As one gets older, pockets of fluid can develop in the vitreous. When these pockets develop near the back of the eye, the vitreous can pull away from the retina and possibly tear it. Posterior vitreous detachment accounts for 3.7–11.7% of vitreous hemorrhage cases.

Less common causes of vitreous hemorrhage make up 6.4–18% of cases, and include:

- Proliferative sickle cell retinopathy

- Macroaneurysm

- Age-related macular degeneration

- Terson syndrome

- Retinal neovascularization as a result of branch or central retinal vein occlusion

- Other – about 7 cases in 100,000 have no known cause attributed to them.

Retinal haemorrhages commonly occur in high attitude climbers, most likely due to the effects of systemic hypoxia on the eye. Risk is correlated with the maximum altitude reached, duration of exposure to high altitude conditions, and climb rate.

Different causes may cause bleeding in different locations.

- Terson's syndrome (as a result of subarachnoid hemorrhage)

- Hemophilia (a severe bleeding disorder, usually hereditary)

- Anticoagulants and thrombolysis (medication to reduce blood clotting tendency or to disperse blood clots, respectively)

Retinal haemorrhages, especially mild ones not associated with chronic disease, will normally resorb without treatment. Laser surgery is a treatment option which uses a laser beam to seal off damaged blood vessels in the retina. Anti-vascular endothelial growth factor (VEGF) drugs like Avastin and Lucentis have also been shown to repair retinal haemorrhaging in diabetic patients and patients with haemorrhages associated with new vessel growth.

Studies have identified the following abnormalities as risk factors for the development of BRVO:

- hypertension

- cardiovascular disease

- obesity

- glaucoma

Diabetes mellitus was not a major independent risk factor.

It may cause seizures but cephalohematoma and caput will not cause seizure

The majority (90%) result from applying a vacuum to the head at delivery (Ventouse assisted delivery). The vacuum assist ruptures the emissary veins (connections between dural sinus and scalp veins) leading to accumulation of blood under the aponeurosis of the scalp muscle and superficial to the periosteum. Subgaleal hematoma has a high frequency of occurrence of associated head trauma (40%), such as intracranial hemorrhage or skull fracture. The occurrence of these features does not correlate significantly with the severity of subgaleal hemorrhage.

Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.

Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.

In general, BRVO has a good prognosis: after 1 year 50–60% of eyes have been reported to have a final VA of 20/40 or better even without any treatment. With time the dramatic picture of an acute BRVO becomes more subtle, hemorrhages fade so that the retina can look almost normal. Collateral vessels develop to help drain the affected area.

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

Eales disease most commonly affects healthy young adults. Male predominance (up to 97.6%) has been reported in a majority of the series. The predominant age of onset of symptoms is between 20 and 30 years. The disease is now seen more commonly in the Indian subcontinent.

Intraocular hemorrhage (sometimes hemophthalmos or hemophthalmia) is bleeding (hemorrhage) into the eyeball ("oculus" in Latin. It may be the result of physical trauma (direct injury to the eye) or medical illness. Severe hemorrhage, particularly when leading to rising pressure inside the eye, may lead to blindness.

Antenatal corticosteroids have a role in reducing incidence of germinal matrix hemorrhage in premature infants.

Terson syndrome or Terson's syndrome is the occurrence of a vitreous hemorrhage of the human eye in association with subarachnoid hemorrhage. Vitreous hemorrhage of the eye can also occur in association with intracranial hemorrhage and elevated intracranial pressure (ICP). Intraocular hemorrhage can be a subretinal, retinal, preretinal, subhyaloidal, or intra-vitreal hemorrhage. Its likely cause is a rapid increase in ICP. The classic presentation is in the subhyaloidal space, which is beneath the posterior vitreous face and in front of the retina.

In subarachnoid hemorrhage, 13% of patients have Terson's syndrome, which is associated with more severe SAH (higher Hunt-Hess score, a marker of severity), and risk of death is significantly increased.

The first known report of the association was by the German ophthalmologist Moritz Litten in 1881. Still, French ophthalmologist Albert Terson's name is more commonly associated with the condition after a report by his hand from 1900.

Inflammatory/Infection:

- Graves' ophthalmopathy due to Graves' disease, usually causes bilateral proptosis.

- Orbital cellulitis – often with unilateral proptosis, severe redness, and moderate to severe pain, sinusitis and an elevated white blood cell count.

- Dacryoadenitis

- Erdheim-Chester Disease

- Mucormycosis

- Orbital pseudotumor – presents with acute, usually unilateral proptosis with severe pain.

- High altitude cerebral edema

- Granulomatosis with polyangiitis

Neoplastic:

- Leukemias

- Meningioma, (of sphenoid wing)

- Nasopharyngeal angiofibroma

- Hand–Schüller–Christian disease

- Hemangioma, cavernous

Cystic:

- Dermoid cyst

Vascular:

- Carotid-cavernous fistula

- Aortic insufficiency: manifests as a pulsatile pseudoproptosis, described by British cardiothoracic surgeon, Hutan Ashrafian in 2006

Others:

- Orbital fracture: apex, floor, medial wall, zygomatic

- Retrobulbar hemorrhage: trauma to the orbit can lead to bleeding behind the eye. The hemorrhage has nowhere to escape and the increased pressure pushes the eye out of the socket, leading to proptosis and can also cause blindness if not treated promptly.

- Cushing's syndrome (due to fat in the orbital cave)

- Pfeiffer syndrome

No laboratory studies usually are necessary, though serum bilurubin level can be used. Vitamin C deficiency has been reported to possibly be associated with development of cephalohematomas. Skull x-ray or CT scanning is used if neurological symptoms appear. Usual management is mainly observation. Phototherapy may be necessary if blood accumulation is significant leading to jaundice. Rarely anaemia can develop needing blood transfusion. Do not aspirate to remove accumulated blood because of the risk of infection and abscess formation. The presence of a bleeding disorder should be considered but is rare. Skull radiography or CT scanning is also used if concomitant depressed skull fracture is a possibility. It may take weeks and months to resolve and disappear completely.

The cause of this condition is not known. However, in a significant number of patients, DNA of the bacterium "Mycobacterium tuberculosis" was detected by PCR.

Nontraumatic intraparenchymal hemorrhage most commonly results from hypertensive damage to blood vessel walls e.g.:

- hypertension

- eclampsia

- drug abuse,

but it also may be due to autoregulatory dysfunction with excessive cerebral blood flow e.g.:

- reperfusion injury

- hemorrhagic transformation

- cold exposure

- rupture of an aneurysm or arteriovenous malformation (AVM)

- arteriopathy (e.g. cerebral amyloid angiopathy, moyamoya)

- altered hemostasis (e.g. thrombolysis, anticoagulation, bleeding diathesis)

- hemorrhagic necrosis (e.g. tumor, infection)

- venous outflow obstruction (e.g. cerebral venous sinus thrombosis).

Nonpenetrating and penetrating cranial trauma can also be common causes of intracerebral hemorrhage.

Exophthalmos (also called exophthalmus, exophthalmia, proptosis, or exorbitism) is a bulging of the eye anteriorly out of the orbit. Exophthalmos can be either bilateral (as is often seen in Graves' disease) or unilateral (as is often seen in an orbital tumor). Complete or partial dislocation from the orbit is also possible from trauma or swelling of surrounding tissue resulting from trauma.

In the case of Graves' disease, the displacement of the eye is due to abnormal connective tissue deposition in the orbit and extraocular muscles which can be visualized by CT or MRI.

If left untreated, exophthalmos can cause the eyelids to fail to close during sleep leading to corneal dryness and damage. Another possible complication would be a form of redness or irritation called "Superior limbic keratoconjunctivitis", where the area above the cornea becomes inflamed as a result of increased friction when blinking. The process that is causing the displacement of the eye may also compress the optic nerve or ophthalmic artery, leading to blindness.

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event.

A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.

Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis.

Risk factors for ICH include:

- Hypertension (high blood pressure)

- Diabetes mellitus

- Menopause

- Cigarette smoking

- Excessive alcohol consumption

- Severe migraine

Traumautic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.

According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.

Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.

The main risk is intracranial hemorrhage. This risk is difficult to quantify since many patients with asymptomatic AVMs will never come to medical attention. Small AVMs tend to bleed more often than do larger ones, the opposite of cerebral aneurysms. If a rupture or bleeding incident occurs, the blood may penetrate either into the brain tissue (cerebral hemorrhage) or into the subarachnoid space, which is located between the sheaths (meninges) surrounding the brain (subarachnoid hemorrhage). Bleeding may also extend into the ventricular system (intraventricular hemorrhage). Cerebral hemorrhage appears to be most common.

One long-term study (mean follow up greater than 20 years) of over 150 symptomatic AVMs (either presenting with bleeding or seizures) found the risk of cerebral hemorrhage to be approximately 4% per year, slightly higher than the 2-3% seen in other studies. A simple, rough approximation of a patient's lifetime bleeding risk is 105 - (patient age in years), assuming a 3% bleed risk annually. For example, a healthy 30-year-old patient would have approximately a 75% lifetime risk of at least one bleeding event. Ruptured AVMs are a significant source or morbidity and mortality; post rupture, as many as 29% of patients will die, and only 55% will be able to live independently.