Distribution A: Approved for public release; distribution is unlimited. Case Number: 88ABW-2013-2090, 3 May 2013 1

Michael Prudhomme, MDLCDR (FS/FMF) MC USN

Naval Aerospace Medical Institute

NAS Pensacola

RAM 2014

Malingering vs Somatization Malingering vs Somatization DisorderDisorder

Disclosure InformationDisclosure Information84th Annual Scientific Meeting84th Annual Scientific Meeting

Dr. Michael PrudhommeDr. Michael Prudhomme

I have no financial relationships to disclose.

I will not discuss off-label use and/or investigational use in our presentation.

• 23-yr-old Female PFC, Aircraft Mechanic

• Past Medical History • Significant for “Elephantchartitis”

• In 3.5 years of active duty she had filled two medical records

• Averaged 3 visits to medical per week

• Multiple GMO’s / FS involved in her care as PCP• Most with 1- 2 years of experience past internship

• Had seen several specialists for various complaints including Mental Health (Network Providers)

Case HistoryCase History

• Symptoms involved multiple organ systems

• Symptoms were vague, no formal diagnosis• GI (IBS?)• Musculoskeletal (fibromyalgia/ patellar femoral pain syndrome?)• Mental (anxiety?)

• Was diagnosed with adjustment disorder / anxiety at one point• Malingering and somatization were suspected but not formally diagnosed

Case Presentation ContinuedCase Presentation Continued

• One morning she presents to medical with a new complaint of fainting. It was sudden onset, and she believed it lasted less than a minute. She was at home and it was not witnessed. It was dismissed as vasovagal or anxiety, and she was returned to work

• Over the next month she presented to different providers with similar stories of syncopal episodes. One of the GMO’s decided to rule out seizures and placed routine Neurology consult.

• Discussion among FS/GMO was she turning from malingering to full blown somatization disorder.

Case Presentation Continued Case Presentation Continued

History and Physical Exam were benign • No PMH or family Hx of syncope, seizures, or sudden death• Not taking any medications or supplements that could explain

symptoms

Lab work• CBC and TSH normal

EvaluationEvaluation

ECGECG

•Computer noted long QTc•It was compared to an ECG taken over a year ago, and was noted and signed as unchanged from previous ECG•No further action taken at this time as she had a pending workup (neuro)

• Several days latter she is leaving a movie theater with her boyfriend. Walking out the door, she suddenly colapses. No Tonic-Clonic movements are noted. She regains consciousness in under a minute. EMS delivers her to Local ER where she is admitted by internal medicine.

• Long QT noted on ECG monitoring• The next morning she is air transported to tertiary care

and had an AICD placed.• Subsequently diagnosed with congenital Long QT

Syndrome, recieved medical board, and was discharged from USMC

Case Presentation ContinuedCase Presentation Continued

Congenital Long QT syndromeCongenital Long QT syndrome

• Disorder of ventricle myocardial repolarization characterized by a prolonged QT interval

• Etiology is not fully understood, but there are 12 known genetic mutations involving ion channels

• incidence of 1 in 3000

http://www.sads.org/Library/Long-QT-Syndrome

• Primary presenting symptoms are:• Palpitations, syncope, seizures (mistaken), cardiac arrest

• Different mutations present differently with initial presentation ranging from infancy to early 20’s

• Probands tend to have later onset of presentation averaging 21 years and most are female

• Typically results in Torsades de points, with potential for sudden cardiac death. (also PVC’s or Monomorphic VT)

• Can be triggered by external events such as exercise, noise, emotion, sudden wakening (alarm) thunder, swimming, diving

Long QT SyndromeLong QT Syndrome

““Normal” QTcNormal” QTc

•normal”QTc is .44 for men and .45 for women

•QTc = QT / RR (corrects for heart rate)

•440-ms line, often referred to as “borderline QTc,” shows the substantial overlap between approximately 10% to 15% of humanity and the subset of patients having “concealed” LQTS

LQTS

Taggart N W et al. Circulation 2007;115:2613-2620

Risk StratificationRisk Stratification

doi: 10.1093/eurheartj/ehl159

Rate of ACA or SCD by Genotype and QTc Category Kaplan-Meier cumulative probabilities of aborted cardiac arrest (ACA) and sudden cardiac death (SCD) by genotype and corrected QT (QTc) subgroup. LQTS = long-QT

syndrome.

...

http://dx.doi.org/10.1016/j.jacc.2010.07.038

Event Risk Even in “normal” Event Risk Even in “normal” QTcQTc

• Congenital LQTS can make its initial presentation in the third and fourth decades, especially in female patients without family history

• Initial presentation may be palpitations or syncope• ECG may or may not be normal, and risk of cardiac event

increases with QTc• Previously asymptomatic patients with undiagnosed LQTS can

have an event precipitated by medicines that prolong QT interval:

• Clarithromycin, azithromycin, SSRIs, Diuretics (electrolyte changes), HIV protease inhibitors

• Stress, Anxiety, Physical Exertion can precipitate an event• Holter Monitor / Genetic testing can help differentiate patients

that fall in the overlap zone

Aeromedical ConcernsAeromedical Concerns

• Duty as a physician to evaluate every patient complaint, even in those suspected of malingering

• Syncope may be the presenting symptom for potentially life threatening disease, and even a single episode warrants a thorough work up.

Lessons LearnedLessons Learned

• T/F Congenital LQTS always becomes symptomatic by the 3rd decade

• T/F: patients with asymptomatic LQTS have a decreasing incidence of Sudden Cardiac Events in the 4th decade as apposed to their second.

Questions?Questions?