The best "treatment" of extravasation is "prevention". Depending on the medication that has extravasated, there are potential management options and treatments that aim to minimize damage, although the effectiveness of many of these treatments has not been well studied. In cases of tissue necrosis, surgical debridement and reconstruction may be necessary. The following steps are typically involved in managing extravasation:

- Stop infusion immediately. Put on sterile gloves.

- Replace infusion lead with a disposable syringe. While doing this, do not exert pressure on the extravasation area.

- Slowly aspirate back blood back from the arm, preferably with as much of the infusion solution as possible.

- Remove the original cannula or other IV access carefully from the arm (removal of the original cannula is not advised by all healthcare institutions, as access to the original cannula by surgeons can be used to help clean extravasated tissue).

- Elevate arm and rest in elevated position. If there are blisters on the arm, aspirate content of blisters with a new thin needle. Warm compresses should be placed initially on the site to help diffuse the contrast medium, and cold compresses are used later to help reduce the swelling.

- If, for the extravasated medication, substance-specific measures apply, carry them out (e.g. topical cooling, DMSO, hyaluronidase or dexrazoxane may be appropriate).

- Recent clinical trials have shown that Totect (USA) or Savene (Europe) (dexrazoxane for extravasation) is effective in preventing the progression of anthracycline extravasation into progressive tissue necrosis. In two open-label, single arm, phase II multicenter clinical trials, necrosis was prevented in 98% of the patients. Dexrazoxane for extravasation is the only registered antidote for extravasation of anthracyclines (daunorubicin, doxorubicin, epirubicin, idarubicin, etc.).

The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase. The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly. A recent study of 59 acute episodes occurring in 37 hospitalized SCLS patients concluded that high-volume fluid therapy was independently associated with poorer clinical outcomes, and that the main complications of SCLS episodes were recovery-phase pulmonary edema (24%), cardiac arrhythmia (24%), compartment syndrome (20%), and acquired infections (19%).

The prevention of episodes of SCLS has involved two approaches. The first has long been identified with the Mayo Clinic, and it recommended treatment with beta agonists such as terbutaline, phosphodiesterase-inhibitor theophylline, and leukotriene-receptor antagonists montelukast sodium.

The rationale for use of these drugs was their ability to increase intracellular cyclic AMP (adenosine monophosphate) levels, which might counteract inflammatory signaling pathways that induce endothelial permeability. It was the standard of care until the early 2000s, but was sidelined afterwards because patients frequently experienced renewed episodes of SCLS, and because these drugs were poorly tolerated due to their unpleasant side effects.

The second, more recent approach pioneered in France during the last decade (early 2000s) involves monthly intravenous infusions of immunoglobulins (IVIG), with an initial dose of 2 gr/kg/month of body weight, which has proven very successful as per abundant case-report evidence from around the world.

IVIG has long been used for the treatment of autoimmune and MGUS-associated syndromes, because of its potential immunomodulatory and anticytokine properties. The precise mechanism of action of IVIG in patients with SCLS is unknown, but it is likely that it neutralizes their proinflammatory cytokines that provoke endothelial dysfunction. A recent review of clinical experience with 69 mostly European SCLS patients found that preventive treatment with IVIG was the strongest factor associated with their survival, such that an IVIG therapy should be the first-line preventive agent for SCLS patients. According to a recent NIH survey of patient experience, IVIG prophylaxis is associated with a dramatic reduction in the occurrence of SCLS episodes in most patients, with minimal side effects, such that it may be considered as frontline therapy for those with a clear-cut diagnosis of SCLS and a history of recurrent episodes.

Treatment has traditionally been splenectomy. However, splenectomy is avoided if possible, particularly in children, to avoid the resulting permanent susceptibility to bacterial infections. Most small, and some moderate-sized lacerations in stable patients (particularly children) are managed with hospital observation and sometimes transfusion rather than surgery. Embolization, blocking off of the hemorrhaging vessels, is a newer and less invasive treatment. When surgery is needed, the spleen can be surgically repaired in a few cases, but splenectomy is still the primary surgical treatment, and has the highest success rate of all treatments.

Complications related to extravasation are possible with any medication.

Since Vesicants are blistering agents, extravasation may lead to irreversible tissue injury.

Extravasation is particularly serious during Chemotherapy, since chemotherapy medications are highly toxic.

In recent years, healthcare professionals are becoming more aware of this problem.

In mostly European experience with 69 patients during 1996-2016, the 5- and 10-year survival rates for SCLS patients were 78% and 69%, respectively, but the survivors received significantly more frequent preventive treatment with IVIG than did non-survivors. Five- and 10-year survival rates in patients treated with IVIG were 91% and 77%, respectively, compared to 47% and 37% in patients not treated with IVIG. Moreover, better identification and management of this condition appears to be resulting in lower mortality and improving survival and quality-of-life results as of late.

Early stage sepsis-associated purpura fulminans may be reversible with quick therapeutic intervention. Treatment is mainly removing the underlying cause and degree of clotting abnormalities and with supportive treatment (antibiotics, volume expansion, tissue oxygenation, etc.). Thus, treatment includes aggressive management of the septic state.

Purpura fulminans with disseminated intravascular coagulation should be urgently treated with fresh frozen plasma (10–20 mL/kg every 8–12 hours) and/or protein C concentrate to replace pro-coagulant and anticoagulant plasma proteins that have been depleted by the disseminated intravascular coagulation process.

Protein C in plasma in the steady state has a half life of 6- to 10-hour, therefore, patients with severe protein C deficiency and presenting with purpura fulminans can be treated acutely with an initial bolus of protein C concentrate 100 IU/kg followed by 50 IU /kg every 6 hours. A total of 1 IU/kg of protein C concentrate or 1 mL/kg of fresh frozen plasma will increase the plasma concentration of protein C by 1 IU/dL. Cases with comorbid pathological bleeding may require additional transfusions with platelet concentrate (10–15 mL/kg) or cryoprecipitate (5 mL/kg).

Established soft tissue necrosis may require surgical removal of the dead tissue, fasciotomy, amputation or reconstructive surgery.

For people who have severe congenital protein C deficiency, protein C replacement therapies are available, which is indicated and approved for use in the United States and Europe for the prevention of purpura fulminans. Protein C replacement is often in combination with anticoagulation therapy of injectable low molecular weight heparin or oral warfarin. Before initiating warfarin therapy, a few days of therapeutic heparin may be administered to prevent warfarin skin necrosis and other progressive or recurrent thrombotic complications.

Systemic corticosteroids such as (prednisone) can produce rapid improvement and are the “gold standard” for treatment. The temperature, white blood cell count, and eruption improve within 72 hours. The skin lesions clear within 3 to 9 days. Abnormal laboratory values rapidly return to normal. There are, however, frequent recurrences. Corticosteroids are tapered within 2 to 6 weeks to zero.

Resolution of the eruption is occasionally followed by milia and scarring. The disease clears spontaneously in some patients. Topical and/or intralesional corticosteroids may be effective as either monotherapy or adjuvant therapy.

Oral potassium iodide or colchicine may induce rapid resolution.

Patients who have a potential systemic infection or in whom corticosteroids are contraindicated can use these agents as a first-line therapy.

In one study, indomethacin, 150 mg per day, was given for the first week, and 100 mg per day was given for 2 additional weeks. Seventeen of 18 patients had a good initial response; fever and arthralgias were markedly attenuated within 48 hours, and eruptions cleared between 7 and 14 days.

Patients whose cutaneous lesions continued to develop were successfully treated with prednisone (1 mg/kg per day). No patient had a relapse after discontinuation of indomethacin.

Other alternatives to corticosteroid treatment include dapsone, doxycycline, clofazimine, and cyclosporine. All of these drugs influence migration and other functions of neutrophils.

Some mucoceles spontaneously resolve on their own after a short time. Others are chronic and require surgical removal. Recurrence may occur, and thus the adjacent salivary gland is excised as a preventive measure.

Several types of procedures are available for the surgical removal of mucoceles. These include laser and minimally-invasive techniques which means recovery times are reduced drastically.

Micro-marsupialization is an alternative procedure to surgical removal. Micro-marsupialization uses silk sutures in the dome of a cyst to allow new epithelialized drainage pathways. It is simpler, less traumatic, and well-tolerated by patients, especially children.

A non-surgical option that may be effective for a small or newly identified mucocele is to rinse the mouth thoroughly with salt water (one tablespoon of salt per cup) four to six times a day for a few days. This may draw out the fluid trapped underneath the skin without further damaging the surrounding tissue. If the mucocele persists, individuals should see a doctor to discuss further treatment.

Smaller cysts may be removed by laser treatment, larger cysts will have to be removed surgically in an operating room.

The objective of this treatment is to treat the imbalances brought about by the illness: edema, hypoalbuminemia, hyperlipemia, hypercoagulability and infectious complications.

- Edema: a return to an unswollen state is the prime objective of this treatment of nephrotic syndrome. It is carried out through the combination of a number of recommendations:

- Rest: depending on the seriousness of the edema and taking into account the risk of thrombosis caused by prolonged bed rest.

- Medical nutrition therapy: based on a diet with the correct energy intake and balance of proteins that will be used in synthesis processes and not as a source of calories. A total of 35 kcal/kg body weight/day is normally recommended. This diet should also comply with two more requirements: the first is to not consume more than 1 g of protein/kg body weight/ day, as a greater amount could increase the degree of proteinuria and cause a negative nitrogen balance. Patients are usually recommended lean cuts of meat, fish, and poultry. The second guideline requires that the amount of water ingested is not greater than the level of diuresis. In order to facilitate this the consumption of salt must also be controlled, as this contributes to water retention. It is advisable to restrict the ingestion of sodium to 1 or 2 g/day, which means that salt cannot be used in cooking and salty foods should also be avoided. Foods high in sodium include seasoning blends (garlic salt, Adobo, season salt, etc.) canned soups, canned vegetables containing salt, luncheon meats including turkey, ham, bologna, and salami, prepared foods, fast foods, soy sauce, ketchup, and salad dressings. On food labels, compare milligrams of sodium to calories per serving. Sodium should be less than or equal to calories per serving.

- Medication: The pharmacological treatment of edema is based on the prescription of diuretic drugs (especially loop diuretics, such as furosemide). In severe cases of edema (or in cases with physiological repercussions, such as scrotal, preputial or urethral edema) or in patients with one of a number of severe infections (such as sepsis or pleural effusion), the diuretics can be administered intravenously. This occurs where the risk from plasmatic expansion is considered greater than the risk of severe hypovolemia, which can be caused by the strong diuretic action of intravenous treatment. The procedure is the following:

- Hypoalbuminemia: is treated using the medical nutrition therapy described as a treatment for edema. It includes a moderate intake of foods rich in animal proteins.

- Hyperlipidaemia: depending of the seriousness of the condition it can be treated with medical nutrition therapy as the only treatment or combined with drug therapy. The ingestion of cholesterol should be less than 300 mg/day, which will require a switch to foods that are low in saturated fats. Avoid saturated fats such as butter, cheese, fried foods, fatty cuts of red meat, egg yolks, and poultry skin. Increase unsaturated fat intake, including olive oil, canola oil, peanut butter, avocadoes, fish and nuts. In cases of severe hyperlipidaemia that are unresponsive to nutrition therapy the use of hypolipidemic drugs, may be necessary (these include statins, fibrates and resinous sequesters of bile acids).

- Thrombophilia: low molecular weight heparin (LMWH) may be appropriate for use as a prophylactic in some circumstances, such as in asymptomatic patients that have no history of suffering from thromboembolism. When the thrombophilia is such that it leads to the formation of blood clots, heparin is given for at least 5 days along with oral anticoagulants (OAC). During this time and if the prothrombin time is within its therapeutic range (between 2 and 3), it may be possible to suspend the LMWH while maintaining the OACs for at least 6 months.

- Infectious complications: an appropriate course of antibacterial drugs can be taken according to the infectious agent.

In addition to these key imbalances, vitamin D and calcium are also taken orally in case the alteration of vitamin D causes a severe hypocalcaemia, this treatment has the goal of restoring physiological levels of calcium in the patient.

- Achieving better blood glucose level control if the patient is diabetic.

- Blood pressure control. ACE inhibitors are the drug of choice. Independent of their blood pressure lowering effect, they have been shown to decrease protein loss.

The first-line treatment for a muscular strain in the acute phase include five steps commonly known as P.R.I.C.E.

- Protection: Apply soft padding to minimize impact with objects.

- Rest: Rest is necessary to accelerate healing and reduce the potential for re-injury.

- Ice: Apply ice to induce vasoconstriction, which will reduce blood flow to the site of injury. Never ice for more than 20 minutes at a time.

- Compression: Wrap the strained area with a soft-wrapped bandage to reduce further diapedesis and promote lymphatic drainage.

- Elevation: Keep the strained area as close to the level of the heart as is possible in order to promote venous blood return to the systemic circulation.

Immediate treatment is usually an adjunctive therapy of NSAID's and Cold compression therapy. Controlling the inflammation is critical to the healing process. Cold compression therapy acts to reduce swelling and pain by reducing leukocyte extravasation into the injured area. NSAID's such as Ibuprofen/paracetamol work to reduce the immediate inflammation by inhibiting Cox-1 & Cox-2 enzymes, which are the enzymes responsible for converting arachidonic acid into prostaglandin. However, NSAIDs, including aspirin and ibuprofen, affect platelet function (this is why they are known as "blood thinners") and should not be taken during the period when tissue is bleeding because they will tend to increase blood flow, inhibit clotting, and thereby increase bleeding and swelling. After the bleeding has stopped, NSAIDs can be used with some effectiveness to reduce inflammation and pain.

A new treatment for acute strains is the use of platelet rich plasma (PRP) injections which have been shown to accelerate recovery from non surgical muscular injuries.

It is recommended that the person injured should consult a medical provider if the injury is accompanied by severe pain, if the limb cannot be used, or if there is noticeable tenderness over an isolated spot. These can be signs of a broken or fractured bone, a sprain, or a complete muscle tear.

The treatment of kidney damage may reverse or delay the progression of the disease. Kidney damage is treated by prescribing drugs:

- Corticosteroids: the result is a decrease in the proteinuria and the risk of infection as well as a resolution of the edema. Prednisone is usually prescribed at a dose of 60 mg/m² of body surface area/day in a first treatment for 4–8 weeks. After this period the dose is reduced to 40 mg/m² for a further 4 weeks. Patients suffering a relapse or children are treated with prednisolone 2 mg/kg/day till urine becomes negative for protein. Then, 1.5 mg/kg/day for 4 weeks. Frequent relapses treated by: cyclophosphamide or nitrogen mustard or cyclosporin or levamisole. Patients can respond to prednisone in a number of different ways:

- Corticosteroid sensitive patient or early steroid-responder: the subject responds to the corticosteroids in the first 8 weeks of treatment. This is demonstrated by a strong diuresis and the disappearance of edemas, and also by a negative test for proteinuria in three urine samples taken during the night.

- Corticosteroid resistant patient or late steroid-responder: the proteinuria persists after the 8-week treatment. The lack of response is indicative of the seriousness of the glomerular damage, which could develop into chronic kidney failure.

- Corticosteroid tolerant patient: complications such as hypertension appear, patients gain a lot of weight and can develop aseptic or avascular necrosis of the hip or knee, cataracts and thrombotic phenomena and/or embolisms.

- Corticosteroid dependent patient: proteinuria appears when the dose of corticosteroid is decreased or there is a relapse in the first two weeks after treatment is completed.

The susceptibility testing in vitro to glucocorticoids on patient's peripheral blood mononuclear cells is associated with the incidence of not optimal clinical responses: the most sensitive patients in vitro have shown a higher incidence of corticodependence, while the most resistant patients in vitro showed a higher incidence of ineffective therapy.

- Immunosupressors (cyclophosphamide): only indicated in recurring nephrotic syndrome in corticosteroid dependent or intolerant patients. In the first two cases the proteinuria has to be negated before treatment with the immunosuppressor can begin, which involves a prolonged treatment with prednisone. The negation of the proteinuria indicates the exact moment when treatment with cyclophosphamide can begin. The treatment is continued for 8 weeks at a dose of 3 mg/kg/day, the immunosuppression is halted after this period. In order to be able to start this treatment the patient should not be suffering from neutropenia nor anaemia, which would cause further complications. A possible side effect of the cyclophosphamide is alopecia. Complete blood count tests are carried out during the treatment in order to give advance warning of a possible infection.

If left untreated, complications may arise including abscess formation, peritonitis, sepsis, and damage to the urinary tract by fibrosis and granuloma formation. It is recommended, as a first step, to drain the lesion with ultrasound or CT guidance. If a patient has an underlying obstructive problem it needs to be addressed according to its cause.

Treatment of ranulas usually involves removal of the sublingual gland. Surgery may not be required if the ranula is small and asymptomatic. Marsupialization may sometimes be used, where the intra-oral lesion is opened to the oral cavity with the aim of allowing the sublingual gland to re-establish connection with the oral cavity.

The treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).

The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by Laser treatment or cryotherapy, and detached retinas are reattached surgically.

Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina,long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.

The aim of the medical treatment is to slow the progression of chronic kidney disease by reducing blood pressure and albumin levels. The current published guidelines define ideal BP of <130/80 mmHg for patients with hypertensive nephropathy; studies show that anything higher or lower than this can increase cardiovascular risk. According to the African American Study of Kidney Disease (AASK) trial, after an additional 5 years follow-up upon completion of the 10-year trial, up to 65% of the cohort had progressive nephropathy despite having controlled the mean systolic BP level <135 mmHg.

ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological treatments that can be used to lower BP to target levels; hence reducing neuropathy and proteinuria progression. The management plan should be individualized based on the condition of the patients including comorbidities and previous medical history.

In addition, there are lifestyle changes that can be made. Weight reduction, exercise, reducing salt intake can be done to manage hypertensive nephropathy.

Blunt splenic trauma most often occurs in automobile accident victims, in which it is a leading cause of internal bleeding. However, any type of major impact directed to the spleen may cause splenic trauma. This can happen in bicycling accidents, when the handlebar is forced into the left subcostal margin, and into the spleen. The degree of injury ranges from subcapsular hematoma, to splenic rupture.

Non-septic prepatellar bursitis can be treated with rest, the application of ice to the affected area, and anti-inflammatory drugs, particularly ibuprofen. Elevation of the affected leg during rest may also expedite the recovery process. Severe cases may require fine-needle aspiration of the bursa fluid, sometimes coupled with cortisone injections. However, some studies have shown that steroid injections may not be an effective treatment option. After the bursitis has been treated, rehabilitative exercise may help improve joint mechanics and reduce chronic pain.

Opinions vary as to which treatment options are most effective for septic prepatellar bursitis. McAfee and Smith recommend a course of oral antibiotics, usually oxacillin sodium or cephradine, and assert that surgery and drainage are unnecessary. Wilson-MacDonald argues that oral antibiotics are "inadequate", and recommends intravenous antibiotics for managing the infection. Some authors suggest surgical irrigation of the bursa by means of a subcutaneous tube. Others suggest that bursectomy may be necessary for intractable cases; the operation is an outpatient procedure that can be performed in less than half an hour.

An ecchymosis is a subcutaneous spot of bleeding (from extravasation of blood) with diameter larger than . It is similar to (and sometimes indistinguishable from) a hematoma, commonly called a bruise, though the terms are not interchangeable in careful usage. Specifically, bruises are caused by trauma whereas ecchymoses, which are the same as the spots of purpura except larger, are not "necessarily" caused by trauma, often being caused by pathophysiologic cell function, and some diseases such as Marburg virus disease.

A broader definition of ecchymosis is the escape of blood into the tissues from ruptured blood vessels. The term also applies to the subcutaneous discoloration resulting from seepage of blood within the contused tissue.

Treatment depends on the proximate cause. In one study, it was reported that 9 of 13 men who underwent vasectomy reversal in an attempt to relieve post-vasectomy pain syndrome became pain-free, though the followup was only one month in some cases. Another study found that 24 of 32 men had relief after vasectomy reversal.

Nerve entrapment is treated with surgery to free the nerve from the scar tissue, or to cut the nerve. One study reported that denervation of the spermatic cord provided complete relief at the first follow-up visit in 13 of 17 cases, and that the other four patients reported improvement. As nerves may regrow, long-term studies are needed.

One study found that epididymectomy provided relief for 50% of patients with post-vasectomy pain syndrome.

Orchiectomy is recommended usually only after other surgeries have failed.

There are many causes of subcutaneous hematomas including ecchymoses. Coagulopathies such as Hemophilia A may cause ecchymosis formation in children. The medication betamethasone can have the adverse effect of causing echhymosis.

A urinoma, also pararenal pseudocyst, is an encapsulated collection of extravasated urine and typically found in the area adjacent to the kidneys or to extend into the retroperitoneum.

Simple surgical excision is considered curative. Rare recurrences have been reported.

Some patients with metastatic breast cancer opt to try alternative therapies such as vitamin therapy, homeopathic treatments, a macrobiotic diet, chiropractic or acupuncture. There is no evidence that any of these therapies are effective; they may be harmful, either because patients pass up effective conventional therapies such as chemotherapy or anti-estrogen therapy in favor of alternative treatments, or because the treatments themselves are harmful (as in the case of apricot-pit therapy—which exposes the patient to cyanide—or in chiropractic, which can be dangerous to patients with cancer metastatic to the spinal bones or spinal cord. A macrobiotic diet is neither effective nor safe as it could hypothetically induce weight loss due to severe dietary restriction. There is limited evidence that acupuncture might relive pain in cancer patients, but data so far is insufficient to recommend its use outside of clinical trials.

There is free peer support and an online platform to interact with others going through various therapies, including Abraxane.

Scheduling of drug treatments and combination treatment can have substantial impact on treatment efficacy.