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Commentaries   |    
In the Aftermath of Tragedy: Medical and Psychiatric Consequences
Charles B. Nemeroff, M.D., Ph.D.; Pascal J. Goldschmidt-Clermont, M.D.
Academic Psychiatry 2011;35:4-7. 10.1176/appi.ap.35.1.4
View Author and Article Information

Address correspondence to Charles B. Nemeroff, M.D., Ph.D., University of Miami Miller School of Medicine, Psychiatry & Behavioral Sciences, 1120 NW 14th St., Miami, FL 33136; cnemeroff@med.miami.edu (e-mail).

Received July 13, 2010; Revised August 2, 2010; Accepted August 5, 2010.

The catastrophic earthquake that ravaged the already fragile Haitian capital of Port-au-Prince on January 12, 2010 unleashed an unprecedented humanitarian crisis. The devastation was beyond belief, the suffering horrific. Yet the brave people of Haiti were stoic in rescuing their neighbors and friends, the injured and the homeless, triggering an impassioned humanitarian response from around the world that showed Haiti will never be forgotten or forsaken.

Led by Dr. Barth Green, the chairman of neurological surgery at the University of Miami Leonard M. Miller School of Medicine, an army of University of Miami doctors, nurses, and staff would be joined by more than 2,000 medical volunteers from the United States and beyond who staffed the most advanced ground zero hospital in the hemisphere's poorest nation. In a 25,000-square-foot tent facility, we collectively treated more than 20,000 patients, saving countless lives. One of us (PGC) dramatically described the experience.

"I will always remember the night of January 17, when I landed in Port-au-Prince, the capital of Haiti, with one of the first hospital shifts. I was joining our medical team to assess the needs and develop a strategy for our long-term relief effort. We were immediately immersed in the formidable rescue, caring for hundreds of injured Haitians who were brought to two cargo tents at the nonfunctioning airport. In an improvised emergency room, our volunteers performed life-saving procedures on patients whose survival hung by a thread. One young man, JC, had a crushed leg and was suffering from rhabdomyolysis. In need of dialysis, which was not available, the 19-year-old was destined to die. With a plastic carpet, we lifted him onto a plane bound for Miami, Florida, where he would receive the treatment that saved his life. As he bravely awaited takeoff, he asked me to speak to his mother who stayed quietly behind.

"The dead, dying, and injured were all around us. I was, to say the least, overwhelmed, as probably everybody else was. Nevertheless our teams in Port-au-Prince and Miami were working remarkably well together ensuring that volunteers, supplies, and other necessary equipment were dispatched like clockwork.

"The next morning a young girl, approximately 11 years old, needed plastic surgery for her chest. A falling rock had sheared off her flesh and rib. A University of Miami professor of surgery and I took her to the Israeli Army Field Hospital, the only facility with a plastic surgery service. Our driver, his hand locked on the horn, drove his makeshift ambulance at 70 mph through roads jammed with people, bicycles, cars, and trucks, all trying to navigate a world of chaos. Remarkably, we made it with our young patient, who uttered not one word, nor shed one single tear. Our Israeli colleagues traded her for a patient who only we were prepared to care for. I could not help but wonder if all our fellow humans would always interact in such a kind, collaborative manner, would not the world be a better place?"

The Miller School of Medicine's relief effort was quite extraordinary—from state-of-the-art trauma care by the University of Miami/Jackson Memorial Hospital team of doctors and nurses to the can-do spirit of our orthopedic surgeons, anesthesiologists, pediatricians, OB/GYNs, dermatologists, neurologists, ophthalmologists, and physical therapists who contributed in every way they could, even taking wounded orphans under their wing to bring them to U.S. hospitals. The rapid expansion of our pre-earthquake programs in comprehensive health care to underserved Haitians and the introduction of telemedicine to transmit real-time images of patients for consultations with faculty back home in Miami was no less extraordinary than the prosthetic limbs and physical therapy provided to hundreds of new amputees and the distribution of hundreds of eyeglasses and the establishment of an eyeglass library by our Bascom Palmer Eye Institute.

Of course little of this would have been possible without the caring generosity of so many individuals who collectively contributed $5.8 million and donated pharmaceuticals; supplies; equipment; and the use of their planes, pilots, personnel, time, and considerable energy to help us help our neighbors in their time of greatest need.

The University of Miami Global Institute for Community Health and Development has now passed the baton for day-to-day operations of our field hospital to our partner in Haiti, Project Medishare, which is leading the effort to establish a much needed national trauma, critical care, and rehabilitation network in the nation as well as the educational components to support them.

Once the initial triage was completed to deal with urgent medical and surgical needs, the mental health consequences of this trauma became evident.

In this issue of Academic Psychiatry, one of our outstanding psychiatric residents, Molly McShane, M.D., shares her remarkable experiences as a volunteer in Haiti. Two of the major tenets of psychiatry that we traditionally highlight to trainees are that "life is uncertain" and "bad things happen to good people." In the last several years, natural disasters such as the tsunami that devastated Sri Lanka; Hurricane Katrina that decimated New Orleans; terrorist acts including the Oklahoma City bombing and the September 11 attacks; and ongoing military conflicts that expose our valiant troops and civilians in Iraq, Afghanistan, the Middle East, and Africa have focused our attention on the psychiatric aftermath of such cataclysmic traumatic events.

Because stress is known to precipitate episodes of, or exacerbate, a variety of severe psychiatric disorders including major depression, bipolar disorder, schizophrenia, and all of the major anxiety and substance abuse disorders, natural disasters are expected to markedly increase the severity and point prevalence of these disorders. Unfortunately, as noted in Dr. McShane's article, the availability of inpatient and outpatient psychiatric facilities, trained mental health professionals, and psychopharmacological medications in Haiti was severely limited prior to the earthquake. In addition to the exacerbation of preexisting psychiatric illness is the marked increase in new cases of depression and posttraumatic stress disorder (PTSD) in response to the loss of loved ones, and the witnessing of widespread death and destruction far beyond what is generally considered within the "normal" range of human experience. Unfortunately, the cultural climate in Haiti is antithetical to early recognition and treatment of psychiatric illness and this further contributed to the burden of psychiatric morbidity after the earthquake. A previous issue of Academic Psychiatry has focused on the devastating consequences of stigma in mental health care (1).

Posttraumatic stress disorder (PTSD) is the fifth most common of the major psychiatric disorders, with a lifetime prevalence rate of 7.8% in the United States (2). PTSD is approximately twice as common in women, and prevalence rates correlate with trauma exposure rates. Prospective studies indicate that the majority of trauma victims experience the cardinal symptoms of reexperiencing, avoidance, and hyperarousal immediately following trauma, but for most these symptoms abate and eventually disappear (3). For a significant minority, symptoms persist and develop into syndromal PTSD. Chronic PTSD is associated with significant comorbidity (e.g., major depression, substance and alcohol abuse, panic disorder), reduced life expectancy and mortality (suicide, medical comorbidity), as well as disability, loss of productivity, and increased health care utilization (4). It is, therefore, crucial to identify individuals at high risk to develop PTSD in the immediate aftermath of trauma, in order to design interventions that are effective in preventing the development of PTSD and its associated disease burden. It is also important to recognize the increasing evidence that providing immediate psychological interventions to all trauma victims is not only costly, but may interfere with normal recovery in the survivors who would not go on to develop PTSD (5).

PTSD is a complex disease in which gene-environment interactions determine vulnerability. Several risk factors have been identified for developing PTSD following trauma exposure (6, 7) including (a) female gender; (b) pretrauma personal and familial psychopathology; (c) prior trauma including child abuse and neglect; (d) trauma severity; (e) perceived life threat and peritraumatic emotional response; (f) lack of social support; (g) reduced hippocampal size; (h) a variety of previously identified risk alleles including FKBP5, DAT, COMT, BDNF, 5-HTTLPR, RGS2, GABRA2, CRFR1; (i) markers of inflammation including IL-6, C-reactive peptide, and tumor necrosis factor (TNF) implicated in the pathophysiology of PTSD and mood disorders; and (j) measures of hypothalamic-pituitary-adrenal (HPA) axis function including blood and hair cortisol concentrations, the latter a validated measure of longitudinal HPA axis activity (713).

Epidemiological studies indicate that about 70% of people will experience a traumatic event in their lifetime, but not all of these individuals will develop PTSD. Identifying which trauma victims will develop PTSD is the agreed upon "holy grail" for the PTSD research field. Clearly, a clinically useful metric using a combination of biological, epidemiological, and psychological variables to predict who, at the time of trauma, will develop PTSD will revolutionize the treatment of this common and severe psychiatric disorder. The savings in terms of human suffering, medical and psychiatric comorbidity, reduction in suicide risk, disability, and loss of life as well as economic gains in terms of reduced health care utilization and increased work productivity are virtually incalculable. Considering the almost universal exposure to traumatic events and the vast public health problem that PTSD represents worldwide, the global impact in civilian and military populations will be substantial.

Functional genomics, transcriptomics, and the related fields of proteomics and epigenetics allow high throughput hypothesis generators. These approaches have proven successful in identifying disease biomarkers in several common complex disorders including Alzheimer's disease, cancer, and diabetes (14). The concern that the use of blood elements instead of brain tissue does not provide valid data in gene expression appears to be unwarranted (15).

We need to accelerate discoveries for the prevention, diagnosis, and treatment of PTSD. Applying genomics, transcriptomics, epigenetics, and proteomics to elucidate biological predicators of PTSD is an active avenue of investigation. Approximately 30% to 40% of the risk to develop PTSD is heritable and our group has identified some of the most promising candidate genes that mediate vulnerability to PTSD. Much of what we have learned concerning the mammalian response to trauma is derived from basic science discoveries, and these findings, in part, provide the scientific rationale for identifying predictors of PTSD (e.g., inflammatory markers and neuroendocrine alterations). PTSD is a major global health problem and success will result in a clear and immediate global health impact.

Personalized medicine has been developed and implemented in, for example, oncology and infectious disease. Based on the extant literature, the development of personalized biomarker signatures for PTSD should be achievable. The promise of personalized medicine has been difficult to realize, not because of the difficulty in whole genome scanning (GWAS) or in its expense, but because of the realization that complex genetic diseases such as PTSD involve a large number of genes, each of which exerts a relatively small effect, rendering it difficult to assess the risk of each variant. Moreover, the gene variants interact with environmental factors such as child abuse and neglect. The disappointing results obtained with GWAS studies have led to the inexorable conclusion that the functional consequences of these myriad polymorphisms are key to understanding the biology and treatment of complex disorders.

A few studies to date have examined candidate gene associations with risk for PTSD, with our study on FKBP5 representing the largest PTSD genetics study ever conducted (10). The FKBP5 gene regulates the HPA axis at the level of glucocorticoid receptor sensitivity. FKBP5 polymorphisms interact with a history of child abuse to predict adult PTSD symptoms.

The use of such genomic, transcriptomic, epigenetic, proteomic, structural and functional brain imaging, inflammation, and neuroendocrine measures taken together with behavioral and psychological measures will likely achieve the much needed goal of predicting which trauma victims will develop syndromal PTSD and, moreover, will likely help identify predictors of response to the effective treatments of PTSD, both psychotherapeutic and psychopharmacological. In the future, such tools can be brought to bear to help manage the psychiatric sequelae of natural disasters similar to the Haiti earthquake. Immediate intervention for medical-surgical and psychiatric consequences of trauma will surely reduce the resultant morbidity and mortality associated with such events.

The authors are indebted to our faculty, staff, students, trainees and all of our volunteers from Haiti, the United States, and beyond, without whom our medical relief efforts would have never been possible. We are also deeply grateful for the steadfast and substantial support that we have received from our wonderful philanthropic partners. We thank our Haitian friends for their help, kindness, generosity, and for providing all of us with an unforgettable lesson of courage and stoicism. Finally, we thank Carmen and Maggie for their exceptional partnership.

Small portions of this commentary were published by Dr. Goldschmidt in the University of Miami MEDICINE Magazine (2010; 12:2—3) and have been modified with consent.

In the past year, Charles B. Nemeroff, M.D., Ph.D., served on the Board of Directors of NovaDel Pharma and Mt. Cook Pharma. He served on the Scientific Advisory Board of AstraZeneca Pharmaceuticals, CeNeRx BioPharma, NovaDel Pharma, PharmaNeuroboost, the American Foundation for Suicide Prevention (AFSP), and NARSAD. He holds stock, stock options, or equity in CeNeRx BioPharma, Corcept, NovaDel Pharma, PharmaNeuroboost, and Revaax Pharma. He holds two U.S. patents: method and devices for transdermal delivery of lithium, and method of assessing antidepressant drug therapy via transport inhibition of monoamine neurotransmitters.

In the past year, Pascal J. Goldschmidt-Clermont, M.D., served on the Board of Mednax and OPKO. He served on the Scientific Advisory Board of Synecor. He holds stock in Synecor, Mednax, and OPKO.

Tsao  CIP;  Tummala  A;  Roberts  LW:  Stigma in mental health care.  Acad Psychiatry   2008; 32:70—72
[PubMed]
[CrossRef]
 
Keane  TM;  Marx  BP;  Sloan  DM:  Posttraumatic stress disorder: definition, prevalence, and risk factors, in Post-Traumatic Stress Disorder: Basic Science and Clinical Practice. Edited by Shiromani  PJ;  Keane  TM;  LeDoux  JE.  New York, NY,  Humana Press, pp 1—19
 
Rothbaum  BO;  Foa  EB;  Riggs  D  et al.:  A prospective examination of post-traumatic stress disorder in rape victims.  J Traumatic Stress   1992; 5:455—475
[CrossRef]
 
McFarlane  AC:  The long-term costs of traumatic stress: intertwined physical and psychological consequences.  World Psychiatry   2010; 9:3—10
[PubMed]
 
Mayou  A;  Ehlers  A:  Psychological debriefing for road traffic accident victims: three year follow-up of a randomized controlled trial.  Br J Psychiatry   2000; 176:589—593
[PubMed]
[CrossRef]
 
Zohar  J;  Fostick  L;  Cohen  A  et al.:  Risk factors for the development of posttraumatic stress disorder following combat trauma: a semiprospective study.  J Clin Psychiatry   2009; 70:1629—1635
[PubMed]
[CrossRef]
 
Heim  C;  Bremner  JD;  Nemeroff  C:  Trauma spectrum disorders, in Principles of Molecular Medicine, 2nd ed. Edited by Runge  MS;  Patterson  C;  McKusick  V.  Totowa, NJ,  Humana Press,  2006, pp 1203—1210
 
Cloitre  M;  Stolbach  BC;  Herman  JL  et al.:  A developmental approach to complex PTSD: childhood and adult cumulative trauma as predictors of symptom complexity.  J Traumatic Stress   2009; 22:399—408
[CrossRef]
 
Gillespie  CF;  Bradley  B;  Mercer  K  et al.:  Trauma exposure and stress-related disorders in inner city primary care patients.  Gen Hosp Psychiatry   2009; 31:505—514
[PubMed]
[CrossRef]
 
Binder  EB;  Bradley  RG;  Liu  W  et al.:  Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.  JAMA   2008; 299:1291—1305
[PubMed]
[CrossRef]
 
Koenen  KC;  Amstadter  AB;  Nugent  NR:  Gene-environment interaction in posttraumatic stress disorder: an update.  J Traumatic Stress   2009; 22:416—426
[CrossRef]
 
Yehuda  R;  Bierer  LM:  The relevance of epigenetics to PTSD: implications for the DSM-5.  J Traumatic Stress   2009; 22:427—434
[CrossRef]
 
Handwerger  K:  Differential patterns of HPA activity and reactivity in adult posttraumatic stress disorder and major depressive disorder.  Harv Rev Psychiatry   2009; 17:184—205
[PubMed]
[CrossRef]
 
Geschwind  DH;  Konopka  G:  Neuroscience in the era of functional genomics and systems biology.  Nature   2009; 461:908—915
[PubMed]
[CrossRef]
 
Jasinska  AJ;  Service  S;  Choi  O  et al.:  Identification of brain transcriptional variation reproduction in peripheral blood: an approach for mapping brain expression traits.  Hum Mol Genet   2009; 18:4415—4427
[PubMed]
[CrossRef]
 
References Container
+

References

Tsao  CIP;  Tummala  A;  Roberts  LW:  Stigma in mental health care.  Acad Psychiatry   2008; 32:70—72
[PubMed]
[CrossRef]
 
Keane  TM;  Marx  BP;  Sloan  DM:  Posttraumatic stress disorder: definition, prevalence, and risk factors, in Post-Traumatic Stress Disorder: Basic Science and Clinical Practice. Edited by Shiromani  PJ;  Keane  TM;  LeDoux  JE.  New York, NY,  Humana Press, pp 1—19
 
Rothbaum  BO;  Foa  EB;  Riggs  D  et al.:  A prospective examination of post-traumatic stress disorder in rape victims.  J Traumatic Stress   1992; 5:455—475
[CrossRef]
 
McFarlane  AC:  The long-term costs of traumatic stress: intertwined physical and psychological consequences.  World Psychiatry   2010; 9:3—10
[PubMed]
 
Mayou  A;  Ehlers  A:  Psychological debriefing for road traffic accident victims: three year follow-up of a randomized controlled trial.  Br J Psychiatry   2000; 176:589—593
[PubMed]
[CrossRef]
 
Zohar  J;  Fostick  L;  Cohen  A  et al.:  Risk factors for the development of posttraumatic stress disorder following combat trauma: a semiprospective study.  J Clin Psychiatry   2009; 70:1629—1635
[PubMed]
[CrossRef]
 
Heim  C;  Bremner  JD;  Nemeroff  C:  Trauma spectrum disorders, in Principles of Molecular Medicine, 2nd ed. Edited by Runge  MS;  Patterson  C;  McKusick  V.  Totowa, NJ,  Humana Press,  2006, pp 1203—1210
 
Cloitre  M;  Stolbach  BC;  Herman  JL  et al.:  A developmental approach to complex PTSD: childhood and adult cumulative trauma as predictors of symptom complexity.  J Traumatic Stress   2009; 22:399—408
[CrossRef]
 
Gillespie  CF;  Bradley  B;  Mercer  K  et al.:  Trauma exposure and stress-related disorders in inner city primary care patients.  Gen Hosp Psychiatry   2009; 31:505—514
[PubMed]
[CrossRef]
 
Binder  EB;  Bradley  RG;  Liu  W  et al.:  Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults.  JAMA   2008; 299:1291—1305
[PubMed]
[CrossRef]
 
Koenen  KC;  Amstadter  AB;  Nugent  NR:  Gene-environment interaction in posttraumatic stress disorder: an update.  J Traumatic Stress   2009; 22:416—426
[CrossRef]
 
Yehuda  R;  Bierer  LM:  The relevance of epigenetics to PTSD: implications for the DSM-5.  J Traumatic Stress   2009; 22:427—434
[CrossRef]
 
Handwerger  K:  Differential patterns of HPA activity and reactivity in adult posttraumatic stress disorder and major depressive disorder.  Harv Rev Psychiatry   2009; 17:184—205
[PubMed]
[CrossRef]
 
Geschwind  DH;  Konopka  G:  Neuroscience in the era of functional genomics and systems biology.  Nature   2009; 461:908—915
[PubMed]
[CrossRef]
 
Jasinska  AJ;  Service  S;  Choi  O  et al.:  Identification of brain transcriptional variation reproduction in peripheral blood: an approach for mapping brain expression traits.  Hum Mol Genet   2009; 18:4415—4427
[PubMed]
[CrossRef]
 
References Container
+
+

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