1879-1970), a Dutch Pediatrician, identified it as an inherited disorder.

It is a genetic disorder with an autosomal dominant inheritance pattern. Heterozygotes are clinically normal, although their neutrophils may be mistaken for immature cells, which may cause mistreatment in a clinical setting. Homozygotes tend to have neutrophils with rounded nuclei that do have some functional problems. Homozygous individuals inconsistently have skeletal anomalies such as post-axial polydactyly, short metacarpals, short upper limbs, short stature, or hyperkyphosis.

Identifying Pelger–Huët anomaly is important to differentiate from bandemia with a left-shifted peripheral blood smear and neutrophilic band forms and from an increase in young neutrophilic forms that can be observed in association with infection.