A retinal haemorrhage is generally diagnosed by using an ophthalmoscope or fundus camera in order to examine the inside of the eye. A fluorescent dye is often injected into the patient's bloodstream beforehand so the administering ophthalmologist can have a more detailed view of the blood vessels in the retina.

The fluorescent dye can have dangerous side effects: see Fluorescein

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.

Many laboratories rely on only the color of the cerebrospinal fluid to determine the presence or absence of xanthochromia. However, recent guidelines suggest that spectrophotometry should be performed. Spectrophotometry relies on the different transmittance, or conversely, absorbance, of light by different substances or materials, including solutes. Bilirubin absorbs light at wavelengths between 450–460 nm. Spectrophotometry can also detect the presence of oxyhemoglobin and methemoglobin, which absorb light at 410-418 nm and 403-410 nm, respectively, and also may indicate that bleeding has occurred; to identify substances in cerebrospinal fluid that absorb light at other wavelengths but are not due to bleeding, such as carotenoids; and to detect very small amounts of yellow color saturation (about 0.62%) which may be missed by visual inspection, especially when the cerebrospinal fluid has been examined under incandescent lighting or a tungsten desk lamp (corresponding to International Commission on Illumination standard illuminant A).

Visual inspection is the most frequent method used in the United States to assess cerebrospinal fluid for xanthochromia, while spectrophotometry is used on up to 94% of specimens in the United Kingdom. There is still disagreement about whether or not to routinely use spectrophotometry or whether visual inspection is adequate, and one group of authors has even advocated measuring bilirubin levels.

Management consists of vigilant observation over days to detect progression. The subgaleal space is capable of holding up to 50% of a newborn baby's blood and can therefore result in acute shock and death. Fluid bolus may be required if blood loss is significant and patient becomes tachycardic. Transfusion and phototherapy may be necessary. Investigation for coagulopathy may be indicated.

The treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).

The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by Laser treatment or cryotherapy, and detached retinas are reattached surgically.

Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina,long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.

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 diagnosis of BRVO is made clinically by finding retinal hemorrhages in the distribution of an obstructed retinal vein.

- Fluorescein angiography is a helpful adjunct. Findings include delayed venous filling, hypofluorescence caused by hemorrhage and capillary nonperfusion, dilation and tortuosity of veins, leakage due to neovascularization and macular edema.

- Optical coherence tomography is an adjunctive test in BRVO. Macular edema is commonly seen in BRVO in OCT exams. Serial OCT is used as a rapid and noninvasive way of monitoring the macular edema.

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

Common symptoms of vitreous hemorrhage include:

- Blurry vision

- Floaters- faint cobweb-like apparitions floating through the field of vision

- Reddish tint to vision

- Photopsia – brief flashes of light in the peripheral vision

Small vitreous hemorrhage often manifests itself as "floaters". A moderate case will often result in dark streaks in the vision, while dense vitreous hemorrhage can significantly inhibit vision.

Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify cause. Some common tests include:

- Examination of the eye with a microscope

- Pupil dilation and examination

- An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye

- Blood tests to check for specific causes such as diabetes

- A CT scan to check for injury around the eye

- Referral to a retinal specialist

Imaging studies such as ultrasonography (US), Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI) can aid diagnosis. On ultrasound, Coats' disease appears as a hyperechoic mass in the posterior vitreous without posterior acoustic shadowing; vitreous and subretinal hemorrhage may often be observed.

On CT, the globe appears hyperdense compared to normal vitreous due to the proteinaceous exudate, which may obliterate the vitreous space in advanced disease. The anterior margin of the subretinal exudate enhances with contrast. Since the retina is fixed posteriorly at the optic disc, this enhancement has a V-shaped configuration.

On MRI, the subretinal exudate shows high signal intensity on both T1- and T2-weighted images. The exudate may appear heterogeneous if hemorrhage or fibrosis is present. The subretinal space does not enhance with gadolinium contrast. Mild to moderate linear enhancement may be seen between the exudate and the remaining vitreous. The exudate shows a large peak at 1-1.6 ppm on proton MR spectroscopy.

Grossly, retinal detachment and yellowish subretinal exudate containing cholesterol crystals are commonly seen.

Microscopically, the wall of retinal vessels may be thickened in some cases, while in other cases the wall may be thinned with irregular dilatation of the lumen. The subretinal exudate consists of cholesterol crystals, macrophages laden with cholesterol and pigment, erythrocytes, and hemosiderin. A granulomatous reaction, induced by the exudate, may be seen with the retina. Portions of the retina may develop gliosis as a response to injury.

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.

It is important that a person receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.

Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes. They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli. Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri.

On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stage of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere since it can cross suture lines, unlike an epidural hemorrhage. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding such as effacement of sulci or medial displacement of the junction between gray matter and white matter may be apparent. A chronic bleed can be the same density as brain tissue (called isodense to brain), meaning that it will show up on CT scan as the same shade as brain tissue, potentially obscuring the finding.

Computed tomography (CT scan): A CT scan may be normal if it is done soon after the onset of symptoms. A CT scan is the best test to look for bleeding in or around your brain. In some hospitals, a perfusion CT scan may be done to see where the blood is flowing and not flowing in your brain.

Magnetic resonance imaging (MRI scan): A special MRI technique (diffusion MRI) may show evidence of an ischemic stroke within minutes of symptom onset. In some hospitals, a perfusion MRI scan may be done to see where the blood is flowing and not flowing in your brain.

Angiogram: a test that looks at the blood vessels that feed the brain. An angiogram will show whether the blood vessel is blocked by a clot, the blood vessel is narrowed, or if there is an abnormality of a blood vessel known as an aneurysm.

Carotid duplex: A carotid duplex is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the carotid arteries. These arteries are the large blood vessels in your neck that feed your brain.

Transcranial Doppler (TCD): Transcranial Doppler is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the blood vessels inside of your brain. It can also be used to see if you have emboli (blood clots) in your blood vessels.

Treatment of Eales’ disease comprises:

1. Medical treatment:

A course of oral corticosteroids for extended periods is the main stay of treatment

during active inflammation. A course of antitubercular therapy has also been

recommended in selective cases.

2. Laser photocoagulation of the retina is indicated in stage of neovascularizion.

3. Vitreoretinal surgery is required for nonresolving vitreous haemorrhage and tractional retinal detachment.

•If active TB present - treat with ATT

•otherwise manage the vitreous hemorrhage -

Partial h’ge - postural management with propped up position

Total h’ge - Pars Plana Vitrectomy

Treatment of a subdural hematoma depends on its size and rate of growth. Some small subdural hematomas can be managed by careful monitoring until the body heals itself. Other small subdural hematomas can be managed by inserting a temporary small catheter through a hole drilled through the skull and sucking out the hematoma; this procedure can be done at the bedside. Large or symptomatic hematomas require a craniotomy, the surgical opening of the skull. A surgeon then opens the dura, removes the blood clot with suction or irrigation, and identifies and controls sites of bleeding. Postoperative complications include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizure. The injured vessels must be repaired.

Depending on the size and deterioration, age of the patient, and anaesthetic risk posed, subdural hematomas occasionally require craniotomy for evacuation; most frequently, simple burr holes for drainage; often conservative treatment; and rarely, palliative treatment in patients of extreme age or with no chance of recovery.

In those with a chronic subdural hematoma, but without a history of seizures, the evidence is unclear if using anticonvulsants is harmful or beneficial.

After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below).

Lumbar puncture, in which cerebrospinal fluid (CSF) is removed from the subarachnoid space of the spinal canal using a hypodermic needle, shows evidence of hemorrhage in 3 percent of people in whom CT was found normal; lumbar puncture is therefore regarded as mandatory in people with suspected SAH if imaging is negative. At least three tubes of CSF are collected. If an elevated number of red blood cells is present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap"). While there is no official cutoff for red blood cells in the CSF no documented cases have occurred at less than "a few hundred cells" per high-powered field.

The CSF sample is also examined for xanthochromia—the yellow appearance of centrifugated fluid. This can be determined by spectrophotometry (measuring the absorption of particular wavelengths of light) or visual examination. It is unclear which method is superior. Xanthochromia remains a reliable ways to detect SAH several days after the onset of headache. An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin from the red blood cells to be metabolized into bilirubin.

Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH. So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign".

Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan.

When due to high blood pressure, they typically occur in the putamen or thalamus (60%), cerebrum (20%), cerebellum (13%) or pons (7%).

The best imaging modality for idiopathic orbital inflammatory disease is contrast-enhanced thin section magnetic resonance with fat suppression. The best diagnostic clue is a poorly marginated, mass-like enhancing soft tissue involving any area of the orbit.

Overall, radiographic features for idiopathic orbital inflammatory syndrome vary widely. They include inflammation of the extraocular muscles (myositis) with tendinous involvement, orbital fat stranding, lacrimal gland inflammation and enlargement (dacryoadenitis), involvement of the optic sheath complex, uvea, and sclera, a focal intraorbital mass or even diffuse orbital involvement. Bone destruction and intracranial extension is rare, but has been reported. Depending on the area of involvement, IOI may be categorized as:

- Myositic

- Lacrimal

- Anterior – Involvement of the globe, retrobulbar orbit

- Diffuse – Multifocal intraconal involvement with or without an extraconal component

- Apical – Involving the orbital apex and with intracranial involvement

Tolosa–Hunt syndrome is a variant of orbital pseudotumor in which there is extension into the cavernous sinus through the superior orbital fissure. Another disease variant is Sclerosing pseudotumor, which more often presents bilaterally and may extend into the sinuses.

CT findings

In non-enhanced CT one may observe a lacrimal, extra-ocular muscle, or other orbital mass. It may be focal or infiltrative and will have poorly circumscribed soft tissue. In contrast-enhanced CT there is moderate diffuse irregularity and enhancement of the involved structures. A dynamic CT will show an attenuation increase in the late phase, contrary to lymphoma where there is an attenuation decrease. Bone CT will rarely show bone remodeling or erosion, as mentioned above.

MR findings

On MR examination there is hypointensity in T1 weighted imaging (WI), particularly in sclerosing disease. T1WI with contrast will show moderate to marked diffuse irregularity and enhancement of involved structures. T2 weighted imaging with fat suppression will show iso- or slight hyperintensity compared to muscle. There is also decreased signal intensity compared to most orbital lesions due to cellular infiltrate and fibrosis. In chronic disease or sclerosing variant, T2WI with FS will show hypointensity (due to fibrosis). Findings on STIR (Short T1 Inversion Recovery) are similar to those on T2WI FS. In Tolosa–Hunt syndrome, findings include enhancement and fullness of the anterior cavernous sinus and superior orbital fissure in T1WI with contrast, while MRA may show narrowing of cavernous sinus internal carotid artery (ICA).

Ultrasonographic findings

On grayscale ultrasound there is reduced reflectivity, regular internal echoes, and weak attenuation, in a way, similar to lymphoproliferative lesions.

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

The most important initial investigation is computed tomography of the brain, which is very sensitive for subarachnoid hemorrhage. If this is normal, a lumbar puncture is performed, as a small proportion of SAH is missed on CT and can still be detected as xanthochromia.

If both investigations are normal, the specific description of the headache and the presence of other abnormalities may prompt further tests, usually involving magnetic resonance imaging (MRI). Magnetic resonance angiography (MRA) may be useful in identifying problems with the arteries (such as dissection), and magnetic resonance venography (MRV) identifies venous thrombosis. It is not usually necessary to proceed to cerebral angiography, a more precise but invasive investigation of the brain's blood vessels, if MRA and MRV are normal.

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)

Cerebrospinal fluid, which fills the subarachnoid space between the arachnoid membrane and the pia mater surrounding the brain, is normally clear and colorless. When there has been bleeding into the subarachnoid space, the initial appearance of the cerebrospinal fluid can range from barely tinged with blood to frankly bloody, depending on the extent of bleeding. Within several hours, the red blood cells in the cerebrospinal fluid are destroyed, releasing their oxygen-carrying molecule heme, which is then metabolized by enzymes to bilirubin, a yellow pigment. The most common cause for bleeding into the subarachnoid space is a subarachnoid hemorrhage from a ruptured cerebral aneurysm.

The most frequently employed initial test for subarachnoid hemorrhage is a computed tomography scan of the head, but it detects only 98% of cases in the first 12 hours after the onset of symptoms, and becomes less useful afterwards. Therefore, a lumbar puncture ("spinal tap") is recommended to obtain cerebrospinal fluid if someone has symptoms of a subarachnoid hemorrhage (e.g., a thunderclap headache, vomiting, dizziness, new-onset seizures, confusion, a decreased level of consciousness or coma, neck stiffness or other signs of meningismus, and signs of sudden elevated intracranial pressure), but no blood is visible on the CT scan. According to one article, a spinal tap is not necessary if no blood is seen on a CT scan done using a third generation scanner within six hours of the onset of the symptoms. However, this is not standard of care.

Heme from red blood cells that are in the cerebrospinal fluid because a blood vessel was nicked during the lumbar puncture (a "traumatic tap") has no time to be metabolized, and therefore no bilirubin is present.

After the cerebrospinal fluid is obtained, a variety of its parameters can be checked, including the presence of xanthochromia. If the cerebrospinal fluid is bloody, it is centrifuged to determine its color.