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.

Although the precise molecular cause of SCLS remains undetermined, scientific research in recent years, conducted mainly at a unit (NIAID) of the U.S. National Institutes of Health, has shed some light on its biological and chemical roots. The study of the peripheral microvasculature from patients’ biopsy specimens has not evidenced gross anomalies, disrupted angiogenesis, or inflammatory cells or other factors suggestive of a disorder prone to damage the blood vessels by inflammation. The absence of structural abnormalities is thus consistent with the hypothesis of some kind of defective but curiously reversible cellular phenomenon in the capillaries.

Studies suggest that the presence of various inflammatory factors during episodes of SCLS may explain the temporarily abnormal permeability of the endothelial cells lining the inner surface of the capillaries. These include transient spikes in monocyte- and macrophage-associated inflammatory mediators and temporary increases in the proteins vascular endothelial growth factors (VEGF) and angiopoietin-2. The impairment of endothelial cells in laboratory conditions provoked by serum taken from patients who were having episodes of SCLS is also suggestive of biochemical factors at work.

There is no evidence that SCLS is hereditary, and the role of specific gene defects in patients with SCLS, which might program their endothelial cells for an overreaction to external stimuli, has not been established. The significance, if any, of the paraprotein (MGUS) present in most patients with SCLS is unknown, other than it has been a precursor to multiple myeloma in a minority (7% in the largest reported cohort) of SCLS patients.

Anasarca, edema, is a medical condition characterized by widespread swelling of the skin due to effusion of fluid into the extracellular space.

It is usually caused by liver failure (cirrhosis of the liver), renal failure/disease, right-sided heart failure, as well as severe malnutrition/protein deficiency. The increase in salt and water retention caused by low cardiac output can also result in anasarca as a long term maladaptive response.

It can also be created from the administration of exogenous intravenous fluid. Certain plant-derived anticancer chemotherapeutic agents, such as docetaxel, cause anasarca through a poorly understood capillary leak syndrome.

In Hb Barts, the high oxygen affinity results in poor oxygen delivery to peripheral tissues, resulting in anasarca.

Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: Between 20% and 50% of patients will die. DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma.

DIC is observed in approximately 1% of academic hospital admissions. DIC occurs at higher rates in people with bacterial sepsis (83%), severe trauma (31%), and cancer (6.8%).

KMS has a mortality rate of about 30%. For patients that survive the acute disease, supportive care may be required through a gradual recovery.

Furthermore, patients may need care from a dermatologist or plastic surgeon for residual cosmetic lesions. On long-term followup, most patients have skin discoloration and/or mild disfiguration from the dormant tumor.

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

Transfusion-related acute lung injury (TRALI) is a serious blood transfusion complication characterized by the acute onset of non-cardiogenic pulmonary edema following transfusion of blood products.

Although the incidence of TRALI has decreased with modified transfusion practices, it was the leading cause of transfusion-related deaths in the United States from fiscal year 2008 through fiscal year 2012.

Treatment varies according to severity, ranging from monitoring of the hematoma (in haemodynamic stability) to emergency surgery (when patients develop hypovolemic shock requiring seminephrectomy or nephrectomy). Vascular causes lead to surgery due to severity of hemorrhage. Robotic-assisted partial nephrectomy has been proposed as a surgical treatment of a ruptured angiomyolipoma causing retroperitoneal hemorrhage, combining the advantages of a kidney preservation procedure and the benefits of a minimally invasive procedure without compromising the safety of the patient.

TRALI is defined as an acute lung injury that is temporally related to a blood transfusion; specifically, it occurs within the first six hours following a transfusion.

It is typically associated with plasma components such as platelets and fresh frozen plasma, though cases have been reported with packed red blood cells since there is some residual plasma in the packed cells. The blood component transfused is not part of the case definition.

Transfusion-related acute lung injury (TRALI) is an uncommon syndrome that is due to the presence of leukocyte antibodies in transfused plasma. TRALI is believed to occur in approximately one in every 5000 transfusions. Leukoagglutination and pooling of granulocytes in the recipient's lungs may occur, with release of the contents of leukocyte granules, and resulting injury to cellular membranes, endothelial surfaces, and potentially to lung parenchyma. In most cases leukoagglutination results in mild dyspnea and pulmonary infiltrates within about 6 hours of transfusion, and spontaneously resolves.

Occasionally more severe lung injury occurs as a result of this phenomenon and acute respiratory distress syndrome (ARDS) results. Leukocyte filters may prevent TRALI for those patients whose lung injury is due to leukoagglutination of the donor white blood cells, but because most TRALI is due to donor antibodies to leukocytes, filters are not helpful in TRALI prevention. Transfused plasma (from any component source) may also contain antibodies that cross-react with platelets in the recipient, producing usually mild forms of posttransfusion purpura or platelet aggregation after transfusion.

Another nonspecific form of immunologic transfusion complication is mild to moderate immunosuppression consequent to transfusion. This effect of transfusion is not completely understood, but appears to be more common with cellular transfusion and may result in both desirable and undesirable effects. Mild immunosuppression may benefit organ transplant recipients and patients with autoimmune diseases; however, neonates and other already immunosuppressed hosts may be more vulnerable to infection, and cancer patients may possibly have worse outcomes postoperatively.

A very large range of medical conditions can cause circulatory collapse. These include, but are not limited to:

- Surgery, particularly on patients who have lost blood.

- Blood clots, including the use of some platelet-activating factor drugs in some animals and humans

- Dengue Fever

- Severe dehydration

- Shock (including, among other types, many cases of cardiogenic shock- e.g., after a myocardial infarction or during heart failure; distributive shock, hypovolemic shock, resulting from large blood loss; and severe cases of septic shock)

- Heart Disease (myocardial infarction- heart attack; acute or chronic congestive or other heart failure, ruptured or dissecting aneurysms; large, especially hemorrhagic, stroke; some untreated congenital heart defects; failed heart transplant)

- Superior mesenteric artery syndrome

- Drugs that affect blood pressure

- Drinking seawater

- As a complication of dialysis

- Intoxicative inhalants

The best course of treatment varies from case to case. The physician must take into account the details in the case before deciding on the appropriate treatment. No treatment is effective for every patient.

Treatment depends on many factors, including:

- Location of lesions

- Anatomy of lesions

- Patient risk factors

- Procedural risk

- Clinical presentation of symptoms

- Duration of symptoms

- etc.

One cause of microangiopathy is long-term diabetes mellitus. In this case, high blood glucose levels cause the endothelial cells lining the blood vessels to take in more glucose than normal (these cells do not depend on insulin). They then form more glycoproteins on their surface than normal, and also cause the basement membrane in the vessel wall to grow abnormally thicker and weaker. Therefore they bleed, leak protein, and slow the flow of blood through the body. As a result, some organs and tissues do not get enough blood (carrying oxygen & nutrients) and are damaged, for example, the retina (diabetic retinopathy) or kidney (diabetic nephropathy). Nerves and neurons, if not sufficiently supplied with blood, are also damaged, which leads to loss of function (diabetic neuropathy, especially peripheral neuropathy).

Massive microangiopathy may cause microangiopathic hemolytic anemia (MAHA).

The incidence of RCVS is unknown, but it is believed to be "not uncommon", and likely under-diagnosed. One small, possibly biased study found that the condition was eventually diagnosed in 45% of outpatients with sudden headache, and 46% of outpatients with thunderclap headache.

The average age of onset is 42, but RCVS has been observed in patients aged from 19 months to 70 years. Children are rarely affected. It is more common in females, with a female-to-male ratio of 2.4:1.

Management of KMS, particularly in severe cases, can be complex and require the joint effort of multiple subspecialists. This is a rare disease with no consensus treatment guidelines or large randomized controlled trials to guide therapy.

Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.

The morbidity and of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increases. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children (though very rarely). Also, women have slightly increased risks of developing hypertension crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.

Gleich's syndrome or episodic angioedema with eosinophilia is a rare disease in which the body swells up episodically (angioedema), associated with raised antibodies of the IgM type and increased numbers of eosinophil granulocytes, a type of white blood cells, in the blood (eosinophilia). It was first described in 1984.

Its cause is unknown, but it is unrelated to capillary leak syndrome (which may cause similar swelling episodes) and eosinophilia-myalgia syndrome (which features eosinophilia but alternative symptoms). Some studies have shown that edema attacks are associated with degranulation (release of enzymes and mediators from eosinophils), and others have demonstrated antibodies against endothelium (cells lining blood vessels) in the condition.

Gleich's syndrome is not a form of the idiopathic hypereosinophilic syndrome in that there is little or no evidence that it leads to organ damage. Rather, recent studies report that a subset of T cells (a special form of lymphocyte blood cell) found in several Gleich syndrome patients have an abnormal immunophenotype, i.e. they express CD3-, CD4+ cluster of differentiation cell surface antigens. These same aberrant T cell immunophenotypes are found in lymphocyte-variant eosinophilia, a disease in which the aberrant T cells overproduce cytokines such as interleukin 5 which simulate the proliferation of eosinophil precursor cells and are thereby responsible for the eosinophilia. It is suggested that most forms of Gleich's syndrome are due to a similar aberrant T cell mechanism and are a subtype of lymphocyte-variant eosinophilia.

Gleich syndrome has a good prognosis. Attack severity may improve with steroid treatment.

It is also possible to classify angiopathy by the associated condition:

- Diabetic angiopathy

- Congophilic angiopathy

Although an estimated 50 million or more adult Americans suffer from hypertension, the relative incidence of hypertensive crisis is relatively low (less than 1% annually). Nevertheless, this condition does affect upward of 500,000 Americans each year, and is therefore a significant cause of serious morbidity in the US. About 14% of adults seen in hospital emergency departments in United States have a systolic blood pressure ≥180 mmHg.

As a result of the use of antihypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of people with high blood pressure. The 1–year survival rate has also increased. Before 1950, this survival rate was 20%, but it is now more than 90% with proper medical treatment.

Estimates indicate that approximately 1% to 2% of people with hypertension develop hypertensive crisis at some point in their lifetime. Men are more commonly affected by hypertensive crises than women.

The rates of hypertensive crises has increased and hospital admissions tripled between 1983 and 1990, from 23,000 to 73,000 per year in the United States. The incidence of postoperative hypertensive crisis varies and such variation depends on the population examined. Most studies report and incidence of between 4% to 35%.

The direct cause of the symptoms is believed to be either constriction or dilation of blood vessels in the brain. The pathogenesis is not known definitively, and the condition is likely to result from multiple different disease processes.

Up to two-thirds of RCVS cases are associated with an underlying condition or exposure, particularly vasoactive or recreational drug use, complications of pregnancy (eclampsia and pre-eclampsia), and the adjustment period following childbirth called "puerperium". Vasoactive drug use is found in about 50% of cases. Implicated drugs include selective serotonin reuptake inhibitors, weight-loss pills such as Hydroxycut, alpha-sympathomimetic decongestants, acute migraine medications, pseudoephedrine, epinephrine, cocaine, and cannabis, among many others. It sometimes follows blood transfusions, certain surgical procedures, swimming, bathing, high altitude experiences, sexual activity, exercise, or coughing. Symptoms can take days or a few months to manifest after a trigger.

Following a study and publication in 2007, it is also thought SSRIs, uncontrolled hypertension, endocrine abnormality, and neurosurgical trauma are indicated to potentially cause vasospasm.

Fat emboli occur in almost 90% of all people with severe injuries to bones, although only 10% of these are symptomatic. The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures and especially by early operative correction. There is also some evidence that steroid prophylaxis of high-risk individuals reduces the incidence. The mortality rate of fat-embolism syndrome is approximately 10–20%.

Fat emboli can be either traumatic (resulting from fracture of long bones, accidents, or trauma to soft tissue) or non-traumatic (resulting from burns or fatty liver).

In medicine, hepatopulmonary syndrome is a syndrome of shortness of breath and hypoxemia (low oxygen levels in the blood of the arteries) caused by vasodilation (broadening of the blood vessels) in the lungs of patients with liver disease. Dyspnea and hypoxemia are worse in the upright position (which is called platypnea and orthodeoxia, respectively).

Patients with hypertensive encephalopathy who are promptly treated usually recover without deficit. However, if treatment is not administered, the condition can lead to death.

Wunderlich syndrome is spontaneous, nontraumatic renal hemorrhage confined to the subcapsular and perirenal space. It may be the first manifestation of a renal angiomyolipoma (AML), or rupture of renal artery or intraparechymal aneurysm.

There are two types of angiopathy: macroangiopathy and microangiopathy.

In macroangiopathy, atherosclerosis and a resultant blood clot forms on the large blood vessels, sticks to the vessel walls, and blocks the flow of blood. Macroangiopathy may cause other complications, such as ischemic heart disease, stroke and peripheral vascular disease which contributes to the diabetic foot ulcers and the risk of amputation.

In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body. The decrease of blood flow through stenosis or clot formation impairs the flow of oxygen to cells and biological tissues (called ischemia) and leads to cellular death (necrosis and gangrene, which in turn may require amputation). Thus, tissues which are very sensitive to oxygen levels, such as the retina, develop microangiopathy and may cause blindness (so-called proliferative diabetic retinopathy). Damage to nerve cells may cause peripheral neuropathy, and to kidney cells, diabetic nephropathy (Kimmelstiel-Wilson syndrome).