cerebral edema
Methanol Overdose
Submitted by GPH on Wed, 2011-06-08 08:53
Methanol Overdose
This is an interesting yet very sad case.
The patient in his early 40s presented to ER with decreased level of consciousness. The patient remained comatose and had to be intubated for airway protection.
His laboratory studies revealed a profound anion gap metabolic acidosis and a significantly elevated serum osmolarity and osmolal gap.
Methanol overdose was suspected and the patient was immediately given Fomepizole IV and started on Bicarbonate drip.
The patient had a long history of alcohol abuse. His initial CT head revealed a diffuse brain atrophy unusual for his young age. Note a diffuse volume loss and enlarged ventricles on the upper image above. Prolonged and severe alcohol abuse is known to cause brain atrophy.
Despite aggressive medical management the patient remained acidotic so hemodialysis treatment was initiated.
Several hours after the admission the patient “blew his pupils” - his pupils became large and unresponsive to light.
Repeat CT head revealed diffuse cerebral edema due to Methanol overdose. Note almost complete collapse of the ventricles and absence of gyri and sulci(bottom image above). This appearance of the brain is very similar to a brain of the patient suffering from a severe anoxic encephalopathy.
Subsequently, the patient was pronounced brain dead based on clinical criteria and confirmatory test (nuclear brain perfusion scan).
The "Aftershock" of Severe Traumatic Brain Injury
Submitted by GPH on Fri, 2010-03-12 10:01
Cerebral edema (brain swelling) is an “aftershock” of severe traumatic brain injury. Caused, primarily, by vasogenic edema, it usually peaks 48 to 72 hours after the injury. By itself cerebral edema could be detrimental and cause a significant deterioration in the patient’s condition.
The skull is a rigid structure with limited space within it. Once the brain starts expanding within the skull, secondary damage to the brain can occur, primarily, via vascular compromise.
The image above demonstrates the consequences of cerebral edema: loss of white-gray matter differentiation, loss of cerebral sulci, compressed ventricles. You can also see the brain is, literally, bulging out through the craniotomy defect.
The pressure inside the skull, in the patient with a head injury, should be closely monitored. Ventricular drains are being used to monitor the intracranial pressure (ICP) and administer therapeutic interventions like draining the cerebrospinal fluid (CSF) to decrease pressure in the brain. Medications, primarily osmotic diuretics, could also be use to alleviate elevated ICP.
Several studies have shown the benefit of decompressive craniectomy – removing part of the patient’s skull to make more room for the injured brain to expand.
Brain Edema due to Anoxic Encephalopathy
Submitted by GPH on Thu, 2009-12-31 12:44
Brain Edema due to Anoxic Encephalopathy
43 year old male with a history of kidney failure due to diabetes mellitus and systemic lupus, presented to ER after he was found unresponsive at home. He was known to be non-compliant with his treatment. In ER he was in asystole and later PEA (pulsless electrical activity). CPR/ACLS were initiated.
He was given multiple doses of epinephrine, atropine and bicarbonate. His potassium level came back at 8.0. Urgent potassium lowering measures were initiated and he was put on hemodialysis. Despite aggressive therapy, his neurological status continued to deteriorate.
CT scan of his brain showed diffuse brain edema (see image above) consistent with anoxic brain injury. The patient subsequently lost all brainstem reflexes. Nuclear medicine brain perfusion scan confirmed the diagnosis of brain death.
