Abstract
The pathogenesis of delirium in critically ill patients is multifactorial. How hypotension and hypoxemia affect brain function and whether they can promote delirium remains unclear. A high cumulative positive fluid balance may also have a negative effect on brain function and promote delirium. We hypothesized that delirium would be more likely to develop in patients with low systemic arterial pressure, hypoxemia and a higher positive fluid balance, and investigated these associations in a prospective observational cohort study in patients with shock. After initial resuscitation, episodes of hypotension, defined as a mean arterial pressure (MAP) <65 mmHg or diastolic pressure <60 mmHg, and hypoxemia, defined as peripheral oxygen saturation (SpO2) <90% for more than one minute or any arterial oxygen concentration (PaO2) <90 mmHg, were recorded during the first 5 days of the ICU stay. Fluid balance was evaluated daily and the 5-day cumulative fluid balance recorded. Delirium was assessed using the Confusion Assessment Method for the ICU. A total of 252 patients were admitted with shock during the study period; 185 (73%) developed delirium. Patients who developed delirium also had more episodes of hypotension with a low MAP (p = 0.013) or diastolic pressure (p = 0.018) during the first five days of the ICU stay than those who did not. Patients with a higher cumulative fluid balance during the same period were also more likely to develop delirium (p = 0.01); there was no significant difference in the occurrence of hypoxemia between groups. Joint modeling, combining a linear-mixed model and an adjusted Cox survival model showed that low diastolic pressure (alpha effect = -0.058±0.0013, p = 0.043) and a positive cumulative fluid balance (alpha effect = 0.04±0.003, p = 0.021) were independently associated with delirium. In conclusion, low diastolic pressure and a cumulative positive fluid balance but not hypoxemia were independently associated with development of delirium in patients with shock.
Highlights
The pathogenesis of delirium in critically ill patients is multifactorial
Maintaining a mean arterial pressure (MAP) ! 65 mmHg is usually suggested as sufficient to maintain adequate organ perfusion in clinical practice [3], whether reduction in MAP below this level affects brain function is unclear, when it falls below the threshold for cerebral autoregulation, i.e., < 50 mmHg [3,4,5]
It has been shown that delirium is more frequent in patients with acute respiratory distress syndrome (ARDS) but it remains uncertain whether delirium is associate with hypoxemia per se [7]
Summary
The pathogenesis of delirium in critically ill patients is multifactorial. Administration of excessive sedative and analgesic agents is a known risk factor for delirium along with high disease severity [1, 2]. Systemic hypotension and hypoxemia have been suggested as potential risk factors, but their role remains unclear because their definitions vary from study to study. 65 mmHg is usually suggested as sufficient to maintain adequate organ perfusion in clinical practice [3], whether reduction in MAP below this level affects brain function is unclear, when it falls below the threshold for cerebral autoregulation, i.e., < 50 mmHg [3,4,5]. It has been shown that delirium is more frequent in patients with acute respiratory distress syndrome (ARDS) but it remains uncertain whether delirium is associate with hypoxemia per se [7]. Fluid administration is necessary for correction of hypotension in shock, excessive fluid administration can impair organ function and worsen outcomes [10, 11, 12]. BBB leakage facilitates the passage of brain S100B protein into the serum, so elevated S100B levels have been used as a marker of brain injury or BBB leakage [13, 14, 15]
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