A 21 y/o male presents with possible seizure. According to EMS they were called for person down. Mom noted her son passed out, and then had some shaking. His family witnessed the event, and his brothers helped him to the ground so he did not strike his head very hard. EMS arrived and noted he was still confused and very diaphoretic. His mom notes he has a history of pseudo seizures. He had another episode just like this last week, and went to another Emergency Department, and was loaded with Dilantin. They did a CT of his head, and it was normal. His mother notes he has had seizures for `many years’ and has been on numerous anticonvulsants. He states he just `feels funny’ then passes out. When he comes to, they tell him he had a seizure. His mother notes he gets sweaty, then drools, then falls. While on the ground he does jerk some. Then eventually he wakes up. One doctor told them he has pseudo seizures.
He had no tongue biting, and no incontinence.
PMH: Negative except for seizures or pseudo seizures.
FH: Neg
ROS: Neg
Meds: Dilantin, but he admits to not taking it.
Allergies: None
PE: RR=20, Blood pressure 120/85, Pulse 140, Temp 98.9F, Sat 96% (RA)
Obese male (BMI=30.5) in no distress. Neurologically non-focal, except for mental status exam and his tachycardia. He’s oriented x3, but slow to answer. He can follow commands, but has difficulty putting words together into a sentence. Per mother, this is his baseline.
Labs: Dilantin: 5.9 mcg/ml, Basic Metabolic panel normal except C02=17, Glu=137, WBC=14.4, Hbg=14.8.
EKG: Sinus Tachycardia, non-specific ST changes (T wave flattening in inferior leads).
He is loaded with Phenytoin, but continues to have persistent sinus tachycardia. Repeat vital signs 3 hours later: RR=24, BP=123/87, HR=138, Sat=99% (RA).
Questions:
1. What should you consider as the causes of the tachycardia?
The most common causes of sinus tachycardia are the normal responses to exercise and conditions where catecholamine release is physiologically increased (flight, fright, anger or stress). (1) Seizures may have contributed to the initial tachycardia, but as it has been 3 hours that should no longer be the reason.
Other causes include:
Hyperthyroidism
Fever
Hypovolemia/dehydration
Sepsis
Anemia
PE
Acute Coronary ischemia/myocardial infarction/myocarditis
Heart failure
Chronic Pulmonary Disease
Hypoxemia
Medications (Albuterol, Caffeine, Cocaine, etc.)
His obesity makes hyperthyroidism less likely, but not impossible. Clearly, the persistent tachycardia is abnormal and needs to be investigated.
Myocarditis is certainly possible. Myocarditis is divided into toxic, infectious, and immunologic etiologies. The most common cause in North America is Viral (37% Parvovirus B-19, 33% enterovirus, 11% Human Herpes virus-6, and 13% had co-infection with both parvovirus B19 AND Herpes virus-6). (2)
Worldwide, the most common bacterial cause is diphtheria, and in South America, the Protozoal Chagas disease is common. (2)
Toxic myocarditis can be from medical agents or environmental agents. Medicines that can cause myocarditis include penicillin, ampicillin, and hydrochlorothiazide. (2). Environmental toxins include lead, arsenic and carbon monoxide. Interestingly some bites (scorpion, black widow spider bites) may cause myocarditis.
The immunologic causes include Lupus, Rheumatoid arthritis, scleroderma, Kawasaki’s disease, sarcoidosis, and giant cell arteritis.
PE is also possible. Although we always look for the classic triad (pleuritic chest pain, hemoptysis, and dyspnea), this is rarely seen. (3). I found these interesting facts regarding PE:
1. Of the patients who go on to die from massive PE, 40% had NO dyspnea, 83% had NO chest pain, and 97% had no hemoptysis. (3)
2. Non-classic presentations of PE include syncope, seizure, abdominal pain, new onset Atrial Fibrillation, or hiccough (3)
3. In patients with PE:
a. 44% have tachycardia
b. 43% have a fever
c. 36% have diaphoresis
d. 19% have cyanosis
2. What is your disposition?
I would not send a patient home with abnormal vital signs, unless there was a clear explanation, and /or it was their baseline. A heart rate of 140 is really pretty fast. My initial approach to the fast heart rate would be to give some fluids, treat pain/anxiety, and see if the tachycardia resolved. In this case, the persistent tachycardia prompted the EM physician to place him in observation (this is not my case, but one of my colleagues).
3. Do you need a CT scan?
If there is a good history that there was no head trauma, and the patient is not on anticoagulants, and returns to baseline after a seizure, I do not order a CT scan. Many patients with difficult seizure disorders (either because of non-compliance or because of the underlying seizure disorder) end up with a significant number of head CT’s in their lifetime. If they have family to watch them, are at baseline, did not suffer significant head trauma, and I have a reason for the seizure (usually low anticonvulsant level), then I do not image them. I really don’t think a new CNS process is causing the tachycardia.
4. What BMI is considered obesity?
According to the WHO, a BMI of 25-29.9 kg/m2 is Grade 1 overweight. Grade 2 overweight (commonly called obesity) is a BMI 30-39.9 kg/m2. Grade 3 overweight is commonly called morbid obesity) is a BMI > 40kg/m2. (4). in the surgical literature, a BMI >40kg/m2 is severe obesity, and a BMI 40-50 kg/m2 is morbid obesity, and a BMI >50kg/m2 is `super obese.’ (4) If you’re wondering about your own BMI, there are several quick `calculators’ available. Here is one: http://www.nhlbisupport.com/bmi/bminojs.htm
Outcome:
Patient was placed in observation. Cardiac enzymes were negative x2. During the night he had one episode of brady-dysrhythmias (Sinus brady at 46) which resolved spontaneously (perhaps related to Dilantin??). In the AM, he was again tachycardic at 140, tachypneic at 34, and sats on 4 L NC were only 93%. At this time he also complained of pleuritic chest pain, and he was sent for a spiral CT of the chest which revealed a large PE in the right main pulmonary artery which was occluding the bifurcation. Numerous other PE’s were noted on right and left side, some not completely occlusive. He was started on heparin (CT of head was neg), and a stat echo revealed Right ventricular dysfunction. During the night in the ICU he became more hypoxic, and was given TPA. In the AM, his chest pain was resolved, repeat echo revealed improved right heart parameters. Ultimately, he was found to have the lupus anticoagulant as the reason for his hypercoaguable state. Ironically, neurology felt he did not have a seizure disorder and his multiple previous `seizures’ may have been secondary to PE’s.
This patient was a challenge for several reasons. First, he already had the known diagnosis of seizures/pseudo seizures. As they had been previously diagnosed, it is logical that the original physician just assumed the diagnosis was correct. Second, his developmental delay/difficulty in explaining what occurred was also a challenge. Once more pointed questions were asked, he did note that he sometimes had chest pain after his episodes of `seizures.’ Finally, the `jerking’ that his mother noted was likely myoclonic jerks from hypoxemia. Sometimes you can see this when someone experiences vasovagal syncope. They may have a few `jerks,’ but this is different from a seizure. The confused state when the patient awoke from his `seizure’ likely represented some hypoxemia. I thought this was an interesting and challenging case.
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References:
1. Arnsdorf MF, Ganz L. Up To Date: Sinus Tachycardia. May 2010 Accessed at: http://www.uptodate.com/patients/content/topic.do?topicKey=~pl2HSiIsiBBDVG
2. Howes DS, Booker EA. Myocarditis. Emedicine Dec 1, 2009 Accessed at: http://emedicine.medscape.com/article/759212-overview
3. Sutherland SF, Pulmonary Embolism. Emedicine. May 8, 2009. Accessed at: http://emedicine.medscape.com/article/759765-overview
4. Uwaifo GI, Arioglu E. Obesity. Emedicine. Aug 17, 2010. Accessed at: http://emedicine.medscape.com/article/123702-overview