To evaluate the effects of delayed vs early fluid resuscitation on cerebral hemodynamics after severe head injury and uncontrolled hemorrhagic shock.
Prospective, randomized, controlled experimental trial.
Surgical research laboratory.
Immature swine (N=16) weighing 40 to 50 kg.
Twelve swine were subjected to cryogenic brain lesion and hemorrhage to maintain a mean arterial pressure (MAP) of 50 mm Hg. Animals were randomized to receive 1 L of Ringer lactate solution in 20 minutes, starting 20 minutes after injury and hemorrhage, followed by 1 L of Ringer lactate solution in 30 minutes (ER group) (n=6), or no fluid resuscitation (DR group) (n=6). The 4 control animals underwent instrumentation only. The study ended 70 minutes after head injury and hemorrhage.
Main Outcome Measurements
Measurements of MAP, bilateral regional cerebral blood flow, serum hemoglobin level, systemic and regional cerebral oxygen delivery, and intracranial pressure performed at baseline and 20 (phase 1), 50 (phase 2), and 70 minutes (phase 3) after head injury and hemorrhage. Lesion size (percentage of ipsilateral cortex) was measured post mortem.
All animals survived the experimental period. Systemic cerebral oxygen delivery in the DR group was significantly lower at phase 3 compared with that of the ER group (31.5% vs 53.1% at baseline) (P=.03). However, bilateral regional cerebral oxygen delivery was significantly greater in the DR group at phase 3 compared with that of the ER group (71.5% vs 47.0% at baseline in the injured side; 72.9% vs 48.4% at baseline in the noninjured side) (P=.02). Bilateral cerebral blood flow was similar in all groups at all times. The ER group showed a trend toward a greater intracranial pressure elevation (6.8 vs −0.25) (P=.07) and lesion size (37.0% vs 28.6%) (P=.07). Hemoglobin level became significantly lower in the ER group at phase 2 (7.0 vs 10.7) (P=.03) and remained lower at phase 3 (6.9 vs 11.7) (P=.01).
Early fluid resuscitation with Ringer lactate solution following head injury and uncontrolled hemorrhagic shock worsens cerebral hemodynamics. Cerebral pressure autoregulation is sufficiently intact following head injury to maintain regional cerebral oxygen delivery without asanguineous fluid resuscitation.