Background and Purpose Many patients with acute basilar artery occlusion may require endotracheal intubation and mechanical ventilation. The circumstances and predictive value for outcome in these patients are not well documented.
Methods We reviewed the medical records of 25 patients admitted into the intensive care unit with a clinical diagnosis of acute basilar artery occlusion and need for mechanical ventilation. The medical records were reviewed for clinical features, breathing patterns, mode of mechanical ventilation, ability to wean from the ventilator, and neurological outcome.
Results Apneic episodes resulted in endotracheal intubation in 8 patients. In the remaining 17 patients, intubation was needed for airway protection. Seven of 8 patients presenting with apneic episodes lost all brain stem reflexes. All 17 patients intubated for airway protection could be successfully weaned to a T-tube circuit. Outcome was generally poor and 22 patients died, of whom 7 died of early systemic complications. Only 3 of 25 patients, all with locked-in syndrome, survived.
Conclusions Mortality is high in patients who require mechanical ventilation after acute basilar artery occlusion. No neurological improvement beyond a locked-in syndrome occurred in survivors. Recurrent apnea appears to predict further progression to brain stem death.
Basilar artery occlusion is a devastating acute neurological event with little prospect for restoration of independent function.1 2 3 4 No definite benefit of heparin or other supportive measures, such as blood pressure augmentation, has been documented. Early intra-arterial thrombolysis, however, has shown promise and may become a first-line treatment.5 6
Many patients continue to deteriorate after admission and may require endotracheal intubation for airway protection. In other patients breathing abnormalities may result in inadequate gas exchange. The circumstances of mechanical ventilation, its predictive value for outcome, and weaning potential have not been addressed in earlier reports.
We reviewed a series of patients with acute basilar occlusion who were placed on mechanical ventilation. We sought answers to the following questions: (1) Do certain breathing abnormalities predict outcome? (2) Which patients can be successfully weaned from the ventilator? (3) If mechanical ventilation is required, which patients are unlikely to benefit from aggressive support?
Subjects and Methods
We reviewed the medical records of all patients with acute basilar artery occlusion admitted from 1980 to 1995 to intensive care units and who required endotracheal intubation and mechanical ventilation. We excluded patients with previous surgery of the posterior circulation and those with end-stage malignant disease. The diagnosis of acute basilar artery occlusion was based on clinical findings and, in most patients, confirmed by CT scan (n=11), MRI (n=3), angiography (n=3), or autopsy (n=9). The circumstances surrounding the endotracheal intubation and mode of ventilation were carefully reviewed, as were the results of arterial blood gas and chest roentgenographic studies. All patients were examined by staff neurologists. The variables investigated were age, sex, risk factors for stroke, and possible cardioembolism.
All 25 patients with a clinical diagnosis of acute basilar artery occlusion were evaluated in medical, surgical, or neurological intensive care units (age range, 29 to 78 years; 11 women, 14 men). The mode of mechanical ventilation was assisted control ventilation in 10, intermittent mandatory ventilation in 9, and pressure support in 6.
In 8 patients, recurrent apneic spells prompted endotracheal intubation. In the remaining 17 patients, endotracheal intubation was performed for airway protection.
The most pertinent clinical features are summarized in Tables 1 and 2⇓⇓. Of 25 patients, 22 presented with sudden vertigo, dysarthria, and quadriparesis. Six patients presented with hemiparesis. Brief rhythmic shaking movements were observed in 2 patients. At the time of endotracheal intubation and institution of mechanical ventilation, 16 patients had progressed to coma with quadriplegia and either pathological withdrawal or extensor motor responses to pain. Of the 25 patients, 7 lost all brain stem reflexes (Table 2⇓). In these 7 patients, loss of triggering of the ventilator prompted clinicians to increase the minute volume by an increase in the intermittent mechanical ventilation rate or a change to an assisted control mode of ventilation. In the remaining patients (Table 2⇓), the maximal neurological deficit was locked-in syndrome in 4 patients and coma in 12 patients. In 2 patients (patients 2 and 10), no further clinical progression was noted. Both patients were drowsy and had ophthalmoparesis and bulbar weakness.
Maximal neurological deficit was reached within 1 day in 7 patients, in 1 to 2 days in 12 patients, and in 3 to 4 days in 6 patients.
Initial CT scans in 11 patients showed occipital, temporal, or thalamic hypodensities. MRI showed flow void signal in the basilar artery and abnormalities in the pons in all 3 patients.
In none of the 8 patients in whom apnea prompted endotracheal intubation was periodic or Cheyne-Stokes type of breathing observed. Before endotracheal intubation, episodes of apnea were brief and recurrent. Chest x-ray films were normal on admission in all 8 patients. Seven of these 8 patients progressed to brain stem death and never triggered the mechanical ventilator. Hypotension (systolic blood pressure <90 mm Hg) was present in 4 of the 8 patients and was controlled with inotropic medication. Hyperthermia was observed at the time of diagnosis of brain stem death in 2 patients. Electroencephalography in 2 patients with absent brain stem reflexes showed alpha coma with superimposed delta waves in 1 patient.
Drowsiness or inability to clear secretions led to endotracheal intubation in 17 patients. Tachypnea was found in 10 of 17 patients, but respiratory alkalosis and significant hypoxemia were noted in only 2 patients. Evidence of aspiration on chest roentgenography was found in 2 of 17 patients.
The 8 patients presenting with apnea could not be weaned from the mechanical ventilator, and all 8 died. All of the remaining 17 patients could be weaned to a T piece with continuous positive airway pressure support of 5 cm H2O. In 5 patients a tracheostomy was performed (average, day 10).
None of the patients improved in neurological function during their stay in the intensive care unit. In fact, 23 patients continued to worsen to their maximal deficit despite heparinization and flat body position. In 17 patients an activated partial thromboplastin time (APTT) value was available at the time of neurological deterioration. Of these 17 patients, 14 had adequate heparinization (APTT, 1.5 to 2.0 times control; normal values, 23 to 37 seconds). Seven of the 17 patients died from systemic complications. In 5 patients significant aspiration pneumonitis was implicated in early death, 1 suffered a fatal gastrointestinal bleed, and another suffered a cardiac arrest in the setting of acute myocardial infarction. Seven comatose patients died without change in their neurological condition within 2 weeks and after extubation was performed according to the request of their families. Three of the 4 patients with a locked-in syndrome survived, and 1 patient improved in motor function. None of the demographic variables significantly affected clinical course or outcome.
It appears that the outcome in patients with basilar artery occlusion who require endotracheal intubation and mechanical ventilation is very poor. None of the patients improved to independent function, and in this series only the patients with locked-in syndrome survived. In fact, many patients continue to worsen despite adequate anticoagulation and blood pressure augmentation.
The majority of patients in this series required endotracheal intubation for airway protection because of an inability to clear secretions or loss of protective pharyngeal reflexes from drowsiness. A subset of patients were intubated because of recurrent apnea. Apneic episodes were generally brief, and none of these patients had periodic breathing or sustained hyperventilation. Except for 1 patient, they progressed over 1 to 2 days to complete loss of brain stem function compatible with a clinical diagnosis of brain stem death. These observations suggest that apnea during presentation of acute basilar artery occlusion may be predictive of a devastating ischemic insult to the brain stem incompatible with survival.
In the majority of patients, weaning from the mechanical ventilator was easily achieved and spontaneous breathing with adequate gas exchange was possible with a T-tube circuit. However, 5 of these 17 patients died from aspiration pneumonia shortly after admission. None of these patients demonstrated neurological improvement during their stay in the intensive care unit, and the majority of the patients remained comatose. Systemic complications led to death in 40% of the patients.
An important observation in our patient series was that a progression of clinical signs and symptoms occurred despite adequate heparin treatment. However, in a retrospective series such as ours it is difficult to exactly correlate APTT values with clinical worsening. This may be further explored in a prospective study. Early thrombolytic intervention may be beneficial in this setting.7
This series of patients with acute basilar occlusion who required mechanical ventilation suggests several possible clinical scenarios: Patients with early apnea at the time of presentation have a high probability of progression to brain stem death. Patients progressing to coma with intubation for airway protection will probably not improve, and many will die from systemic complications early in the clinical course. In our series only patients with locked-in syndrome survived.
Early prognostic indicators in comatose patients with acute basilar occlusion may assist in management decisions or in planning of future aggressive therapeutic measures.
- Received September 25, 1995.
- Revision received April 11, 1996.
- Accepted April 11, 1996.
- Copyright © 1996 by American Heart Association
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