Contrast-induced encephalopathy: a clinical enigma

Contrast-induced encephalopathy: a clinical enigma

Contrast-induced encephalopathy (CIE) is a rare but well-known complication of percutaneous coronary and carotid interventions and presents with a variety of neurological deficits that are attributed to disruption of the blood-brain barrier. [1-3]. All forms of contrast media, including ionic, nonionic, low-osmolar, iso-osmolar, and high-osmolar solutions, have been reported to cause ICP. [1,2]. The most common manifestations include encephalopathy, seizures, motor and sensory disturbances, transient cortical blindness, and focal neurological deficits. Most symptoms usually resolve within 48-72 hours, but there have been cases of fatal cerebral edema and death secondary to ICP associated with the use of high-osmolarity ionic contrast agents. [4]. Although the exact etiology is unknown, some risk factors identified over time include chronic hypertension, diabetes mellitus, renal failure, administration of large volumes of iodinated contrast, percutaneous coronary intervention, impaired cerebral autoregulation, and prior adverse reactions to iodinated contrast. [5]. Almost all but one of the cases reported in the literature have occurred after intra-arterial administration of contrast media. [6]. Diagnosis is confirmed by typical radiologic signs on noncontrast computed tomography of the brain in a symptomatic patient after exclusion of thromboembolic and hemorrhagic complications; however, cases are known to present without the typical radiological signs. [7]. ICP developed after intravenous contrast administration for a CT pulmonary embolism study in our patient, and brain imaging was found to be normal.

A woman in her 70s with a history of diabetes mellitus, hypertension, post-partial thyroidectomy Hashimoto’s thyroiditis status, and chronic obstructive pulmonary disease (COPD) presented with complaints of shortness of breath and chest tightness that progressively worsened over a period of time. week, which got worse over time. the course of a day. On presenting to the emergency department, she was found to be tachycardic at 140 in atrial fibrillation and hypoxic at 70. Respiratory examination revealed diffuse wheezing. She was started on a non-rebreather and managed with one dose of IV metoprolol. Laboratory investigations revealed leukocytosis with bandemia, negative cardiac enzymes, and respiratory acidosis with COtwo arterial blood gas (ABG) retention. Chest X-ray demonstrated features of multifocal pneumonia. He was started on antibiotics in the form of ceftriaxone and azithromycin, IV methylprednisone, and IV fluids. He was also started on bilevel positive airway pressure (BiPAP) ventilation to increase work of breathing and increase oxygen requirements. Computed tomography pulmonary angiography (CTPE) was planned to rule out pulmonary embolism in the setting of new-onset atrial fibrillation and worsening hypoxia. A total of 100 cc of Isovue 370 (iopamidol 76%), a low osmolarity, non-ionic, monomeric, iodine-based contrast medium was administered during the procedure. Minutes after contrast administration, the patient developed an altered sensorium in the form of confusion and agitation. He was also found to have elevated blood pressure in the range of 180/120 mmHg. She was transferred to the ICU, but she continued to be drowsy and disoriented. CTPE turned out to be negative. Neurological evaluation revealed no focal gross motor or cranial nerve deficits and bilateral 2+ reflexes with silent plantar response. There was no neck stiffness or any seizure-like activity. Stat’s laboratory investigations, including a complete blood count and comprehensive metabolic panel, were unchanged. Thyroid-stimulating hormone (TSH) and thyroid profile were within normal limits. ABG did not show any hypercapnia. Blood cultures were negative with normal procalcitonin, so infectious aetiology was ruled out and antibiotic treatment was postponed. A brain CT scan performed within two hours of symptom onset revealed no intracranial abnormalities and only chronic microangiopathic senescent changes. She began hourly neurological checks, a nicardipine drip to control her blood pressure, which was gradually lowered and stopped in six hours, and intravenous fluids to promote excretion of the contrast agent. She also continued the treatment instituted for her pneumonia, including steroids. Within 48 hours of support management, her sensorium improved. She planned to repeat the neuroimaging in the form of an MRI of the brain, but her symptoms improved sooner and she requested to postpone it due to her claustrophobia. She was added apixaban for new-onset atrial fibrillation and she was discharged after four days without neurological deficit with resolution of respiratory symptoms.

ICP is a known but rare complication associated with the use of intra-arterial contrast media during percutaneous carotid and coronary interventions, with an incidence ranging from 0.3% to 1.0%, but higher rates have been documented. high with the use of hyperosmolar iodinated contrast media. [4]. In this report we present a highly probable case of ICP after intravenous administration of a small amount of low osmolarity nonionic contrast agent, with severe symptoms and spontaneous recovery.

Although there have been more than 50 cases of ICP identified in the literature since the clinical description in 1970, all but one have occurred after angiographic procedures and intra-arterial administration of contrast. [5,6]. This supports the hypothesis that the symptoms are the result of the chemotoxic effect of hyperosmolar media resulting in microvascular sedimentation and arterial spasm, causing shrinkage of endothelial cells and disruption of tight junctions. Accumulation of iodinated contrast is also known to cause a localized neurotoxic effect on the blood-brain barrier by increasing endothelin expression, amplifying endothelial cell permeability, and causing brain edema. [7-9]. However, in our case, the contrast was administered intravenously for a CTPE study. The patient did not have kidney failure or a history of previous neurological interventions, but he did have diabetes and systemic hypertension.

The presentation of ICP has been found to be highly variable, from subtle symptoms, such as headache, to more extreme features, such as coma or unresponsiveness. Transient cortical blindness is the most common manifestation [10]. Literature review indicated that symptoms of neurologic dysfunction developed within minutes to hours after contrast agent administration, with most patients fully recovering within 48 to 72 hours with supportive care. . [7-9]. In our patient, symptoms completely resolved within 48 hours, which was consistent with the clinical course of ICP. We suspect that the severity of symptoms in our patient was related to her advanced age, hypertension, and other risk factors, which may have increased the permeability of the blood-brain barrier, resulting in neurotoxicity and ICP.

A small dose of contrast medium, even as low as 25 mL, has been reported to cause ICP and can occur with contrast agents of high or low osmolarity. There has been no defined amount of dye beyond which CIE is safe or more likely to occur [5]. The culprit in our case was Iopaque 370, a low osmolarity, non-ionic, monomeric, iodine-based contrast medium containing 755 mL of iopamidol equivalent to 370 mg of iodine per milliliter. Since 100 ml were used in our patient, the diagnosis of ICP was highly probable even without the associated typical radiological signs.

The diagnosis of ICP requires a high index of suspicion, and brain imaging is often pathognomonic and shows contrast enhancement in the cortical, subarachnoid, striatal spaces, or cerebral edema, which are important in differentiating ICP from other pathologies such as thromboembolism and thromboembolism. hemorrhage. [8,9,11]. Symptoms usually resolve within days and the disease follows a benign course, but cases of persistent neurological deficit and even fatal cerebral edema secondary to contrast injection have been reported. However, the review of the literature revealed multiple cases in which patients were diagnosed with ICP in the absence of classic radiological signs, as was the case with our patient. [7]. Cerebrospinal fluid (CSF) examination has also been found helpful in ruling out subarachnoid hemorrhage and high concentrations of iodine contrast in the CSF and extravasation of serum-supporting contrast. [12]. Differentials considered for our patient included hypoxia and hypercapnia (normal GSA), hypoglycemia (normal blood glucose levels), transient ischemic attack (sensory disturbance took more than 24 hours to resolve), stroke, and venous sinus thrombosis ( Noncontrast brain CT was normal, no focal neurological deficits), toxic metabolic encephalopathy (electrolytes and urea were normal), meningitis (no neck stiffness and symptoms resolved without antibiotics), status epilepticus (no seizure activity), and thyrotoxicosis ( TSH and thyroid profile were normal).

The mainstay of management is supportive treatment with intravenous hydration and anticonvulsants for seizure control. Intravenous steroids and mannitol have been used sporadically with favorable results. In patients with kidney failure on dialysis who develop ICP, hemodialysis has been shown to be beneficial [5,8,9,11]. Our patient was managed with hydration and steroids, which she was receiving for her underlying COPD exacerbation, and her symptoms resolved.

As a limitation of our case report, brain MRI was not performed despite a negative brain CT. It has been found that MRI of the brain frequently reveals vasogenic edema with swelling of the gyrus and increased signal on T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences, with greater intensity on Diffusion-weighted imaging (DWI) sequences. In addition, a repeat brain CT scan was not performed due to complete resolution of symptoms within 48 hours of onset.

Our case highlights a case of ICP that is usually attributed to intra-arterial administration of contrast, but can occur even with intravenous injection, something clinicians should be aware of.

The presentation of ICP is highly variable, ranging from cortical blindness to encephalopathy, seizures, and hemiparesis. In any acutely confused patient with a history of recent contrast administration, it is important to evaluate and investigate as ICP is often a diagnosis of exclusion. Although there is no specific treatment for ICP, management is usually supportive with an excellent prognosis.

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