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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?