It is important to correlate physical findings with patient history and reported symptoms.CT scan and MRI of the orbits are two imaging modalities that are commonly used to aid in the diagnosis and monitoring of orbital cellulitis, as they can provide detailed images that can show the extent of inflammation along with possible abscess location, size, and involvement of surrounding structures. Ultrasound has also been used as an imaging modality in the past, but it cannot provide the same level of detail as CT or MRI.Blood cultures, electrolytes, and a complete blood count (CBC) with differential showing elevated white blood cell count is a useful laboratory test that may aid in diagnosis. Differential Diagnosis
A variety of pathologies and diseases can present similarly to orbital cellulitis, including:
Inflammatory causes (thyroid eye disease, idiopathic orbital inflammatory syndrome, sarcoidosis, granulomatosis with polyangiitis)
Infectious causes (subperiosteal abscess)
Neoplastic, benign and malignant (dermoid cyst, capillary hemangioma, rhabdomyosarcoma, optic nerve glioma, lymphangioma, neurofibroma, leukemia)
Trauma (orbital fracture, retrobulbar hemorrhage, orbital foreign body, carotid cavernous fistula)
Malformation (congenital, vascular)

Treatment
Immediate treatment is very important, and it typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Several lab tests should be ordered, including a complete blood count, differential, and blood culture. Antibiotic therapy – Since orbital cellulitis is commonly caused by Staphylococcus and Streptococcus species, both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant Staphylococcus aureus) orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline.
Neutrophil-specific granule deficiency ( previously known as lactoferrin deficiency) is a rare congenital immunodeficiency characterized  by an increased risk for pyogenic infections due to defective production of specific granules and gelatinase granules in patient neutrophils. Symptoms and signs
Atypical infections are the key clinical manifestation of SGD. Within the first few years of life, patients will experience repeated pyogenic infections by species such as Staphylococcus aureus, Pseudomonas aeruginosa or other Enterobacteriaceae, and Candida albicans. Cutaneous ulcers or abscesses and pneumonia and chronic lung disease are common. Patients may also develop sepsis, mastoiditis, otitis media, and lymphadenopathy. Infants may present with vomiting, diarrhea, and failure to thrive.Diagnosis can be made based upon CEBPE gene mutation or a pathognomonic finding of a blood smear showing lack of specific granules. Neutrophils and eosinophils will contain hyposegmented nuclei (a pseudo-Pelger–Huet anomaly). Genetics
A majority of patients with SGD have been found to have mutations in the CEBPE (CCAAT/enhancer-binding protein epsilon) gene, a transcription factor primarily active in myeloid cells. Almost all patients have been found to be homozygous for the mutation, suggesting the disease is autosomal recessive. One patient, heterozygous for the mutation, was found to be deficient in GFI1, a related gene. Pathophysiology
The defect in CEBPE appears to block the ability of neutrophils to mature past the promyelocyte stage in bone marrow. Since specific (secondary) and gelatinase (tertiary) granules are only produced past the promyelocyte stage of development, these are deficient in SGD.