It thus overall does not result in better outcomes in those without hemophilia. Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy. Platelets however appear to worsen outcomes in those with spontaneous intracerebral bleeding on antiplatelet medication. The specific reversal agents idarucizumab and andexanet alfa may be used to stop continued intracerebral hemorrhage in people taking directly oral acting anticoagulants (such as factor Xa inhibitors or direct thrombin inhibitors). However, if these specialized medications are not available, prothrombin complex concentrate may also be used. Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage. H2 antagonists or proton pump inhibitors are commonly given for to try to prevent stress ulcers, a condition linked with ICH. Corticosteroids, were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended. Surgery
Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a structural vascular lesion or lobar hemorrhage in a young patient. A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures. Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited. A craniectomy holds promise of reduced mortality, but the effects of long‐term neurological outcome remain controversial. Prognosis
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.
Lack of functional sulfite oxidase causes a disease known as sulfite oxidase deficiency. This rare but fatal disease causes neurological disorders, mental retardation, physical deformities, the degradation of the brain, and death. Reasons for the lack of functional sulfite oxidase include a genetic defect that leads to the absence of a molybdopterin cofactor and point mutations in the enzyme. A G473D mutation impairs dimerization and catalysis in human sulfite oxidase. See also
Sulfur metabolism
Bioinorganic chemistry

References
Further reading
External links
Sulfite+oxidase at the US National Library of Medicine Medical Subject Headings (MeSH)
Research Activity of Sarkar Group
PDBe-KB provides an overview of all the structure information available in the PDB for Human Sulfite oxidase, mitochondrial