Guest post: Syncope primer

CDI Blog - Volume 13, Issue 19

by Alba Kuqi, MD, CICA, CCS, CDIP, CCDS, CRCR, CSMC

Syncope is a sudden/transient loss of consciousness with loss of postural tone. It accounts for 3% of emergency room visits and 1%-6 % of all hospital admissions. Several different disease processes can cause syncope. Reflex mediated syncope and orthostatic intolerance are most common, whereas neurological, cardiovascular, and psychogenic causes occur with decreasing frequency. Up to 45% of patients will be labeled as having a “syncope of unknown cause” despite a thorough evaluation.

The etiology of syncope has important prognostic significance. Younger patients more frequently have syncope due to non-cardiovascular cause or syncope of unknown origin and overall have a more favorable prognosis. Older patients more often have a cardiac etiology or syncope due to polypharmacy. 

The importance of an H&P

The initial diagnostic evaluation’s goal is to differentiate between benign and potentially life-threatening causes. The presence of cardiovascular diseases identifies patients at increased risk of death. History and physical (H&P) examination alone allow diagnosis of syncope cause in 45% of patients and suggest a diagnosis in another 40%. Physicians need to obtain patient’s and eyewitnesses’ reports of the event and search for situational or provocative factors, postural or exertional symptoms, and symptoms of cardiac or neurologic origin. 

A past medical history should focus on prior syncopal events, as well as prior cardiac, neurologic, and psychiatric history. A family history of familial cardiomyopathy, sudden cardiac death, or syncope should also be investigated. It’s not hard to diagnose syncope; you can get there with the H&P alone. Secondary testing and imaging are ancillary, and it is only done if you’re not sure of the etiology. The goal is to decide whether this is cardiogenic or not because of the mortality risk associated with it.

Diagnosing syncope 

In her paper, “Documentation and data improvement fundamentals,” Ruthann Russo, JD, MPH, RHIT, writes that if a patient is admitted with syncope, and the physician orders both a neurological as well as a cardiology consultation, it is important to know that the attending physician is working with differential diagnoses of “possible cerebral vascular accident (CVA)” and “arrhythmia.” These diagnoses justify the ordering of consultation from each clinical area. 

The ACDIS Pocket Guide says that the most common cause (if not due to orthostatic hypotension) is a cardiac arrhythmia, which may be difficult to diagnose without prolonged cardiac event monitoring, particularly when no cause is identified by the initial work-up.

Other causes may include heart block (second or third degree), acute blood loss anemia, electrolyte imbalance, hypoglycemia, stenosis of vertebrobasilar (VB), or bilateral carotid arteries or diabetic neuropathy. Up to 25% of patients with syncope of unknown etiology have a psychiatric diagnostic of panic disorder, generalized anxiety, or major depression. 

Differential diagnoses

Tongue biting, aching muscles, or disorientation following a syncopal episode suggests a seizure, whereas sweating, nausea, vertigo, incontinence, injury, headache, family history of epilepsy, and history of prior concussion are not predictive of seizures. The most important distinction between syncope from seizure is the length of time it took the patient to recover from the loss of consciousness. Was there a postictal state? The postictal state is a transient deficit, occurring between the end of an epileptic seizure and the patient’s return to baseline. In syncope, there is a rapid return of consciousness and in seizure, there is a postictal state.

 If someone passed out because they didn’t perfuse the brain when they fell over, they would again perfuse the brain and should wake up quickly. The length of loss of consciousness should be brief and they should have a rapid return of consciousness once they wake back up. 

In a seizure, however, the patient loses consciousness not because of perfusion to the brain, but because of the abnormal firing of the neurons. As such, it takes a long time for the body to readjust. So, if there is a postictal state greater than five minutes, we should be thinking about a seizure. On the other hand, if there is a rapid return of consciousness less than three minutes, we should be thinking about syncope. 

Remember, encephalopathy due to the postictal state is not coded separately since it is integral to the condition. Coding Clinic only advises the diagnosis of encephalopathy being integral to seizures, not to a CVA. Coding Clinic, first quarter 2014, says to report any neurological deficits caused by a CVA (Other encephalopathies, G93.49), with or without treatment, even if they are resolved at the time of discharge from the hospital. When in doubt, CDI professionals need to query the provider to provide further clarification.  

Differential diagnosis

An advanced organizer is a mnemonic (WOMAN 321 PE)

  • Vasovagal (visceral organs/carotid baroreceptors/psychogenic) 
  • Orthostatic (volume depletion/autonomic nervous system dysfunction) 
  • Mechanical cardiac 
  • Arrhythmias  
  • Neurogenic 
  • Psych + Electrolytes = Pulmonary embolism (PE)

Treatment

Syncope is a symptom that can be caused by many different factors. When it comes to treatment, there is no one-size-fits-all approach, making an accurate diagnosis very important. Treatment should address the underlying cause of syncope.

Intensive care unit (ICU) admission should be strongly considered in syncope patients with sustained ventricular tachycardia (VT), symptomatic non-sustained VT, second or third degree heart block, pauses greater than three seconds, symptomatic bradycardia, severe aortic stenosis, severe CHF, evidence of acute ischemia, or ongoing hemodynamic inability. 

Editor’s note: Kuqi is the CDI supervisor at Prime Healthcare in Philadelphia. Click here to read the first part of this series. Contact her at albakuqi88@gmail.com. Opinions expressed are those of the author and do not necessarily reflect those of ACDIS, HCPro, or any of its subsidiaries.  

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Clinical & Coding

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