Postpartum blues, also known as baby blues and maternity blues, is a very common but self-limited condition that begins shortly after childbirth and can present with a variety of symptoms such as mood swings, irritability, and tearfulness. Mothers may experience negative mood symptoms mixed with intense periods of joy. Up to 85% of new mothers are affected by postpartum blues, with symptoms starting within a few days after childbirth and lasting up to two weeks in duration. Treatment is supportive, including ensuring adequate sleep and emotional support. If symptoms are severe enough to affect daily functioning or last longer than two weeks, the individual should be evaluated for related postpartum psychiatric conditions, such as postpartum depression and postpartum anxiety. It is unclear whether the condition can be prevented, however education and reassurance are important to help alleviate patient distress. Signs and symptoms
Symptoms of postpartum blues can vary significantly from one individual to another, and from one pregnancy to the next. Many symptoms of postpartum blues overlap both with normal symptoms experienced by new parents and with postpartum depression. Individuals with postpartum blues have symptoms that are milder and less disruptive to their daily functioning compared to those with postpartum depression. Symptoms of postpartum blues include, but are not limited to:
Tearfulness or crying "for no reason"
Mood swings
Irritability
Anxiety
Questioning ones ability to care for the baby
Difficulty making choices
Loss of appetite
Fatigue
Difficulty sleeping
Difficulty concentrating
Negative mood symptoms interspersed with positive symptoms

Onset
Symptoms of postpartum blues generally begin within a few days of childbirth and often peak by day four or five.
Concerning the pathology underlying these causes (except idiopathic), "some of the more frequent causes include atheromatous disease of the internal carotid or ophthalmic artery, vasospasm, optic neuropathies, giant cell arteritis, angle-closure glaucoma, increased intracranial pressure, orbital compressive disease, a steal phenomenon, and blood hyperviscosity or hypercoagulability." Embolic and hemodynamic origin
With respect to embolic and hemodynamic causes, this transient monocular visual loss ultimately occurs due to a temporary reduction in retinal artery, ophthalmic artery, or ciliary artery blood flow, leading to a decrease in retinal circulation which, in turn, causes retinal hypoxia. While, most commonly, emboli causing amaurosis fugax are described as coming from an atherosclerotic carotid artery, any emboli arising from vasculature preceding the retinal artery, ophthalmic artery, or ciliary arteries may cause this transient monocular blindness. Atherosclerotic carotid artery: Amaurosis fugax may present as a type of transient ischemic attack (TIA), during which an embolus unilaterally obstructs the lumen of the retinal artery or ophthalmic artery, causing a decrease in blood flow to the ipsilateral retina. The most common source of these athero-emboli is an atherosclerotic carotid artery. However, a severely atherosclerotic carotid artery may also cause amaurosis fugax due to its stenosis of blood flow, leading to ischemia when the retina is exposed to bright light. "Unilateral visual loss in bright light may indicate ipsilateral carotid artery occlusive disease and may reflect the inability of borderline circulation to sustain the increased retinal metabolic activity associated with exposure to bright light." Atherosclerotic ophthalmic artery: Will present similarly to an atherosclerotic internal carotid artery.