Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2589_Библиотеки_им_академика_М_И_Перельмана

returning if the blood pressure remains con-

While microaneurysms are the sine qua non of diabetic retinopathy, dot and blot haemorrhages are the hallmarks of non-proliferative diabetic retinopathy. Most of these arise from the extrav­asation of RBCs from the retinal microaneu­rysms and capillary segments. The collections of blood elements from the leaking microaneu­rysms in the ganglion cell layer and the inner nuclear layer take a dot-like appearance due to the vertical orientation of the tightly packed retinal cells in these layers, while in the inner and outer plexiform layers, these haemorrhages appear larger blot-like due to a comparatively less density of the interstitial tissue and the hori­zontal orientation of the neural bres (Fig.5.8a

In the elderly, this is due to age-related choroidal neovascular membrane/s (CNVM) or polypoidal choroidal vasculopathy (PCV). Other less com­mon causes of submacular haemorrhages at any age include CNVM complicating myopia, angi­oid streaks, ocular histoplasmosis, toxoplasmosis retinochoroiditis scars, and tubercular choroidi­tis. Because of its transparency, blood under the neurosensory retina appears bright red, while that under the RPE appears dark due to the pigmented nature of the RPE.Unlike the boat-shaped sub­ILM or subhyaloid haemorrhage, blood under the neurosensory retina or sub-RPE space is clotted and shows no uid level. Depending upon its location, brin strands pull the photoreceptors or the RPE and cause irreversible damage and the loss of central vision. As most of these haemor­rhages are due to abnormal CNVM, the treatment revolves around using only an intravitreal anti­VEGF agent if the haemorrhage is small and thin; however, if it is large and thick, the tissue plas­minogen activator (tPA) administered either intravitreal or subretinal (this approach necessi­tates pars plana vitreous surgery and some sur­geons also combine it with a subretinal air bubble) for clot lysis is followed by pneumatic displacement of the blood by injecting a long­acting gas bubble (SF6 or C3F8) into the vitreous cavity or if PPV has been done by doing a uid gas exchange. The patient lies prone for a few days, so that the lysed blood gets displaced from the macula [6, 7]. Monthly injections of an anti­VEGF agent follow this to keep the CNVM regressed. If thick and large, submacular haemor­rhage following blunt trauma may require tPA and pneumatic displacement. The mild and thin haemorrhages resolve spontaneously.

Intrapapillary haemorrhage with adjacent peri­papillary subretinal haemorrhage may be seen in young myopic women due to a uniquely tilted optic disc with an elevated nasal margin. These resolve spontaneously and carry an excellent prognosis [9]. Most of these haemorrhages are unilateral. These are seen as a crescent nasal to the optic disc. The nasal margin of the disc appears thick, and the disc may be smaller and tilted [10, 11]. Occasionally there may be a small vitreous haemorrhage. These haemorrhages arise from a partial detachment of the posterior vitre­ous tightly adherent to the optic disc margins

of congenital amblyopia might be due to unilat-

with or without retinal haemorrhages were fol-

lowed for 4years, there was no difference in the

Unlike the transient nature of retinal haemor­rhages that occur during normal childbirth, severe

Diminution of vision due to retinal haemorrhages in the macula of one or both eyes usually prompts the patient to seek medical attention (Fig.5.13). On the other hand, peripheral retinal haemor­rhages are often asymptomatic. Their detection on a routine ophthalmoscopic examination may lead to the discovery of potentially life­threatening or disabling systemic disorders such as von Willebrand disease, one of the common bleeding disorders that may show a high degree of variation in its clinical presentations [27].

Retinal haemorrhages are frequently (28%) seen in patients with anaemia and thrombocytopenia and 38% if both are present concomitantly (Fig.5.13).

Patients with acute leukaemias often present with fever, fatigue, loss of appetite, recurrent infec­tions, and easy bruising. They may present with petechial haemorrhages on their arms and legs. Retinal haemorrhages may be asymptomatic and seen in nearly half the patients with leukaemia who, besides leukocytosis, have anaemia, Thrombocytopenia and cellular hyperviscosity.

their cell surface, making them vulnerable to hae-

the post pole of the retina (Terson syndrome) is diagnostic of this condition (Fig. 5.15). Subarachnoid haemorrhage and Terson’s syn­drome may occasionally occur due to cortical venous thrombosis (CVT). While a ruptured aneurysm requires embolization, the CVT needs anticoagulation. Such patients, thus, should undergo imaging studies in an emergency setting to rule out the presence of either a ruptured aneu­rysm or CVT [48, 49].

Patients, mostly obese women in their 40s, pre­senting with headache, pulsatile tinnitus, and transient blurring of vision but without cranial nerve palsies, are suspected of having idiopathic intracranial hypertension [50]. Optic disc oedema (papilloedema) is a highly characteristic feature of IIH. In long-standing cases, it may lead to visual loss (Fig. 5.16). Increased intracranial pressure gets transmitted to the vaginal space in the optic nerve sheath surrounding the optic nerve, leading to axoplasmic stasis and possibly ischaemia of the optic nerve head. In severe cases of IIH, there may be retinal vascular changes, including retinal venous dilation and retinal haemorrhages mimicking a picture of bilateral central retinal vein occlusion. In such cases rarely, a Terson’s syndrome-like picture may also be seen [51–53]. Patients with IIH are often asso­ciated with CVT.Initiation of anticoagulant ther­apy in such patients may precipitate peripapillary haemorrhages, however, without any long-term visual consequences [54]. Rarely, patients with IIH may develop a juxtapapillary choroidal neo­vascular membrane and produce a juxtapapillary subretinal haemorrhage which may or may not be vision threatening. Often, treatment of IIH will cause spontaneous regression of these neovascu­lar membranes. However, if persistent, these will require an intravitreal injection of one of the anti­VEGF agents [55].