PMC9352937_01
From day 11 to 13, the patient's systolic blood pressure increased rapidly with bradycardia, which appeared to be a Cushing reflex. HR, heart rate; SBP, systolic blood pressure.
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F1
Spontaneous breathing disappeared and central diabetes insipidus developed on day 14, and all auditory brainstem response waves were undetectable starting from day 15 (Figures 1, 2A).
(A) TP rose rapidly in parallel with bilateral pupil dilation and fixation, reached a peak a few days later, and then dropped sharply, the timing of which coincided with the disappearance of spontaneous breathing and the full waves of ABR. LF/HF peaked a few days after TP and declined simultaneously with TP. (B) ACTH levels declined dramatically in parallel with progressive brain damage. ADH levels also showed a similar trend despite the higher Posm. Meanwhile, FT3 and FT4 levels both fluctuated at low levels with normal TSH levels after initial brain damage. ABR, acoustic brainstem response; ACTH, adrenocorticotropic hormone; Ad, adrenaline; ADH, antidiuretic hormone; EEG, electroencephalogram; FT3, free triiodothyronine; FT4, free thyroxine; HF, high frequency; LF, low frequency; Na, sodium; PLR, pupillary light reflex; Posm, plasma osmolality; SB, spontaneous breathing; TH, therapeutic hypothermia; TP, total power; TSH, thyroid-stimulating hormone.
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F2
Spontaneous breathing disappeared and central diabetes insipidus developed on day 14, and all auditory brainstem response waves were undetectable starting from day 15 (Figures 1, 2A). Meanwhile, the steep decrease in total power was linked to the disappearance of spontaneous breathing and all auditory brainstem response waves (Figure 2A). Free triiodothyronine and free thyroxine levels fluctuated at low levels whereas thyroid-stimulating hormone levels remained normal (Figure 2B).