It is not uncommon for a patient to complain of a lump on his or her back. Most of the time, the lesion is a sebaceous cyst or lipoma. However, there are other types of back masses, and a simple method of recall is needed. Anatomy is the key. If the mnemonic MINT is applied to most of these structures, all of the important lesions can be recalled.

Muscle is frequently nodular in fibromyositis, and a bursa may occasionally swell significantly. Rupture of a muscle or ligament and contusions are traumatic lesions that may present a mass. Muscle spasm from back injuries is often significant enough to cause a “mass.”

Lesions of the bone are usually responsible for the deeper masses in the back.

Wilms tumors of the kidney and perinephric abscesses may present as a mass in the back.

A clever mnemonic to apply here is HAIR. The H stands for hereditary baldness and hormonal baldness, such as that caused by hypothyroidism and hyperthyroidism. The A stands for alopecia areata and autoimmune disease, such as lupus erythematosus. The I stands for inflammatory conditions, most notably tinea capitis, impetigo, or any condition associated with prolonged fever. The I also stands for intoxication, with arsenic and gold therapy most important here. Finally, the R stands for radiation. This is particularly significant today with so many victims of neoplasms being treated with this modality.

Conditions of the skin, subcutaneous tissue, vascular wall, and blood may all be associated with bleeding under the skin or purpura; thus both anatomy and physiology must be used to develop this differential (Table 12). The skin may hemorrhage from infections such as smallpox, scabies, chickenpox, and measles, especially when the patient traumatizes the area to relieve the itching. A bug bite also may cause hemorrhage by this means. Focal and metastatic neoplasms may cause hemorrhage in the skin, whereas degeneration of the skin may lead to senile purpura. Trauma is by far the most common cause of hemorrhage of the skin.

The subcutaneous tissue is distinguished separately, so that one will recall the Ehlers–Danlos syndrome and pseudoxanthoma elasticum. The vascular wall may be damaged by numerous etiologies. The most important infectious etiologies are subacute bacterial endocarditis and meningococcemia, but typhoid fever, Weil disease, and Rocky Mountain spotted fever should not be forgotten. Systemic neoplasms that infiltrate the vascular wall (such as leukemia) are significant causes, but these usually cause purpura by inducing thrombocytopenia. Vascular degeneration and deficiency diseases (such as scurvy) are uncommon causes of purpura. Toxic conditions are more likely to be related to bone marrow suppression of platelets. Congenital lesions such as hereditary telangiectasias are important to remember.

Most important of all are the allergic and autoimmune disorders, because something can be done to alleviate the condition (e.g., steroids or immunosuppressants). Henoch–Schönlein purpura is a significant form

of allergic vasculitis, but periarteritis nodosa is important as well. Trauma is just as important here as in the skin. Thus, a ruptured varicose vein, crush injury, whooping cough, or contusions are important causes of purpura. Endocrine disorders also cause vascular purpura (as in Cushing syndrome).

Disorders of the blood figure prominently in purpura. Significant among these are the numerous disorders that cause suppression or increased destruction of platelets. Toxic disorders such as gold injections, salicylate ingestion, potassium iodide, quinidine, ergot, and chloral hydrate are just a few of these. It is best to assume that any drug
may cause purpura until proven otherwise. Leukemic overgrowth of the bone marrow may cause purpura because of thrombocytopenia, but any neoplasm that infiltrates the marrow (myelophthisic anemia) must be considered. Autoimmune disease suggests the purpura of idiopathic thrombocytopenic purpura (ITP) and lupus erythematosus.