ARDS and the Treatment of Head Injury
February 1, 2000 5 minutes read
ARDS and the Treatment of Head Injury
Abstract & Commentary
Synopsis: In a prospective, randomized comparison of management of head injury directed by ICP vs. CBF, no difference in long-term functional outcome or death was identified. However, the incidence of ARDS was five times greater in the CBF group than in the ICP-directed group (15% vs 3.3%, P = 0.007), which may have accounted for failure to show benefit of the CBF-directed approach.
Source: Robertson CS, et al. Crit Care Med 1999; 27:2086-2095.
In general there are two approaches used to improve brain perfusion in hopes of preventing secondary injury following head injury. The goal is to improve neurologic outcome and prevent death. Therapy can be directed at reducing elevated intracranial pressure (ICP) to improve global brain oxygen and nutrient delivery by using hyperventilation and dehydration therapy. Alternatively, cerebral perfusion can be improved by increasing arterial blood pressure above normal, increasing cerebral perfusion pressure (CPP), avoiding dehydration, and supporting cardiac function using vasopressors.
The systemic and regional brain tissue consequences of these two approaches are markedly different. ICP-directed treatment might be expected to result in hypoperfusion of uninjured brain tissues, kidneys, and other organs, while cerebral blood flow-directed therapy might result in secondary brain hemorrhage.
In this study, these two approaches were compared in a series of 189 head-injured patients. Adult patients with Glascow Coma Scale (GCS) score less than 6 but higher than 3 (or higher on entry but deterioration to < 6 in the first 48 hours of treatment) who presented within 12 hours of injury were treated either by cerebral blood flow (CBF) or by an ICP-directed protocol. All patients admitted during each two-month block were treated using the same protocol; the blocks were randomly assigned to one of the two protocols during the 32 months of the study that was performed at a single institution.
All patients received a ventriculostomy for ICP monitoring and treatment and jugular bulb venous catheters for continuous oxyhemoglobin saturation monitoring. The primary outcome measures were the number of times that jugular venous saturation was less than 50% (SjvO2 < 50) for 10 minutes or more, and the number of times ICP exceeded 20 torr. Other outcome measures included survival and the patients’ functional capacity at three and six months.
All patients received mechanical ventilation and sedation with morphine, and normothermia was maintained. All patients who developed an ICP of more than 20 torr were treated with CSF drainage, sedation, paralysis, and infusions of mannitol. In addition, the ICP protocol patients were hyperventilated to a PaCO2 of 25-30 torr if the ICP was above 20 torr. This group had a blood pressure goal of between 70-160 torr (mean). The CBF group had a blood pressure goal greater than 90 torr mean pressure with no upper limit. PaCO2 was maintained at 35 torr or greater in the CBF group. Similar treatments for hypotension (e.g., infusions of volume, dopamine, and phenylephrine) were followed in both groups, although with a different lower limit. In the ICP group, hypertension was treated with labetalol.
One hundred patients were randomized to the CBF group and 89 received ICP-directed therapy. There were fewer women in the ICP group (20% vs 10%) and fewer gunshot injuries (4% vs 11%); otherwise, the groups were similar. The treatment goals were achieved: cerebral perfusion pressure (CPP), mean arterial BP, and PaCO2 were higher in the CBF group. The duration of time spent below a CPP of 60 and BP of 80 were also less in the CBF group. SjvO2 was lower on average in the ICP group (70.8% vs 73.2%) and more patients experienced at least one period of SjvO2 less than 50 (50.6% vs 39.7%) and these periods lasted longer. There was no difference in the number of episodes of ICP of more than 20 or in how often a barbiturate coma was needed for ICP control between the groups. There was also no difference in secondary intracranial bleeding in the groups.
There was no difference in death or disability between the groups. There was, however, a striking difference in the incidence of development of the acute respiratory distress syndrome (ARDS), which was 15% in the CBF group and 3.3% in the ICP group. ARDS directly contributed to death in five patients. The CBF group received more fluids and pressors, and had higher blood pressures throughout the treatment period. Only one patient developed renal failure, and it was attributed to sepsis and multiple organ failure rather than to head injury therapy.
Comment by Charles G. Durbin, Jr., MD, FCCM
This is an important study for several reasons. It demonstrates that complex clinical conditions can be adequately studied in the real world of ICU care. While there was no group difference in neurological outcome, CPP was an independent predictor of outcome when all patients were considered. This supports the clinical practice of monitoring CPP and aggressively treating critical values and maintaining CBF at higher levels.
The incidence of global cerebral hypoxemia (reflected in reduced SjvO2) was clearly less in the CBF targeted treatment group. Failure to demonstrate a long-term improved outcome due to this approach is likely due to several factors. Since critical SjvO2 desaturations and raised ICP were aggressively treated in both groups, systemic treatment differences were less. Also, because of the severe pulmonary complications and associated morbidity in the CBF-directed group, improvement in neurologic outcome may have been overridden by this complication. The best treatment to prevent secondary injury following traumatic brain injury is not clear from this study.
The higher incidence of ARDS and its significant effect on mortality in the CBF group was a surprise finding. The etiology is not clear. Higher intravenous fluid rates, more positive fluid balance, higher cardiac output, higher filling pressures, and higher arterial pressures were the consequences of being treated with CBF-directed therapy. But these also could result from infection, being necessary to maintain hemodynamic stability. There was no difference in the use of vasopressors in patients developing ARDS and those who did not develop the syndrome, although the duration and dosage may have been different.
Not all relevant information about this problem is available in this paper. Because the finding of increased incidence of ARDS was only observed following completion of the study, many important pieces of information were not obtained prospectively. No information is reported regarding the possibility of infection or the systemic inflammatory response syndrome (SIRS), a common occult cause of ARDS. Drug therapy not specifically related to neurologic treatment may have been different between the groups. The frequency of use of neuromuscular blockade was not different between the groups, although the duration of paralysis was not reported and prolonged paralysis may be a risk factor for pulmonary infection.
The relationship between fluid administration and the development of ARDS in head-injured patients remains speculative but merits further investigation. Further evaluation of information collected about the patients in this study might shed needed light on this issue. This might also help to increase our understanding of the pathophysiology of ARDS in general.
Treatment of severe head injury with fluids and pressors to preserve cerebral blood flow:
a. is associated with more early deaths.
b. often results in intracranial hemorrhage.
c. should be abandoned due to increased disabilities at six months.
d. is associated with a higher incidence of ARDS.
e. uncovers significant latent cardiac disease.
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