Traumatization, secondary

Go back to the Center for the Study of Traumatic Stress Web site at www.centerforthestudy-oftraumaticstress.org and click on Terrorism Preparedness. Then click on the New Normal. What is Secondary Traumatization and who may be affected When should children be referred to a pediatrician or mental health specialist ... 

Creamer, T. L., Liddle, B. J. (2005). Secondary traumatic stress among disaster mental health workers responding to the September Hth attacks. Journal of Traumatic Stress, 18(1), 89-96. 

In terms of prevention and management of secondary traumatic stress, both organizational and individual (self-care) approaches need to be considered (Morante, Moreno, Rodriquez, Stamm, 2006). The disaster or first responder agency has an obligation to minimize the impact of a disaster event on its workers by incident management strategies such as rotating worker... 

Beaton, R., Murphy, S. (1995). Secondary traumatic stress of crisis workers Research implications. In C. Figley (Ed.), Compassion fatigue Coping with secondary traumatic stress disorder in those who treat the traumatized (pp. 51-81). New York Brunner/Mazel. 

Figley, C. (1995). Compassion fatigue Coping with secondary traumatic stress disorder in those who treat the traumatized. New York Brunner/Mazel. 

Morante, M., Moreno, B., Rodriquez, A., Stamm, B. (2006). Conceptualizing secondary traumatic stress among emergency service workers in Madrid, Spain. Traumatic StressPoints, 20, 6. 

Moderate to severe corneal abrasions usually are accompanied by other ocular signs. Diffnse or focal conjunctival injection is present depending on the size and location of the abrasion. Eyelid edema is common when profuse reflex lacrimation occurs. If the lesion has been present for at least 12 to 24 hours, a secondary traumatic anterior... 

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... 

In secondary peritonitis, bacteria most often enter the peritoneum or retroperitoneum as a result of disruption of the integrity of the GI tract caused by diseases or traumatic injuries. 

Generalized vaccinia Secondary lesions of the skin following vaccination which may occur in subjects with previously healthy skin but are more common in the case of traumatized skin, especially in the case of eczema(eczema vaccinatum). In the latter instance, generalized vaccinia may result from mere contact with a vaccinated person. Secondary vaccinial lesions may also occur following transfer of virus from the vaccination to another site by means of the fingers (autoinnoculation). 

Hickling, E.J., and Blanchard, E.B. (1997) The private practice psychologist and manual-based treatments post-traumatic stress disorder secondary to motor vehicle accidents [see comments]. Be-havi Rese Ther 35 191-203. 

Jorge RE, Robinson RG, Starkstein SE, et al Secondary mania following traumatic brain injury. Am J Psychiatry 150 916-921, 1993 Jovanovic UJ Studies with maprotihne on waking states and on sleep patterns in healthy subjects and in depressed patients, in Depression The Biochemical and Physiological Role of Ludiomil. Edited by Jukes A. England, CIBA, 1977, pp 85-101... 

Like spinal cord trauma, traumatic head injury consists of a primary injury, attributable to the mechanical insult itself, and a secondary injury, attributable to the series of systemic and local neurochemical changes that occur in brain after the initial traumatic insult (Klussmann and Martin-Villalba, 2005). The primary injury causes a rapid deformation of brain tissues, leading to rupture of neural cell membranes, release of intracellular contents, and disruption of blood flow and breakdown of the blood-brain barrier. In contrast, secondary injury to the brain tissue includes many neurochemical alterations such as release of cytokines, glial cell reactions involving both activated microglia and astroglia, and demyelination... 

Morphine releases histamine and may cause peripheral vasodilation and orthostatic hypotension (Figure 47.7). The cutaneous blood vessels dilate around the blush areas such as the face, neck, and upper thorax. Morphine causes cerebral vasodilation (due to increased carbon dioxide retention secondary to respiratory depression), and hence, it increases the cerebrospinal fluid pressure. Therefore, morphine should be used cautiously in patients with either meningitis or a recent head injury. When given subcutaneously, morphine is absorbed poorly whenever there is either traumatic or hemorrhagic shock. 

Topical antibiotics are typically available as ointments and are excellent for use on open wounds. Coupled with the antibacterial action of the antibiotic ingredient, topical antibiotic ointments provide a safe and effective option in wound healing. In addition, topical antibiotics are effective for the localized treatment of primary and secondary pyodermas with minimal systemic side effects.14 Prophylactic uses include application for traumatic and surgical wounds, burns, intravascular catheters, and eradication of S. aureus nasal carriage.16 42 The advantage of antibiotic therapy in the treatment of eczematous skin will be discussed in the following article considering AD as an example. 

Traumatic brain injury leads to inflammatory events that are believed to contribute to outcome through secondary injury mechanisms (67,68). 

Matsushita Y., BramlettH. M., Alonso O., and Dietrich W. D. (2001) Posttraumatic hypothermia is neuroprotective in amodel of traumatic brain injury complicated by a secondary hypoxic insult. Crit. Care Med. 29, 2060-2066. 

Hypothermia-induced coagulopathy in patients with severe TBI has important clinical implications. In addition to the intracranial hemorrhages caused by their primary traumatic injury, these patients have a 20-30% incidence of delayed posttraumatic intracranial hemorrhage. However, at least one report found that treatment with moderate hypothermia did not result in increased rates of secondary delayed intracranial hemorrhages as compared to normothermic controls (19). 

It is known from animal models with global ischemia and traumatic brain injury that moderate hypothermia attenuates secondary brain damage by reducing cerebral ischemia and postischemic brain edema and preserving the blood-brainbarrier. Even though hypothermia has potent cerebroprotective effects after experimental focal ischemia, clinical studies on hypothermic therapy after MCA infarction were not available until recently. We performed a pilot study investigating the efficacy, feasibility, and safety of induced moderate hypothermia in the therapy of patients with acute, severe MCA infarction and increased ICP. 

A significant reduction of the ICP was seen, which was similar to the results of Marion and Shiozaki, who used hypothermic therapy in traumatic brain injuries (37,38). With an unaffected mean arterial blood pressure (MABP) and increased cerebral perfusion pressure (CPP), hypothermic therapy appeared to benefit stroke patients, as uncontrolled intracranial hypertension is the main cause of death in the first week after stroke. However, rewarming the patients consistently led to a secondary rise of ICP, which required additional ICP therapy with mannitol. In some cases it even exaggerated the initial ICP levels (Fig. 3). 

Role in post-traumatic hypoperfusion (secondary ischemia)... 

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