Vascular congestion is the engorgement of an entity, such as the blood vessels of the erectile tissues, with blood. It is known to occur with deep venous thrombosis (DVT).

Hyperaemia, hyperæmia, or hyperemia (Greek ὑπέρ (hupér, "over") + αἷμα (haîma, “blood”)) is the increase of blood flow to different tissues in the body. It can have medical implications but is also a regulatory response, allowing change in blood supply to different tissues through vasodilation. Clinically, hyperaemia in tissues manifest as erythema (redness of the skin) because of the engorgement of vessels with oxygenated blood. Hyperaemia can also occur due to a fall in atmospheric pressure outside the body.

Functional hyperaemia is an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. When a tissue increases activity there is a well-characterized fall in the partial pressure of oxygen and pH, an increase in partial pressure of carbon dioxide, and a rise in temperature and the concentration of potassium ions. The mechanisms of vasodilation are predominantly local metabolites and myogenic effects. Increased metabolic activity of the tissue leads to a local increase in the extracellular concentration of such chemicals as adenosine, carbon dioxide, and lactic acid, and a decrease in oxygen and pH. These changes cause significant vasodilation. The reverse occurs when metabolic activity is slowed and these substances wash out of the tissues. The myogenic effect refers to the inherent attempt of vascular smooth muscle surrounding arterioles and arteries to maintain the tension in the wall of these blood vessels by dilating when internal pressure is reduced and to constrict when wall tension increases.

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

Various classifications have been proposed for CCF. They may be divided into low-flow or high-flow, traumatic or spontaneous and direct or indirect. The traumatic CCF typically occurs after a basal skull fracture. The spontaneous dural cavernous fistula which is more common usually results from a degenerative process in older patients with systemic hypertension

and atherosclerosis. Direct fistulas occur when the Internal Carotid artery (ICA) itself fistulizes into the Cavernous sinus whereas indirect is when a branch of the ICA or External Carotid artery (ECA) communicates with the cavernous sinus.

A popular classification divides CCF into four varieties depending on the type of arterial supply.

The treatment of choice is percutaneous balloon valvuloplasty and is done when a resting peak gradient is seen to be >60mm Hg or a mean >40mm Hg is observed.

Carotid cavernous fistulae may form following closed or penetrating head trauma, surgical damage, rupture of an intracavernous aneurysm, or in association with connective tissue disorders, vascular diseases and dural fistulas.

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

ROP prevalence varies, from 5–8% in developed countries with adequate neonatological facilities, to up to 30% in middle-income developing countries.

There is increasing evidence that ROP and blindness due to ROP are now public health problems in the middle income countries of Latin America, Eastern Europe and the more advanced economies in South East Asia and the Middle east region. In these countries ROP is often the most common cause of blindness in children. ROP is highly likely to become an increasing problem in India, China and other countries in Asia as these countries expand the provision of services for premature infants.

There is also evidence that the population of premature infants at risk of severe ROP varies depending on the level of neonatal intensive care being provided. In countries with high development indices and very low neonatal mortality rates (e.g. North America, western Europe), severe ROP is generally limited to extremely preterm infants i.e. those weighing less than 1 kg (2.2 lbs) at birth. At the other end of the development spectrum, countries with very low development indices and very high neonatal mortality rates (e.g. much of subSaharan Africa) ROP is rare as most premature babies do not have access to neonatal intensive care and so do not survive. Countries with moderate development indices are improving access to neonatal intensive care, and in these settings bigger, more mature babies are also at risk of severe ROP as neonatal care may be suboptimal i.e. those weighing 1.5–2 kg (3.3-4.4 lbs) at birth. These findings have two main implications: firstly, much can be done in countries with moderate development indices to improve neonatal care, to reduce the risk of severe ROP in bigger babies and increase survival of extremely preterm infants, and secondly, in these settings bigger more mature babies need to be included in ROP programs and examined regularly so as to detect those babies developing ROP requiring treatment.

In 2012, the World Health Organization published data on rates of preterm birth and the number of premature babies born in different regions of the world. This report contained three main findings:

- Premature birth has many different causes, and prevention is challenging,

- Prematurity is the most common cause of neonatal death in many countries, totaling as many as 1 million infants annually due to complications of preterm birth, and

- the number of preterm births is currently estimated to be 15 million, and increasing.

Treatment is directed largely to removing the cause, or, where that is impossible, to modifying its effects. Thus, therapy aimed at improving right heart function will also improve congestive hepatopathy. True nutmeg liver is usually secondary to left-sided heart failure causing congestive right heart failure, so treatment options are limited.

Several complications can occur as a result of SCSFLS including decreased cranial pressure, brain herniation, infection, blood pressure problems, transient paralysis, and coma. The primary and most serious complication of SCSFLS is spontaneous intracranial hypotension, where pressure in the brain is severely decreased. This complication leads to the hallmark symptom of severe orthostatic headaches.

People with cranial CSF leaks, the rarer form, have a 10% risk of developing meningitis per year. If cranial leaks last more than seven days, the chances of developing meningitis are significantly higher. Spinal CSF leaks cannot result in meningitis due to the sterile conditions of the leak site. When a CSF leak occurs at the temporal bone surgery becomes necessary in order to prevent infection and repair the leak. Orthostatic hypotension is another complication that occurs due to autonomic dysfunction when blood pressure drops significantly. The autonomic dysfunction is caused by compression of the brainstem, which controls breathing and circulation.

Low CSF volume can cause the cerebellar tonsil position to descend, which can be mistaken for Chiari malformation; however when the CSF leak is repaired the tonsil position often returns to normal (as seen in upright MRI) in this "pseudo-Chiari" condition.

A further, albeit rare, complication of CSF leak is transient quadriplegia due to a sudden and significant loss of CSF. This loss results in hindbrain herniation and causes major compression of the upper cervical spinal cord. The quadriplegia dissipates once the patient lies supine. An extremely rare complication of SCSFLS is third nerve palsy, where the ability to move one's eyes becomes difficult and interrupted due to compression of the third cranial nerve.

There are documented cases of reversible frontotemporal dementia and coma. Coma due to a CSF leak has been successfully treated by using blood patches and/or fibrin glue and placing the patient in the Trendelenburg position. Empty sella syndrome, a boney structure that surround the pituitary gland, occurs in CSF leak patients.

Various risk factors contribute to the development of ROP. They are:

- Prematurity

- High exposure to oxygen

- Low birth weight

- Various types of infections

- Cardiac defects

When pulmonic stenosis (PS) is present, resistance to blood flow causes right ventricular hypertrophy. If right ventricular failure develops, right atrial pressure will increase, and this may result in a persistent opening of the foramen ovale, shunting of unoxygenated blood from the right atrium into the left atrium, and systemic cyanosis. If pulmonary stenosis is severe, congestive heart failure occurs, and systemic venous engorgement will be noted. An associated defect such as a patent ductus arteriosus partially compensates for the obstruction by shunting blood from the left ventricle to the aorta then back to the pulmonary artery (as a result of the higher pressure in the left ventricle) and back into the lungs.

Initial treatment of bleeding from gastric varices focuses on resuscitation, much as with esophageal varices. This includes administration of fluids, blood products, and antibiotics.

The results from the only two randomized trials comparing band ligation vs cyanoacrylate suggests that endoscopic injection of cyanoacrylate, known as gastric variceal obliteration or GVO is superior to band ligation in preventing rebleeding rates. Cyanoacrylate, a common component in 'super glue' is often mixed 1:1 with lipiodol to prevent polymerization in the endoscopy delivery optics, and to show on radiographic imaging. GVO is usually performed in specialized therapeutic endoscopy centers. Complications include sepsis, embolization of glue, and obstruction from polymerization in the lumen of the stomach.

Other techniques for refractory bleeding include:

- Transjugular intrahepatic portosystemic shunts (TIPS)

- Balloon occluded retrograde transvenous obliteration techniques (BORTO)

- Gastric variceal ligation, although this modality is falling out of favour

- Intra-gastric balloon tamponade as a bridge to further therapy

- a caveat is that a larger balloon is required to occupy the fundus of the stomach where gastric varices commonly occur

- Liver transplantation

Normally, the ovarian vein crosses over the ureter at the level of the fourth or fifth lumbar vertebral bone. The ureter itself courses over the external iliac artery and vein. Thus, these vessels can impinge on the ureter causing obstruction. The left ovarian vein ends in the renal vein whereas the right ovarian vein normally enters into the inferior vena cava. In the case of right ovarian vein syndrome, the vein often ends in the renal vein. This is thought to contribute to venous engorgement, in analogy to what is seen in varicoceles, which arise more commonly on the left side. The straight angle between the ovarian vein (or testicular vein in males in the case of varicocoele) and the renal vein has been proposed as a cause of decreased blood return.

A related diagnosis is "Nutcraker Syndrome" where the left renal vein is described as being compressed between the aorta and the superior mesenteric artery. This is reported to cause collateral flow paths to open up to drain the left kidney i.e. reversed flow (reflux caudally) in the left renal vein. Pelvic Congestion Syndrome, vaginal and vulval varices, lower limb varices are clinical sequelae. Virtually all such patient are female and have been pregnant, often multiply.

The ovarian vein often displays incompetent valves. This has been observed more often in women with a higher number of previous pregnancies. Pressure from the baby might hinder the return of blood through the ovarian vein. It has to be noted however that dilation of the urinary tract is a normal observation in pregnancy, due to mechanical compression and the hormonal action of progesterone. Ovarian vein dilatation might also follow venous thrombosis (clotting inside the vein).

Another proposed mechanism of obstruction is when the ovarian vein and ureter both run through a sheath of fibrous tissue, following a local inflammation. This could be seen as a localised form of retroperitoneal fibrosis.

Following obstruction, the ureter displays an abnormal peristalsis (contractions) towards the kidney instead of towards the bladder. This is thought to cause the colicky pain (similar to renal colic), and it is relieved after surgical decompression.

In medicine, ovarian vein syndrome is a rare (possibly not uncommon, certainly under-diagnosed) condition in which a dilated ovarian vein compresses the ureter (the tube that brings the urine from the kidney to the bladder). This causes chronic or colicky abdominal pain, back pain and/or pelvic pain. The pain can worsen on lying down or between ovulation and menstruation. There can also be an increased tendency towards urinary tract infection or pyelonephritis (kidney infection). The right ovarian vein is most commonly involved, although the disease can be left-sided or affect both sides. It is currently classified as a form of pelvic congestion syndrome.

Increased pressure in the sublobular branches of the hepatic veins causes an engorgement of venous blood, and is most frequently due to chronic cardiac , especially those affecting the right heart (e.g., right-sided heart failure), the blood being dammed back in the inferior vena cava and hepatic veins. Central regions of the hepatic lobules are red–brown and stand out against the non-congested, -coloured liver. Centrilobular necrosis occurs.

Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver cells surrounding the central venule of the liver) to become deoxygenated compared to the relatively better-oxygenated periportal hepatocytes adjacent to the hepatic arterioles. This retardation of the blood also occurs in lung lesions, such as chronic interstitial pneumonia, pleural effusions, and intrathoracic tumors.

Papilledema (or papilloedema) is optic disc swelling that is caused by increased intracranial pressure. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare. Papilledema is mostly seen as a symptom resulting from another pathophysiological process.

In intracranial hypertension, the optic disc swelling most commonly occurs bilaterally. When papilledema is found on fundoscopy, further evaluation is warranted due to the fact that vision loss can result if the underlying condition is not treated. Further evaluation with a CT or MRI of the brain and/or spine is usually performed. Recent

research has shown that point-of-care ultrasound can be used to measure optic nerve sheath diameter for detection of increased intracranial pressure and shows good diagnostic test accuracy compared to CT. Thus, if there is a question of papilledema on fundoscopic examination or if the optic disc cannot be adequately visualized, ultrasound can be used to rapidly assess for increased intracranial pressure and help direct further evaluation and intervention. Unilateral papilledema can suggest a disease in the eye itself, such as an optic nerve glioma.

The causes of macular edema are numerous and different causes may be inter-related.

- It is commonly associated with diabetes. Chronic or uncontrolled diabetes type 2 can affect peripheral blood vessels including those of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.

- Age-related macular degeneration may cause macular edema. As individuals age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.

- Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) also known as Irvine-Gass syndrome The surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. Less common today with modern lens replacement techniques.

- Chronic uveitis and intermediate uveitis can be a cause.

- Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma.

- A number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.

- A few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis.

Lobar pneumonia is a form of pneumonia that affects a large and continuous area of the lobe of a lung.

It is one of the two anatomic classifications of pneumonia (the other being bronchopneumonia).

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The cause for CME can be remembered with the mnemonic "DEPRIVEN" (diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin).

Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

Raised intracranial pressure as a result of one or more of the following:

Episcleritis is a common disease, and its exact prevalence and incidence are unknown. It typically affects young adults, and may be more common in women.

Some women who have pain in one or both breasts may fear breast cancer. However, breast pain is not a common symptom of cancer. The great majority of breast cancer cases do not present with symptoms of pain, though breast pain in older women is more likely to be associated with cancer.

In a survey in New York city 35% of nursing mothers stopped breastfeeding after one week due to the pain of cracked nipples. Thirty percent stopped breastfeeding between weeks one and three. Another survey of breastfeeding mothers in Brazil reported that there was 25% higher risk of interruption of exclusive breastfeeding when the women had cracked nipples. Mothers with higher education levels are more likely to continue breastfeeding despite the pain of cracked nipples.