To counter the effects of high-altitude diseases, the body must return arterial p toward normal. Acclimatization, the means by which the body adapts to higher altitudes, only partially restores p to standard levels. Hyperventilation, the body’s most common response to high-altitude conditions, increases alveolar p by raising the depth and rate of breathing. However, while p does improve with hyperventilation, it does not return to normal. Studies of miners and astronomers working at 3000 meters and above show improved alveolar p with full acclimatization, yet the p level remains equal to or even below the threshold for continuous oxygen therapy for patients with chronic obstructive pulmonary disease (COPD). In addition, there are complications involved with acclimatization. Polycythemia, in which the body increases the number of red blood cells in circulation, thickens the blood, raising the danger that the heart can’t pump it.

In high-altitude conditions, only oxygen enrichment can counteract the effects of hypoxia. By increasing the concentration of oxygen in the air, the effects of lower barometric pressure are countered and the level of arterial p is restored toward normal capacity. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 4000 m, raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an altitude equivalent of 3000 m, which is much more tolerable for the increasing number of low-landers who work in high altitude. In a study of astronomers working in Chile at 5050 m, oxygen concentrators increased the level of oxygen concentration by almost 30 percent (that is, from 21 percent to 27 percent). This resulted in increased worker productivity, less fatigue, and improved sleep.

Oxygen concentrators are uniquely suited for this purpose. They require little maintenance and electricity, provide a constant source of oxygen, and eliminate the expensive, and often dangerous, task of transporting oxygen cylinders to remote areas. Offices and housing already have climate-controlled rooms, in which temperature and humidity are kept at a constant level. Oxygen can be added to this system easily and relatively cheaply.

A prescription renewal for home oxygen following hospitalization requires an assessment of the patient for ongoing hypoxemia.

There is no standard medical or surgical treatment for acrocyanosis, and treatment, other than reassurance and avoidance of cold, is usually unnecessary. The patient is reassured that no serious illness is present. A sympathectomy would alleviate the cyanosis by disrupting the fibers of the sympathetic nervous system to the area. However, such an extreme procedure would rarely be appropriate. Treatment with vasoactive drugs is not recommended but traditionally is mentioned as optional. However, there is little, if any, empirical evidence that vasoactive drugs (α-adrenergic blocking agents or calcium channel blockers) are effective.

Differential cyanosis is the bluish coloration of the lower but not the upper extremity and the head. This is seen in patients with a patent ductus arteriosus. Patients with a large ductus develop progressive pulmonary vascular disease, and pressure overload of the right ventricle occurs. As soon as pulmonary pressure exceeds aortic pressure, shunt reversal (right-to-left shunt) occurs. The upper extremity remains pink because the brachiocephalic trunk, left common carotid trunk and the left subclavian trunk is given off proximal to the PDA.

Cyanosis is defined as the bluish or purplish discolouration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation. Based on Lundsgaard and Van Slyke's work, it is classically described as occurring if 5.0 g/dL of deoxyhemoglobin or greater is present. This was based on an estimate of capillary saturation based on a mean of arterial versus peripheral venous blood gas measurements. Since estimation of hypoxia is usually now based either on arterial blood gas measurement or pulse oximetry, this is probably an overestimate, with evidence that levels of 2.0 g/dL of deoxyhemoglobin may reliably produce cyanosis. Since, however, the presence of cyanosis is dependent upon there being an absolute quantity of deoxyhemoglobin, the bluish color is more readily apparent in those with high hemoglobin counts than it is with those with anemia. Also, the bluer the color, the more difficult it is to detect on deeply pigmented skin. When signs of cyanosis first appear, such as on the lips or fingers, intervention should be made within 3–5 minutes because a severe hypoxia or severe circulatory failure may have induced the cyanosis.

The name "cyanosis" literally means "the blue disease" or "the blue condition". It is derived from the color cyan, which comes from κυανός, "kyanós", the Greek word for "blue".

While there is no cure for acrocyanosis, patients otherwise have excellent prognosis. Unless acrocyanosis results from another condition (e.g. malignancy, antiphospholipid syndrome, atherosclerosis, acute ischemic limb, bacterial endocarditis), there is no associated increased risk of disease or death, and there are no known complications. Aside from the discoloration, there are no other symptoms: no pain, and no loss of function. Patients can expect to lead normal lives. In secondary acrocyanosis treatment of the primary condition defines outcomes.

The risk may be reduced by administering a non-particulate antacid (e.g. Sodium Citrate) or an H-antagonist like Ranitidine.

Chloramphenicol therapy should be stopped immediately. Exchange transfusion may be required to remove the drug. Sometimes, phenobarbital (UGT induction) is used.

When the pulmonary capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of carrying fluid away from the interstitial spaces perhaps as much as 10-fold. Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mm Hg have been measured without the development of lethal pulmonary edema.[Guytun and Hall physiology]

Hypoxia exists when there is a reduced amount of oxygen in the tissues of the body. Hypoxemia refers to a reduction in PO2 below the normal range, regardless of whether gas exchange is impaired in the lung, CaO2 is adequate, or tissue hypoxia exists. There are several potential physiologic mechanisms for hypoxemia, but in patients with COPD the predominant one is V/Q mismatching, with or without alveolar hypoventilation, as indicated by PaCO2. Hypoxemia caused by V/Q mismatching as seen in COPD is relatively easy to correct, so that only comparatively small amounts of supplemental oxygen (less than 3 L/min for the majority of patients) are required for LTOT. Although hypoxemia normally stimulates ventilation and produces dyspnea, these phenomena and the other symptoms and signs of hypoxia are sufficiently variable in patients with COPD as to be of limited value in patient assessment. Chronic alveolar hypoxia is the main factor leading to development of cor pulmonale—right ventricular hypertrophy with or without overt right ventricular failure—in patients with COPD. Pulmonary hypertension adversely affects survival in COPD, to an extent that parallels the degree to which resting mean pulmonary artery pressure is elevated. Although the severity of airflow obstruction as measured by FEV1 is the best correlate with overall prognosis in patients with COPD, chronic hypoxemia increases mortality and morbidity for any severity of disease. Large-scale studies of LTOT in patients with COPD have demonstrated a dose-response relationship between daily hours of oxygen use and survival. There is reason to believe that continuous, 24-hours-per-day oxygen use in appropriately selected patients would produce a survival benefit even greater than that shown in the NOTT and MRC studies.

The condition can be prevented by using chloramphenicol at the recommended doses and monitoring blood levels, or alternatively, third generation cephalosporins can be effectively substituted for the drug, without the associated toxicity.

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.

A living person can look deathly pale. This can happen when circumstances make the blood escape from the surface of the skin, as in deep shock. Also heart failure ("insufficientia cordis") can make the face look grey; the person then also has blue lips. Skin can also look deathly pale as a result of vasoconstriction as part of the body's homeostatic systems in cold conditions, or if the skin is deficient in vitamin D, as seen in people who spend most of the time indoors, away from sunlight.

Pallor mortis results from the cessation of capillary circulation throughout the body. Gravity then causes the blood to sink down into the lower parts of the body, creating livor mortis.

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.

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

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.

Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.

If the condition of the ischemic limb is stabilized with anticoagulation, recently formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.

Direct arteriotomy may be necessary to remove the clot. Surgical revascularization may be used in the setting of trauma (e.g., laceration of the artery). Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.

Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury.

Fournier gangrene is a urological emergency requiring intravenous antibiotics and debridement (surgical removal) of necrotic (dead) tissue. In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) may be useful and acts to inhibit the growth of and kill the anaerobic bacteria.

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.

Medications that may alleviate the symptoms of airsickness include:

- meclozine

- dimenhydrinate

- diphenhydramine

- scopolamine (available in both patch and oral form).

Pilots who are susceptible to airsickness should not take anti-motion sickness medications (prescription or over-the-counter). These medications can make one drowsy or affect brain functions in other ways.

If the inciting defect in the heart is identified "before" it causes significant pulmonary hypertension, it can normally be repaired through surgery, preventing the disease. After pulmonary hypertension is sufficient to reverse the blood flow through the defect, however, the maladaptation is considered irreversible, and a heart–lung transplant or a lung transplant with repair of the heart is the only curative option.

Transplantation is the final therapeutic option and only for patients with poor prognosis and quality of life. Timing and appropriateness of transplantation remain difficult decisions. 5-year and 10-year survival ranges between 70% and 80%, 50% and 70%, 30% and 50%, respectively. Since the average life expectancy of patients after lung transplantation is as low as 30% at 5 years, patients with "reasonable functional status" related to Eisenmenger syndrome have "improved survival with conservative medical care" compared with transplantation.

Various medicines and therapies for pulmonary hypertension are under investigation for treatment of the symptoms.

The formation of a TIF is a medical emergency and requires immediate intervention. Blood volume control, management of the hemorrhage, and adequate oxygenation should be insured in these patients. In a majority of TIF cases (85%), hyperinflation of the tracheostomy cuff will control the bleeding, while the patient is prepared for surgery. However, if this fails the tracheostomy cuff must be removed, and the patient must be intubated from above. Next, pressure from the index finger can be applied on the bleeding site from within the tracheostomy to control the bleeding. In addition, the "Utley Maneuver", which involves digital compression of the artery against the posterior wall of the manubrium of the sternum following a right infraclavicular incision, may be used to urgently control the bleeding When the bleeding is controlled the patient should be immediately transferred on the operating room.

There are numerous alternative remedies for motion sickness. One such is ginger, but it is ineffective.

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.

Disease progression may be slowed with immunosuppressives and other medications, and esophageal reflux, pulmonary hypertension and Raynaud phenomenon may benefit from symptomatic treatment. However, there is no cure for this disease as there is no cure for scleroderma in general.

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.