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Try out PMC Labs and tell us what you think. Learn More. A year-old incarcerated male presented to the emergency department ED after an episode concerning for syncope.
The patient had nystagmus and ataxia on initial examination. There is a broad differential diagnosis for syncope, and for patients presenting to the ED we tend to focus on cardiogenic and neurologic causes. This case takes the reader through the differential diagnosis and systemic work-up of a patient presenting to the ED with syncope. A year-old male who was currently incarcerated presented to the emergency department ED with a chief complaint of syncope. The patient reported that the event occurred after he stood up from dinner.
There were no witnesses, but the patient believes that he hit his head. He said he had a headache since the fall, and it had not responded to the acetaminophen that he received from the prison infirmary. He denied any tongue biting or loss of bowel or bladder control. The patient stated that he had felt dizzy and lightheaded over the prior few days, and that sensation continued in the ED.
He also felt numb across his shoulders and had been nauseous since the fall. He had a past medical history of seizures and bipolar disorder. He had no prior surgical history. 36 year old male family history included diabetes in his grandmother. The patient drank alcohol socially and had used marijuana and abused prescription 36 year old male in the past but had not used any substances recently.
On physical examination, he was awake, alert, and in no acute distress. He was afebrile He was Another abrasion on his upper lip was not actively bleeding. His external ears were normal without evidence of trauma. His nose was normal. His oropharynx was clear and moist.
His pupils were 3 millimeters mm equal, round, and reactive to light and accommodation, and eyes were without scleral icterus. His neck was supple without tracheal deviation. He had normal range of motion of his neck and he had no cervical spinous process or paraspinal muscular 36 year old male.
His heart was regular rate and rhythm without murmurs, rubs, or gallops. He had capillary refill of less than two seconds in all extremities. His lungs were clear to auscultation bilaterally without wheezes, rhonchi, or rales. He had regular respiratory effort without accessory muscle use. His abdomen was soft with normal bowel sounds without tenderness, rebound, or guarding. There was no costovertebral tenderness.
He had no spinous process or paraspinal process tenderness in his thoracic or lumbar spine.
He was found to have bilateral and direction-changing 36 year old male nystagmus that was provoked on lateral gaze. No vertical or torsional nystagmus was seen. He had decreased sensation across his shoulders bilaterally, but the remainder of his sensation was intact. He had slow finger to nose with overshoot bilaterally. His ambulation was limited secondary to feeling unsteady. He was oriented to person, place and time, answered questions appropriately, and followed commands without difficulty.
Initial laboratory are shown in Table 1. His electrocardiogram ECG is shown in Image 1. He had a chest radiograph Image 2. Computed tomography CT of his head and neck were performed Image 3; full study is found in Supplemental Material 1. A diagnostic test was then performed, which confirmed the diagnosis. Chest 36 year old male posterior-anterior left and lateral right of a year-old male with syncope.
Kthousand; ggrams; mgmiligrams; mmoLmillimole; Lliter; mcLmicroliter; dLdeciliter; uunits. He has a range of subacute and acute symptoms, and it is challenging to determine which one is the root cause, necessitating a wide differential diagnosis. The combination of syncope and other neurologic symptoms brought to mind five of illness:.
The patient did not experience chest pain, trouble breathing, or other symptoms that I would attribute to atypical angina to suggest an ischemic event. The fact that he had dizziness for several days could possibly indicate persistent arrhythmia or hypotension. However, his physical exam and vital s do not indicate s of either of these, and his ECG confirms that he does not have an arrhythmia currently despite being symptomatic. Therefore, I eliminated a cardiovascular etiology from my differential.
Primary neurologic causes, such as seizures, would certainly be plausible in a patient with his past medical history. However, the history provided does not describe specific seizure-like activity and does not describe a notable post-ictal period. Furthermore, the patient has been compliant with his seizure medications and, from the information I have, does not have a clear reason to have a lower seizure threshold.
This makes seizure an unlikely primary diagnosis. Stroke thrombotic, embolic, or direct vascular injury is certainly a diagnosis that must be explored in any patient with dizziness, with particular attention being paid to the cerebellum and posterior fossa. It does not provide ificant further information regarding the timing and triggers of the dizziness.
The patient has nystagmus, dysmetria and ataxia, but his cranial nerve exam is normal, 36 year old male full extraocular motions and equally reactive pupils. The patient also has intact strength and overall sensation, with the exception of the neck and shoulders. This exam does not support a focal cranial infarct as the etiology.
Basilar artery strokes can sometimes present with several days of subacute or flow-dependent symptoms, but I would expect many more global symptoms if this were the case. While a 36 year old male posterior ischemic stroke is still possible, I believe other investigation is needed. The presentation of headache with neurologic symptoms raises concern for a subarachnoid bleed.
The CT of the head was also negative. Although lumbar puncture would be considered the gold standard test for this diagnosis, I think the likelihood of the diagnosis being an occult subarachnoid hemorrhage is unlikely based on the history provided. I was told that the patient struck his head when he passed out.
This brings into question whether there is actually a traumatic injury causing some of his presenting symptoms. His history of prodromal dizziness tends to lead me away from this; however, he complaints of, and on examination is found to have, numbness across the neck and shoulders.
Injury to the cervical spine could possibly cause injury in this dermatome; however, he does not have any weakness in the upper or lower extremities, any distal sensation deficits, or tenderness on his neck exam. Overall, I think that although he does have this complaint of numbness, his overall history and exam makes it unlikely that he has a cervical spine injury.
Another traumatic etiology to consider is vertebral artery dissection since this can cause posterior neurologic symptoms such as gait instability and dysmetria. Most of his symptoms, however, are bilateral. It would be extremely unlikely for the patient to injure both vertebral arteries simultaneously.
The direction-changing horizontal nystagmus, bilateral dysmetria, and limited ambulation found on his examination are all concerning for a central neurologic injury but can also be due to other centrally acting insults, such as medication toxicity. Phenytoin and valproic acid toxicity can each present with diffuse or vague neurologic symptoms. Valproic acid toxicity typically causes tachycardia, thermal dysregulation, respiratory depression, and hypotension.
Our patient has not experienced any of these effects. Phenytoin toxicity classically causes nystagmus, nausea, confusion, and ataxia. I believe this le to the answer and can explain his bilateral neurologic symptoms. The remaining question is this: Why would this patient have phenytoin toxicity without a recent change in dose or medication? The answer lies in his medication list.
Fluoxetine and valproic acid are known to increase the systemic concentration of phenytoin due to similar cytochrome P metabolism, and there are case reports of both agents causing phenytoin toxicity. I believe that this interaction increased his risk of phenytoin toxicity over a longer period of time, even though there were no changes in his dosing and he was compliant. The confirmatory test will be a phenytoin level. The diagnostic test was a total phenytoin level, which confirmed phenytoin toxicity. The patient had a total phenytoin level of He was given intravenous IV fluids and ondansetron for his nausea.
He was admitted to the internal medicine service, 36 year old male phenytoin was held, and his phenytoin levels were trended. His phenytoin level reached a peak of He thereafter had resolution of his symptoms and return of normal gait. He was ultimately discharged back to prison on HD 6. During his hospitalization, neurology was consulted. Neurology recommended changing his valproic acid medication to alternate mood stabilizer due to concern for possible interaction.
After discharge, he remained stable on his phenytoin but had other presentations to the ED for musculoskeletal injuries. Phenytoin toxicity occurs when a patient develops an excess of phenytoin in the blood related to either an acute ingestion or chronic accumulation of the drug. Phenytoin is a voltage-gated sodium channel blocker 36 year old male predominant targets in neuronal and cardiac tissue. This fact becomes important when interpreting serum phenytoin levels.
Most institutions will only have total phenytoin levels, which is typically related to the available phenytoin in the blood, but one should consider ordering a free phenytoin level if suspecting a low-protein state. Phenytoin toxicity can affect a multitude of systems including neurologic, cardiac, skin, and immunologic. The degree of neurologic toxicity occurs in relatively predictable manner in correlation to the concentration of phenytoin in the blood 6 Table 2.
The drug levels in the patient presented here correlate with some of his physical exam findings including nystagmus and ataxia. It is also important to note that an excess of phenytoin can lead to seizures, and other anti-epileptics have also been shown to have this effect. However, this effect is rarely, if ever, seen with oral phenytoin toxicity. It is more commonly occurs with IV phenytoin toxicity, seen often with rapid infusion. Symptoms of phenytoin toxicity as related to total phenytoin level.
Neurologic phenytoin toxicity can occur from a variety of mechanisms. A patient may have an acute toxicity secondary to either an accidental or intentional ingestion. Valproic acid inhibits the P system, so medications like phenytoin last longer than expected in the body, which could result in a phenytoin toxicity.
Lastly, phenytoin is sometimes mixed with cocaine, and there are cases in the literature of phenytoin toxicity occurring in cocaine users. Treatment of phenytoin toxicity revolves predominantly around supportive care. Fatality from phenytoin poisoning is rare, with only two deaths reported in Treatment should also be targeted 36 year old male symptoms including treatment with anti-emetics and institution of fall precautions. Phenytoin toxicity can present with a range of symptoms and s depending on the phenytoin level; common early symptoms include nystagmus and ataxia.
Section Editor: Rick A. McPheeters, DO. The authors attest that their institution requires neither Institutional Review Board approval, nor patient consent for publication of this clinicopathological case. Documentation on file. Conflicts of Interest : By the CPC-EM article submission agreement, all authors are required to disclose all affiliations, funding sources and financial or 36 year old male relationships that could be perceived as potential sources of bias.
The authors disclosed none. National Center for Biotechnology InformationU. Clin Pract Cases Emerg Med. Published online Jul Samantha A. Zachary D. Laura J.36 year old male
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