Most patients experience an improvement of their symptoms, but for some, OI can be gravely disabling and can be progressive in nature, particularly if it is caused by an underlying condition which is deteriorating. The ways in which symptoms present themselves vary greatly from patient to patient; as a result, individualized treatment plans are necessary.

OI is treated both pharmacologically and non-pharmacologically. Treatment does not cure OI; rather, it controls symptoms.

Physicians who specialize in treating OI agree that the single most important treatment is drinking more than two liters (eight cups) of fluids each day. A steady, large supply of water or other fluids reduces most, and for some patients all, of the major symptoms of this condition. Typically, patients fare best when they drink a glass of water no less frequently than every two hours during the day, instead of drinking a large quantity of water at a single point in the day.

For most severe cases and some milder cases, a combination of medications are used. Individual responses to different medications vary widely, and a drug which dramatically improves one patient's symptoms may make another patient's symptoms much worse. Medications focus on three main issues:

Medications that increase blood volume:

- Fludrocortisone (Florinef)

- Erythropoietin

- Hormonal contraception

Medications that inhibit acetylcholinesterase:

- Pyridostigmine

Medications that improve vasoconstriction:

- Stimulants: (e.g., Ritalin or Dexedrine)

- Midodrine (ProAmatine)

- Ephedrine and pseudoephedrine (Sudafed)

- Theophylline (low-dose)

- Selective serotonin reuptake inhibitors (SSRI's - Prozac, Zoloft, and Paxil)

Behavioral changes that patients with OI can make are:

- Avoiding triggers such as prolonged sitting, quiet standing, warm environments, or vasodilating medications

- Using postural maneuvers and pressure garments

- Treating co-existing medical conditions

- Increasing fluid and salt intake

- Physical therapy and exercise unless contraindicated by an underlying condition such as chronic fatigue syndrome where traditional exercise can worsen the condition

When treating iron-deficiency anemia, considerations of the proper treatment methods are done in light of the "cause and severity" of the condition. If the iron-deficiency anemia is a downstream effect of blood loss or another underlying cause, treatment is geared toward addressing the underlying cause when possible. In severe acute cases, treatment measures are taken for immediate management in the interim, such as blood transfusions or even intravenous iron.

Iron-deficiency anemia treatment for less severe cases includes dietary changes to incorporate iron-rich foods into regular oral intake. Foods rich in ascorbic acid (vitamin C) can also be beneficial, since ascorbic acid enhances iron absorption. Other oral options are iron supplements in the form of pills or drops for children.

As iron-deficiency anemia becomes more severe, or if the anemia does not respond to oral treatments, other measures may become necessary. In addition to the previously mentioned indication for intravenous iron or blood transfusions, intravenous iron may also be used when oral intake is not tolerated, as well as for other indications. Specifically, for those on dialysis, parenteral iron is commonly used. Individuals on dialysis who are taking forms of erythropoietin or some "erythropoiesis-stimulating agent" are given parenteral iron, which helps the body respond to the erythropoietin agents and produce red blood cells.

The various forms of treatment are not without possible adverse effects. Iron supplementation by mouth commonly causes negative gastrointestinal effects, including constipation. Intravenous iron can induce an allergic response that can be as serious as anaphylaxis, although different formulations have decreased the likelihood of this adverse effect.

Definitive therapy depends on the cause:

- Symptomatic treatment can be given by blood transfusion, if there is marked anemia. A positive Coombs test is a relative contraindication to transfuse the patient. In cold hemolytic anemia there is advantage in transfuse warmed blood

- In severe immune-related hemolytic anemia, steroid therapy is sometimes necessary.

- In steroid resistant cases, consideration can be given to rituximab or addition of an immunosuppressant ( azathioprine, cyclophosphamide)

- Association of methylprednisolone and intravenous immunoglobulin can control hemolysis in acute severe cases

- Sometimes splenectomy can be helpful where extravascular hemolysis, or hereditary spherocytosis, is predominant (i.e., most of the red blood cells are being removed by the spleen).

The goal of treatment is to reduce inflammation. Treatment usually does not require hospitalization unless tongue swelling is severe. Good oral hygiene is necessary, including thorough tooth brushing at least twice a day, and flossing at least daily. Corticosteroids such as prednisone may be given to reduce the inflammation of glossitis. For mild cases, topical applications (such as a prednisone mouth rinse that is not swallowed) may be recommended to avoid the side effects of swallowed or injected corticosteroids. Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of glossitis is an infection. Anemia and nutritional deficiencies (such as a deficiency in niacin, riboflavin, iron, or Vitamin E) must be treated, often by dietary changes or other supplements. Avoid irritants (such as hot or spicy foods, alcohol, and tobacco) to minimize the discomfort.

In some cases, tongue swelling may threaten the airway, a medical emergency that needs immediate attention.

PRCA is considered an autoimmune disease as it will respond to immunosuppressant treatment such as ciclosporin in many patients, though this approach is not without risk.

It has also been shown to respond to treatments with Rituximab and Tacrolimus.

Good nutrition with adequate intake of iron may prevent this disorder. Good nutrition should also include balanced diet and exercise.

Blood transfusion is sometimes used to treat iron deficiency with hemodynamic instability. Sometimes transfusions are considered for people who have chronic iron deficiency or who will soon go to surgery, but even if such people have low hemoglobin, they should be given oral treatment or intravenous iron.

At present there is no specific treatment. Many patients with haemolytic anaemia take folic acid (vitamin B) since the greater turnover of cells consumes this vitamin. During crises transfusion may be required. Clotting problems can occur for which anticoagulation may be needed. Unlike hereditary spherocytosis, splenectomy is contraindicated.

Patients generally respond well to treatment. Iron supplementation usually resolves the anemia, and corrects the glossodynia (tongue pain).

It is a synthetic compound developed by Osbond "et al." and Brossi "et al." in 1959. It is as effective as emetine in its amoebicidal properties. Given parenterally dehydroemetine is surprisingly painless. Oral tablets have been introduced. But for some reason, these tablets have not become popular. A high cure rate can be obtained with this drug. Compared to emetine, its concentration in the heart is less. Electrocardiographic changes are not seen so often. When present, they are more transient than with emetine.

Dehydroemetine is excreted by the kidneys, heart and the other organs more rapidly than emetine. Therefore, a daily dose of 1.25 mg or 1.5 mg/kg body weight is necessary. The total daily dose should not exceed 90 mg. The course should not be repeated in less than 14 days.

Ipecac or ipecacuanha consists of the dried rhizome and roots of "Cephaelis ipecacuanha".

The medical virtues of ipecac are almost entirely due to the action of its alkaloids-emetine and cephaline. Till today, emetine remains one of the best drugs for treating amoebic liver abscess. It has a direct action on the trophozoites.

Its greater concentration and duration of action in the liver as compared to that in the intestinal wall explains its high efficacy in amoebic liver abscess and also its low parasitic cure rate for intestinal amoebiasis.

The drug is detoxicated and eliminated slowly. It may, therefore, produce cumulative effects. In man, emetine poisoning is characterized by muscular tremors, weakness and pain in the extremities which tend to persist until drug administration is stopped. Gastro-intestinal symptoms include nausea, vomiting and bloody diarrhoea. The latter may be mistaken for a recurrence of amoebic dysentery.

Many clinicians fear the occurrence of cardiac toxicity due to this drug and hence avoid using it. Serious cardiac toxicity, however, is rare. Both recovered with the treatment for heart failure and withdrawal of emetine. One patient who was given fifteen injections of emetine in a dose of 60 mgm per day, died.

Overdosage of emetine produces focal necrosis of cardiac muscle resulting in cardiac failure and sudden death.

Emetine, like digitalis may produce mild ST and T wave changes in the electrocardiogram which does not necessarily mean serious toxicity. In fact, they are encountered, though less commonly, after the use of chloroquine and metronidazole as well.

Toxic effects on the myocardium have been described even in doses generally considered safe. These are rise in pulse rate, fall in systolic blood pressure and ST-T changes in the electrocardiogram.

The other rare E.C.G. changes include deformity of QRS complexes, prolongation of PR interval, atrial premature beats, and atrial tachycardia. In adults, fatal cases have been reported with a total dose of 0.6 G. or less. The incidence of toxic heart damage greatly increases in patients with anaemia.

In patients having myocardial disease or marked hypertension, emetine can be used for amoebic liver abscess, as the benefits from it may outweigh possible hazards. This situation is unlikely to arise these days, as equally good alternative drugs like metronidazole are available. Patients receiving emetine should be monitored for changes in pulse, blood pressure and electrocardiography. Absolute bed rest during and several days after emetine therapy has been recommended, although we have often seen patients in whom no untoward reactions have occurred in spite of neglecting the above precaution.

Theoretically the use of emetine in children is not advised. However, in practice it has been used as discussed elsewhere. It should not be administered during pregnancy unless absolutely necessary.

Although emetine is undeniably moderately toxic, the risk of using it would be worth accepting in such a serious illness were it not for the fact that less toxic drugs like chloroquine and metronidazole are now available.

In practice, emetine still produces a more dramatic clinical response thanchloroquine or metronidazole. This point would score in favour of emetine in places where facilities for a proper diagnosis are not available and a therapeutic test remains as the only weapon with a practitioner.

Emetine should always be given deep intramuscularly or deep subcutaneously but never intravenously. The total dose in amoebic liver abscess should not exceed 650 mg or 10 mg/kg. This should be given over a period of 10 days in a dose of 6G65 mg. daily. A relapse rate of 7% follows one such course. Therefore, the treatment could be repeated after a period of 2–6 weeks. Of late such a need does not arise, as drug combinations are commonly used. When parenteral emetine is combined with oral chloroquine or two courses of emetine are given, the relapse rate can be brought down to 1 percent.

No treatment is required and the patches in time will settle.

The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.

As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required.

Tacrolimus has been reported as speeding resolution.

In exceptionally severe cases PUVA therapy may be considered.

Medications can be helpful for moderate or severe RP.

- Vasodilators – calcium channel blockers, such as the dihydropyridines nifedipine or amlodipine, preferably slow release preparations – are often first line treatment. They have the common side effects of headache, flushing, and ankle edema; but these are not typically of sufficient severity to require cessation of treatment. The limited evidence available shows that calcium channel blockers are only slightly effective in reducing how often the attacks happen. Peoples whose RP is secondary to erythromelalgia often cannot use vasodilators for therapy as they trigger 'flares' causing the extremities to become burning red due to there being too much blood.

- People with severe RP prone to ulceration or large artery thrombotic events may be prescribed aspirin.

- Sympatholytic agents, such as the alpha-adrenergic blocker prazosin, may provide temporary relief.

- Losartan can, and topical nitrates may, reduce the severity and frequency of attacks, and the phosphodiesterase inhibitors sildenafil and tadalafil may reduce their severity.

- Angiotensin receptor blockers or ACE inhibitors may aid blood flow to the fingers, and there is some evidence that angiotensin receptor blockers (often losartan) reduce frequency and severity of attacks, and possibly better than nifedipine.

- The prostaglandin iloprost is used to manage critical ischemia and pulmonary hypertension in RP, and the endothelin receptor antagonist bosentan is used to manage severe pulmonary hypertension and prevent finger ulcers in scleroderma.

- Statins have a protective effect on blood vessels, and SSRIs such as fluoxetine may help RP symptoms but the data is weak.

Before commencing treatment, there should be definitive diagnosis of the underlying cause for iron deficiency. This is particularly the case in older patients, who are most susceptible to colorectal cancer and the gastrointestinal bleeding it often causes. In adults, 60% of patients with iron deficiency anemia may have underlying gastrointestinal disorders leading to chronic blood loss.

It is likely that the cause of the iron deficiency will need treatment as well.

Upon diagnosis, the condition can be treated with iron supplements. The choice of supplement will depend upon both the severity of the condition, the required speed of improvement (e.g. if awaiting elective surgery) and the likelihood of treatment being effective (e.g. if has underlying IBD, is undergoing dialysis, or is having ESA therapy).

Examples of oral iron that are often used are ferrous sulfate, ferrous gluconate, or amino acid chelate tablets. Recent research suggests the replacement dose of iron, at least in the elderly with iron deficiency, may be as little as 15 mg per day of elemental iron.

Pallor mortis (Latin: "pallor" "paleness", "mortis" "of death"), the first stage of death, is an after death paleness that occurs in those with light/white skin.

Evidence does not support the use of alternative medicine, including acupuncture and laser therapy.

Pallor mortis occurs almost immediately (within 15–25 minutes) post-mortem; paleness develops so rapidly after death that it has little to no use in determining the time of death, aside from saying that it either happened less than 30 minutes ago or more, which could help if the body were found very soon after death.

Treating immune-mediated aplastic anemia involves suppression of the immune system, an effect achieved by daily medicine intake, or, in more severe cases, a bone marrow transplant, a potential cure. The transplanted bone marrow replaces the failing bone marrow cells with new ones from a matching donor. The multipotent stem cells in the bone marrow reconstitute all three blood cell lines, giving the patient a new immune system, red blood cells, and platelets. However, besides the risk of graft failure, there is also a risk that the newly created white blood cells may attack the rest of the body ("graft-versus-host disease"). In young patients with an HLA matched sibling donor, bone marrow transplant can be considered as first-line treatment, patients lacking a matched sibling donor typically pursue immunosuppression as a first-line treatment, and matched unrelated donor transplants are considered a second-line therapy.

Medical therapy of aplastic anemia often includes a course of antithymocyte globulin (ATG) and several months of treatment with ciclosporin to modulate the immune system. Chemotherapy with agents such as cyclophosphamide may also be effective but has more toxicity than ATG. Antibody therapy, such as ATG, targets T-cells, which are believed to attack the bone marrow. Corticosteroids are generally ineffective, though they are used to ameliorate serum sickness caused by ATG. Normally, success is judged by bone marrow biopsy 6 months after initial treatment with ATG.

One prospective study involving cyclophosphamide was terminated early due to a high incidence of mortality, due to severe infections as a result of prolonged neutropenia.

In the past, before the above treatments became available, patients with low leukocyte counts were often confined to a sterile room or bubble (to reduce risk of infections), as in the case of Ted DeVita.

There is no known cure for CVS, but there are medications that can be used for treatment, intervention, and prevention. There is a growing body of publications on both individual cases and the experiences of the CVS cohort. Treatment is usually on an individual basis, based on trial and error.

The most common therapeutic strategies for those already in an attack are maintenance of salt balance by appropriate intravenous fluids and, in some cases, sedation. Having vomited for a long period prior to attending a hospital, patients are typically severely dehydrated. For a number of patients, potent anti-emetic drugs such as ondansetron (Zofran) or granisetron (Kytril), and dronabinol (Marinol) may be helpful in either preventing an attack, aborting an attack, or reducing the severity of an attack. Lifestyle changes may be recommended, such as extended rest and reduction of stress. Because the symptoms of CVS are similar (or perhaps identical) to those of the disease well-identified as "abdominal migraine", treatment of CVS with a regimen of anti-migraine drugs, such as topiramate and amitriptyline, is showing promise in preventing recurrent attacks.

Good oral hygiene (thorough tooth brushing and flossing and regular professional cleaning and examination) may be helpful to prevent these disorders. Drinking plenty of water and the production of enough saliva, aid in the reduction of bacterial growth. Minimizing irritants or injury in the mouth when possible can aid in the prevention of glossitis. Avoiding excessive use of any food or substance that irritates the mouth or tongue may also help.

It is unclear if screening pregnant women for iron-deficiency anemia during pregnancy improves outcomes in the United States. The same holds true for screening children who are "6 to 24 months" old.

While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement. The mineralocorticoid medication fludrocortisone can also improve the low sodium level.

The clinician must protect the patient against hypotension, renal failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas.

Intravenous hydration of up to 1.5 L/hour should continue to prevent hypotension. A urinary output of at least 300 ml/hour should be maintained with IV fluids and mannitol, and hemodialysis considered if this amount of diuresis is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys.

To prevent hyperkalemia/hypocalcemia, consider the following adult doses:

- calcium gluconate 10% 10ml or calcium chloride 10% 5 ml IV over 2 minutes

- sodium bicarbonate 1 meq/kg IV slow push

- regular insulin 5–10 U

- 50% glucose 1–2 ampules IV bolus

- kayexalate 25–50 g with sorbitol 20% 100 ml by mouth or rectum.

Even so, cardiac arrhythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.

Exercise can improve symptoms, as can revascularization. Both together may be better than one intervention of its own.

Pharmacological options exist, as well. Medicines that control lipid profile, diabetes, and hypertension may increase blood flow to the affected muscles and allow for increased activity levels. Angiotensin converting enzyme inhibitors, beta-blockers, antiplatelet agents (aspirin and clopidogrel), naftidrofuryl, pentoxifylline, and cilostazol (selective PDE3 inhibitor) are used for the treatment of intermittent claudication. However, medications will not remove the blockages from the body. Instead, they simply improve blood flow to the affected area.

Catheter-based intervention is also an option. Atherectomy, stenting, and angioplasty to remove or push aside the arterial blockages are the most common procedures for catheter-based intervention. These procedures can be performed by interventional radiologists, interventional cardiologists, vascular surgeons, and thoracic surgeons, among others.

Surgery is the last resort; vascular surgeons can perform either endarterectomies on arterial blockages or perform an arterial bypass. However, open surgery poses a host of risks not present with catheter-based interventions.

Pallor is a pale color of the skin that can be caused by illness, emotional shock or stress, stimulant use, or anemia, and is the result of a reduced amount of oxyhaemoglobin and is visible in skin conjuctivae or mucous membrane.

Pallor is more evident on the face and palms. It can develop suddenly or gradually, depending on the cause. It is not usually clinically significant unless it is accompanied by a general pallor (pale lips, tongue, palms, mouth and other regions with mucous membranes). It is distinguished from similar presentations such as hypopigmentation (lack or loss of skin pigment) or simply a fair complexion.