Posters
Presenting Author Academic/Professional Position
Francisco Arias
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Academic Level (Author 2)
Resident
Discipline/Specialty (Author 2)
Internal Medicine
Academic Level (Author 3)
Resident
Discipline/Specialty (Author 3)
Internal Medicine
Academic Level (Author 4)
Resident
Discipline/Specialty (Author 4)
Internal Medicine
Academic Level (Author 5)
Faculty
Discipline/Specialty (Author 5)
Internal Medicine
Discipline Track
Clinical Science
Abstract Type
Case Report
Abstract
Introduction: Clonidine, an agonist of central α2-adrenergic and imidazoline receptors, possesses the capacity to elicit transient episodes of hypertension succeeded by hypotension and bradycardia. This particular case underscores a rare yet significant complication, Posterior Reversible Encephalopathy Syndrome (PRES), that can occur subsequent to the abrupt cessation of clonidine administration.
Case Presentation: An 18-year-old male with severe asthma and prior ICU admissions presented to the emergency department after two seizures. He had recently been treated for an asthma exacerbation complicated by hypertension, for which clonidine was initiated. He was discharged on clonidine and prednisone but discontinued clonidine the day before admission due to anxiety.
On arrival, he was hypertensive (BP 170–200/90–120 mm Hg) with signs of seizure activity, including tongue/lip bites and left homonymous hemianopia. He was alert but complained of fatigue, blurry vision, and anxiety. CT revealed vasogenic/cytotoxic edema in the right occipital lobe. MRI and EEG were ordered. Treatment included lorazepam, levetiracetam, and antihypertensives. He was admitted to the ICU for hypertensive emergency with new-onset seizures.
In the ICU, he developed mild hypoxemia requiring BiPAP and was treated with bronchodilators, steroids, and antibiotics. Neurology diagnosed PRES secondary to clonidine withdrawal. He was started on nicardipine infusion and increased levetiracetam. MRI confirmed subcortical white matter changes consistent with PRES. His blood pressure and visual symptoms gradually improved, and he was transferred to the general medical floor.
The patient was discharged with nifedipine, losartan, and carvedilol for blood pressure control, along with gabapentin for neuropathic pain. A neurology follow-up was arranged, and he was advised to avoid clonidine in the future.
Discussion: PRES is a neurotoxic syndrome that is characterized by the presence of vasogenic edema, primarily localized in the posterior regions of the brain, and manifests through symptoms such as seizures, headaches, visual impairments, and altered cognitive states. This condition is frequently correlated with hypertensive crises, renal insufficiency, autoimmune disorders, or exposure to cytotoxic substances. The underlying pathophysiological mechanisms are thought to involve endothelial dysfunction resulting from abrupt fluctuations in blood pressure or toxic insults to the vascular system.
Although uncommon, the withdrawal from clonidine can provoke hypertensive crises and subsequently contribute to the development of PRES via catecholamine surges that interfere with cerebral autoregulation. Magnetic Resonance Imaging (MRI) typically demonstrates reversible subcortical edema. Timely diagnosis and supportive management including the regulation of blood pressure and the control of seizures are crucial to avert further complications. While prognostic outcomes are generally positive, delays in intervention can lead to lasting neurological deficits or mortality.
Conclusion: This case underscores the risks of abrupt clonidine cessation and its potential to trigger PRES. It highlights the necessity of gradual tapering protocols and prompt recognition of PRES symptoms, especially in patients presenting with seizures and visual changes amid hypertensive emergencies, to improve prognosis and prevent long-term sequelae
Presentation Type
Poster
Recommended Citation
Calderon, Aura M. C.; Arias, Francisco; Mogollon, Ivan; Salcedo, Luis; and Arredondo, Hector, "Case Report: Clonidine Withdrawal-Induced Posterior Reversible Encephalopathy Syndrome (PRES)" (2025). Research Colloquium. 15.
https://scholarworks.utrgv.edu/colloquium/2025/posters/15
Included in
Case Report: Clonidine Withdrawal-Induced Posterior Reversible Encephalopathy Syndrome (PRES)
Introduction: Clonidine, an agonist of central α2-adrenergic and imidazoline receptors, possesses the capacity to elicit transient episodes of hypertension succeeded by hypotension and bradycardia. This particular case underscores a rare yet significant complication, Posterior Reversible Encephalopathy Syndrome (PRES), that can occur subsequent to the abrupt cessation of clonidine administration.
Case Presentation: An 18-year-old male with severe asthma and prior ICU admissions presented to the emergency department after two seizures. He had recently been treated for an asthma exacerbation complicated by hypertension, for which clonidine was initiated. He was discharged on clonidine and prednisone but discontinued clonidine the day before admission due to anxiety.
On arrival, he was hypertensive (BP 170–200/90–120 mm Hg) with signs of seizure activity, including tongue/lip bites and left homonymous hemianopia. He was alert but complained of fatigue, blurry vision, and anxiety. CT revealed vasogenic/cytotoxic edema in the right occipital lobe. MRI and EEG were ordered. Treatment included lorazepam, levetiracetam, and antihypertensives. He was admitted to the ICU for hypertensive emergency with new-onset seizures.
In the ICU, he developed mild hypoxemia requiring BiPAP and was treated with bronchodilators, steroids, and antibiotics. Neurology diagnosed PRES secondary to clonidine withdrawal. He was started on nicardipine infusion and increased levetiracetam. MRI confirmed subcortical white matter changes consistent with PRES. His blood pressure and visual symptoms gradually improved, and he was transferred to the general medical floor.
The patient was discharged with nifedipine, losartan, and carvedilol for blood pressure control, along with gabapentin for neuropathic pain. A neurology follow-up was arranged, and he was advised to avoid clonidine in the future.
Discussion: PRES is a neurotoxic syndrome that is characterized by the presence of vasogenic edema, primarily localized in the posterior regions of the brain, and manifests through symptoms such as seizures, headaches, visual impairments, and altered cognitive states. This condition is frequently correlated with hypertensive crises, renal insufficiency, autoimmune disorders, or exposure to cytotoxic substances. The underlying pathophysiological mechanisms are thought to involve endothelial dysfunction resulting from abrupt fluctuations in blood pressure or toxic insults to the vascular system.
Although uncommon, the withdrawal from clonidine can provoke hypertensive crises and subsequently contribute to the development of PRES via catecholamine surges that interfere with cerebral autoregulation. Magnetic Resonance Imaging (MRI) typically demonstrates reversible subcortical edema. Timely diagnosis and supportive management including the regulation of blood pressure and the control of seizures are crucial to avert further complications. While prognostic outcomes are generally positive, delays in intervention can lead to lasting neurological deficits or mortality.
Conclusion: This case underscores the risks of abrupt clonidine cessation and its potential to trigger PRES. It highlights the necessity of gradual tapering protocols and prompt recognition of PRES symptoms, especially in patients presenting with seizures and visual changes amid hypertensive emergencies, to improve prognosis and prevent long-term sequelae
