Neurological Complications In

Neurological complications in the hyperglycemic hyperosmolar state present as a spectrum of abnormalities and can range from lucidity to confusion or lethargy to complete coma. Other neurological manifestations, including hemiparesis, hemianopsia, chorea, and partial motor or generalized seizure activity, have also been described (14, 64).

Altered Sensorium and Coma

The most common and classic clinical presentation in the hyperglycemic hyperosmolar state is an altered sensorium (14). Varying degrees of mental status alterations can be observed. Early in the process, patients can present with weakness and visual disturbances (65). As the process worsens with increasing hyperosmolarity and dehydration, lethargy, confusion, and coma may develop.

Those with higher degrees of hyperosmolarity are at increased risk of mental obtundation and coma (13, 63, 66). Neurological deterioration can occur after plasma osmolality climbs higher than 320-330 mOsmol/kg (14, 66). It is also important to note that the stuporous patient with an effective osmolality less than 320 mosmol/Kg should be evaluated for other causes of altered mental status (14).

Hyperosmolarity may cause dehydration of brain tissue leading to diffuse cortical abnormalities. Yet, post-mortem studies suggest no evidence of dehydration in cerebral tissue (67). In laboratory animals, cerebral dehydration and death occur within 60-90 min if plasma glucose is elevated rapidly (68). However, if plasma glucose is elevated at slower rates, brain water content is initially lost but regained in 4-6 h. In these studies, water was ultimately retained in brain cells because of osmotic equilibrium between the brain osmole content increased to that of the plasma. The compensation by glucose, lactate, sorbitol, myoinositol, urea, sodium, potassium, and chloride only partially accounts for the rise and therefore unidentified "idio-genic osmoles" likely exist (67). Glucose levels likely play less of a role in altered sensorium. Despite glucose levels in excess of 600 mg/dl, coma rarely occurs if the plasma osmolality is near-normal (69). Although brain edema is common in patients with DKA, it is rare in those with non-ketotic coma (67).

Hemiparesis/Hemiplegia

The hyperglycemic hyperosmolar state can present as a stroke-like picture with hemiparesis or hemiplegia. There may be some difficulty in determining the cause or effect (i.e., stroke precipitating HHS or HHS precipitating hemiparesis). In fact, stroke was the most common admitting diagnosis in patients with HHS in the 1960s (67). Although hemiparesis may occur independently in HHS, it is more often related to post-ictal activity after a seizure (70). As per one report, hemiparesis is temporary and relieved within days after treatment of the underlying hyperglycemic hyperosmolar state (70).

Hemianopsia

Transient homonymous hemianopsia has been reported as a reversible complication of the hyperglycemic hyperosmolar state (64). There have been at least 12 cases of homonymous hemianopsia reported in patients with hyperosmolar hyperglycemia (64, 71-75). In addition to hemianop-sia, these patients have noted other visual disturbances including blurred or fragmented vision, visual-field hallucinations, and flashing lights (64, 74). MRI findings such as decreased T2 signal of the white matter, subtle gyral swelling, and enhancement of the overlying meninges have been observed in these patients (64). Other studies have reported transient hemianopsia without MRI changes (74). Case reports range from mild improvement to total resolution in visual disturbances after treatment of the underlying hyper-glycemic state (64, 74). In cases of hemianopsia, it is important to consider HHS as the cause when no lesion is detected on MRI. Other visual phenomena reported in patients with HHS include polyopia, flashing and flickering lights, hallucinations, and a persistence and transposition of objects in the visual fields (74).

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