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Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.[1] Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal.[1] In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the oedematus cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome.[1] Lower extremity function is more spared than that of the faciobrachial region.[2] The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.it is important to note that middle cerebral artery lesions mostly affect the dominant hemisphere i.e. the left cerebral hemisphere.
Proper placement of sutures enhances the precise approximation of the wound edges, which helps minimize and redistribute skin tension. Wound eversion is essential to maximize the likelihood of good epidermal approximation. Eversion is desirable to minimize the risk of scar depression secondary to tissue contraction during healing. Usually, inversion is not desirable, and it probably does not decrease the risk of hypertrophic scarring in an individual with a propensity for hypertrophic scars. The elimination of dead space, the restoration of natural anatomic contours, and the minimization of suture marks are also important to optimize the cosmetic and functional results.
In neonates, hypocalcemia is more likely to occur in infants born of diabetic or preeclamptic mothers. Hypocalcemia also may occur in infants born to mothers with hyperparathyroidism. Clinically evident hypocalcemia generally presents in milder forms and is usually the result of a chronic disease state. In emergency department patients, chronic or subacute complaints secondary to mild or moderate hypocalcemia are more likely to be a chief complaint than severe symptomatic hypocalcemia. Once laboratory results demonstrate hypocalcemia, the first question is whether the hypocalcemia is true—that is, whether it is representative of a decrease in ionized calcium. The presence of chronic diarrhea or intestinal disease (eg, Crohn disease, sprue, chronic pancreatitis) suggests the possibility of hypocalcemia due to malabsorption of calcium and/or vitamin D. The patient's past medical history should be explored for pancreatitis, anxiety disorders, renal or liver failure, gastrointestinal disorders, and hyperthyroidism or hyperparathyroidism. Previous neck surgery suggests hypoparathyroidism; a history of seizures suggests hypocalcemia secondary to anticonvulsants. The patient may have a recent history of thyroid, parathyroid, or bowel surgeries or recent neck trauma. The length of time that a disorder is present is an important clue. Hypoparathyroidism and pseudohypoparathyroidism are lifelong disorders. Instead, acute transient hypocalcemia may be associated with acute gastrointestinal illness, nutritional deficiency, or acute or chronic renal failure. In an elderly patient, a nutritional deficiency may be associated with a low intake of vitamin D. A history of alcoholism can help diagnose hypocalcemia due to magnesium deficiency, malabsorption, or chronic pancreatitis. Inquire about recent use of drugs associated with hypocalcemia, including the following: Radiocontrast Estrogen Loop diuretics Bisphosphonates Calcium supplements Antibiotics Antiepileptic drugs Cinacalcet Other considerations in the history include the following: Family history of hypocalcemia Low-calcium diet Lack of sun exposure