Acute cerebral edema reduction due to dexamethasone in a patient with acute respiratory distress syndrome due to severe acute respiratory syndrome coronavirus 2

TO THE EDITOR Neurological condition as a presentation has been reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) patients due to intrinsic clotting effect and worsening of co-morbid conditions. The neuroinvasive potential of the new coronavirus has been related to the development of neurological complications.[1] Recent reports confirm the risk of developing cerebrovascular disease in patients with SARS-CoV2 infection and very little is known about the catastrophic evolution of complications inherent in the development of stroke.[2] Cerebral edema is one of the complications that can compromise the patient’s life and impoverish the prognosis.[3] Herein, we report an unexcepted impact of use of dexamethasone for acute pulmonary SRAS-CoV2 infection.Figure 1.: Top images are 3rd day and bottom are 5th day (on dexamethasone) of admission. Original images without markers are on the right side for comparison. A 57 year right-handed male patient, who was visiting his family from Mexico, was found down at home in the morning with left side weakness, unable to walk and not able to talk clearly. He was brought to the emergency department. His head Computed Tomography Angiography showed acute embolic occlusion of right middle cerebral artery (MCA). Recombinant tissue plasminogen activator (rTPA) was not given due to unknown time of onset of left sided weakness. His nasal swab for SARS-CoV2 came back positive. He was also found to be in pulmonary edema, atrial fibrillation and unable to lay flat. He was intubated and a successful embolectomy of right MCA was performed. On arrival to neurocritical care unit, he was awake, able to move all four extremities and had a good cough. Due to marked improvement in neurological status, he was extubated. He had pitting edema till knees, bilateral basal crackles and atrial fibrillation. Patient was not taking any medications and not seen any doctor in the past. After 30 min of extubation, he lost function of left side of his body and unable to follow commands. He was reintubated and repeat CT-A showed patent right MCA flow but evolving stroke in the MCA territory. Bedside formal echocardiogram next day showed marked reduction in cardiac function with left ventricle ejection fraction of 25%. His fluid balance was kept negative throughout his intensive care unit (ICU) stay. Repeat CT in 48 h showed worsening edema and shift from left to right. Hypertonic saline for cytotoxic edema was not used due to CHF. His pulmonary status declined with high need of oxygenation with low grade fever. Due to active SARS-CoV2 infection and PaO2/FiO2 ratio under 200, he was started on dexamethasone 6 mg every 12h. The CT-scan next day (5th day of stroke) showed reduction in left to right shift. His strength on the left side improved to level that he could keep his extremities off the bed. He was extubated on the 7th day and he left ICU the following day on nasal oxygen. Corticosteroids have traditionally been used for the management of vasogenic cerebral edema. The excessive accumulation of water in the cerebral parenchyma leads to the development of cerebral edema. The failure of intracranial compensatory mechanisms described in the Monroe-Kelli doctrine are the central axis of this condition. Stroke has been associated with cytotoxic edema caused by early brain injury and the disruption of ionic cell pumps. At an experimental level, the use of corticosteroids has led to the reduction of edema in preclinical models of ischemia.[4] The new pandemic associated with SARS-CoV2 infection and the potential risk of developing cerebral ischemic events, makes it necessary to consider various pharmacological strategies, which may be useful in situations associated with cerebral edema. Our case represents the first case in the literature of the use of corticosteroids in cerebral edema associated with coronavirus. This signifies the potential for the use of corticosteroids for this potential complication of coronavirus infections. Corticosteroids are very inexpensive drugs and are readily available for use in neurocritical patients. Future studies should confirm these preliminary findings.

Authors

Institutions

Publication Details

Journal
Journal of Translational Critical Care Medicine
Published
2024-09-27
DOI
https://doi.org/10.1097/jtccm-d-23-00007
Primary Topic
Long-Term Effects of COVID-19
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Acute cerebral edema reduction due to dexamethasone in a patient with acute respiratory distress syndrome due to severe acute respiratory syndrome coronavirus 2

Tariq Janjua, Luis Rafael Moscote‐Salazar
Journal of Translational Critical Care Medicine
Long-Term Effects of COVID-19
article

Acute cerebral edema reduction due to dexamethasone in a patient with acute respiratory distress syndrome due to severe acute respiratory syndrome coronavirus 2

Tariq Janjua, Luis Rafael Moscote‐Salazar
article en

Abstract

TO THE EDITOR Neurological condition as a presentation has been reported in severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) patients due to intrinsic clotting effect and worsening of co-morbid conditions. The neuroinvasive potential of the new coronavirus has been related to the development of neurological complications.[1] Recent reports confirm the risk of developing cerebrovascular disease in patients with SARS-CoV2 infection and very little is known about the catastrophic evolution of complications inherent in the development of stroke.[2] Cerebral edema is one of the complications that can compromise the patient’s life and impoverish the prognosis.[3] Herein, we report an unexcepted impact of use of dexamethasone for acute pulmonary SRAS-CoV2 infection.Figure 1.: Top images are 3rd day and bottom are 5th day (on dexamethasone) of admission. Original images without markers are on the right side for comparison. A 57 year right-handed male patient, who was visiting his family from Mexico, was found down at home in the morning with left side weakness, unable to walk and not able to talk clearly. He was brought to the emergency department. His head Computed Tomography Angiography showed acute embolic occlusion of right middle cerebral artery (MCA). Recombinant tissue plasminogen activator (rTPA) was not given due to unknown time of onset of left sided weakness. His nasal swab for SARS-CoV2 came back positive. He was also found to be in pulmonary edema, atrial fibrillation and unable to lay flat. He was intubated and a successful embolectomy of right MCA was performed. On arrival to neurocritical care unit, he was awake, able to move all four extremities and had a good cough. Due to marked improvement in neurological status, he was extubated. He had pitting edema till knees, bilateral basal crackles and atrial fibrillation. Patient was not taking any medications and not seen any doctor in the past. After 30 min of extubation, he lost function of left side of his body and unable to follow commands. He was reintubated and repeat CT-A showed patent right MCA flow but evolving stroke in the MCA territory. Bedside formal echocardiogram next day showed marked reduction in cardiac function with left ventricle ejection fraction of 25%. His fluid balance was kept negative throughout his intensive care unit (ICU) stay. Repeat CT in 48 h showed worsening edema and shift from left to right. Hypertonic saline for cytotoxic edema was not used due to CHF. His pulmonary status declined with high need of oxygenation with low grade fever. Due to active SARS-CoV2 infection and PaO2/FiO2 ratio under 200, he was started on dexamethasone 6 mg every 12h. The CT-scan next day (5th day of stroke) showed reduction in left to right shift. His strength on the left side improved to level that he could keep his extremities off the bed. He was extubated on the 7th day and he left ICU the following day on nasal oxygen. Corticosteroids have traditionally been used for the management of vasogenic cerebral edema. The excessive accumulation of water in the cerebral parenchyma leads to the development of cerebral edema. The failure of intracranial compensatory mechanisms described in the Monroe-Kelli doctrine are the central axis of this condition. Stroke has been associated with cytotoxic edema caused by early brain injury and the disruption of ionic cell pumps. At an experimental level, the use of corticosteroids has led to the reduction of edema in preclinical models of ischemia.[4] The new pandemic associated with SARS-CoV2 infection and the potential risk of developing cerebral ischemic events, makes it necessary to consider various pharmacological strategies, which may be useful in situations associated with cerebral edema. Our case represents the first case in the literature of the use of corticosteroids in cerebral edema associated with coronavirus. This signifies the potential for the use of corticosteroids for this potential complication of coronavirus infections. Corticosteroids are very inexpensive drugs and are readily available for use in neurocritical patients. Future studies should confirm these preliminary findings.

Journal of Translational Critical Care MedicineVol. 6(4)
Regions Hospital (US), Advanced Dermatology (US)
Good health and well-being
Openalex Percentile: Top 74%
Long-Term Effects of COVID-19
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.