For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset. Signs and symptoms
The extent and severity of the symptoms of cerebral edema depend on the exact etiology but are generally related to an acute increase of the pressure within the skull. As the skull is a fixed and inelastic space, the accumulation of cerebral edema can displace and compress vital brain tissue, cerebral spinal fluid, and blood vessels, according to the Monro-Kellie doctrine.Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness. Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness. Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex. The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death. Causes
Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:
Traumatic brain injury
Stroke
Tumors
Infections (such as a brain abscess or meningitis)
Hepatic encephalopathy
Posterior reversible encephalopathy syndrome
Radiation-induced brain edema
Post-surgical changes
Amyloid-related imaging abnormalities associated with edema (ARIA-E)
Hyponatremia
High-altitude cerebral edema

Risk factors
Cerebral edema is present with many common cerebral pathologies and risk factors for development of cerebral edema will depend on the cause. The following were reliable predictors for development of early cerebral edema in ischemic strokes.
Differential diagnosis
A renal colic must be differentiated from the following conditions:
biliary colic and cholecystitis
aortic and iliac aneurysms (in older patients with left-side pain, hypertension or atherosclerosis)
interstitial: appendicitis, diverticulitis or peritonitis (in this case patients prefer to lie still rather than being restless)
gynaecological: endometriosis, ovarian torsion and ectopic pregnancy
testicular torsion

Treatment
Most small stones are passed spontaneously and only pain management is required. Above 5 mm (0.20 in) the rate of spontaneous stone passage decreases. NSAIDs (non-steroidal anti-inflammatory drugs), such as diclofenac or ibuprofen, and antispasmodics like butylscopolamine are used. Although morphine may be administered to assist with emergency pain management, it is often not recommended as morphine is addictive and raises ureteral pressure, worsening the condition. Vomiting is also considered an important adverse effect of opioids, mainly with pethidine. Oral narcotic medications are also often used.There is typically no antalgic position for the patient (lying down on the non-aching side and applying a hot bottle or towel to the area affected may help). Larger stones may require surgical intervention for their removal, such as shockwave lithotripsy, laser lithotripsy, ureteroscopy or percutaneous nephrolithotomy. Patients can also be treated with alpha blockers in cases where the stone is located in the ureter. References


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