Development of PAT may adversely affect the process of BD determination and could limit the opportunity for organ donation. Each institution should have preventive measures in place.
Background and Purpose:
It remains uncertain which patients with malignant edema after large hemispheric infarction (LHI) remain at risk of death despite decompressive hemicraniectomy (DHC). We investigated factors associated with in-hospital mortality in a cohort of patients with LHI who underwent DHC.
Methodology:
This retrospective cohort study conducted over a five-year period identified 24 LHI patients who underwent DHC. Patient demographics, pre- and post-DHC clinical and neuro-imaging data were recorded (including midline shift [MLS] at the level of lateral ventricles). These variables were then analyzed in relation to in-hospital mortality.
Results:
Patients were predominantly male (17/24), with mean age of 55±15 years and baseline NIHSS score of 18.5± 4. Despite DHC, performed at a median of 52 hours, mortality still occurred in 9 patients (38%), with 11 (46%) going to acute rehabilitation and remainder to long-term care facility (LTC). Patients had a mean pre-operative MLS of 11 ± 3 mm. When compared with a head CT obtained 48 hours after DHC, MLS improved the most in patients going to rehabilitation (by 6 ± 4.2 mm), compared to those going to LTC (3.2 ± 5 mm), while the least improvement was seen in those who died (1 ± 5 mm). Survivors had significant improvement in MLS (5.3 ± 4.4 mm) compared to the non-survivors (1 ± 5 mm), p = 0.04. The survivors were also significantly younger (50 ± 17 years) compared to those who died (62 ± 7 years). Thirteen patients (54% of the cohort) received intracranial pressure (ICP) monitors ipsilateral to the infarct during DHC but measured ICPs were statistically similar in survivors vs non-survivors. Other variables (baseline NIHSS score, MLS and time to surgery) did not predict death in the cohort.
Conclusion:
Mortality remains high in LHI patients even after DHC. Improvement in MLS after DHC appears to separate survivors from non-survivors while post-DHC ICPs do not. However, our sample size is small and additional studies with larger population sizes are required for validation of our findings.
Reversible cerebral vasoconstriction syndrome (RCVS) manifests with a thunderclap headache and reversible vascular abnormalities. Red blood cell transfusions have not been well identified as a risk factor for RCVS. We report a rare case of acute brain injury resulting from RCVS after a packed red blood cell (PRBC) transfusion. A 49-year-old female with a history of menorrhagia initially presented with generalized weakness. She was found to have a hemoglobin (Hgb) of 1.7 g/dL in the setting of a fundal fibroid for which she received five units of PRBCs. Post transfusion, she complained of several days of thunderclap headache and later returned with new-onset seizures. She was admitted to the neurocritical care unit for the treatment of status epilepticus. Metabolic, infectious and toxic work-up were unremarkable except for an elevated lactate. MRI of the brain with contrast showed extensive bilateral hemispheric and cerebellar white matter T2-weighted fluid-attenuated inversion recovery (T2/FLAIR) hyperintensities with areas of enhancement. A diagnostic cerebral angiogram was performed to evaluate for a vascular etiology and revealed focal segmental stenoses in bilateral A1 segments of the anterior cerebral arteries and in branches of the bilateral middle cerebral arteries. These findings were suggestive of RCVS. Clinicians should have a high degree of suspicion for RCVS in patients presenting with neurological manifestations, such as thunderclap headache or seizures after recent transfusion. The window for injury may be longer than that seen in other organs, such as in transfusion-related acute lung injury (TRALI).
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