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Meningococcal infections: With particular reference to fulminant meningococcemia (Waterhouse-Friderichsen Syndrome) treated with cortisone and norepinephrine
21. Maguire P. Barriers to psychological care of the dying. BMJ 1985;291: 1171-712. 22. Serwint JR, Rutherford LE, Hutton N, Rowe PC, Barker S, Adamo G. ‘‘I learned that no death is routine’’: description of a death and bereavement seminar for pediatric residents. Acad Med 2002;77:278-84. 23. Davies B. Shadows in the sun: the experiences of sibling bereavement in childhood. Philadelphia (PA): Brunner/Mazel; 1998. 24. Lundin T. Morbidity following sudden and unexpected bereavement. Br J Psych 1984;144:84-8.
25. Ahrens WR, Hard RG. Emergency physicians’ experience with pediatric death. Am J Emerg Med 1997;15:642-3. 26. Mitchell JT, Everly GS. Critical incident stress debriefing: an operations manual for CISD: defusing and other group crisis interventions services. 3rd ed. Ellicott City (MD): Chevron Publishing Corporation; 1997. 27. Scurry MT, Bruhn JG, Bunce H. The house officer and the dying patient: attitudes, experiences, and needs. Gen Hosp Psychiatry 1979;4: 301-5. 28. McCue JD. The naturalness of dying. JAMA 1995;273:1039-43.
50 Years Ago in The Journal of Pediatrics MENINGOCOCCAL INFECTIONS: WITH PARTICULAR REFERENCE TO FULMINANT MENINGOCOCCEMIA (WATERHOUSE-FRIDERICHSEN SYNDROME) TREATED WITH CORTISONE AND NOREPINEPHRINE
Grifn JW, Daeschner CW. J Pediatr 1954;45:264-72 Neisseria meningitidis remains one of the leading causes of bacterial meningitis and sepsis worldwide. In this case series the authors describe 32 patients with documented or presumed meningococcal infections. Two aspects that are worth remembering from this description are the significant risk of intrafamilial transmission (as documented by one family that had four members affected) and that the microorganism can be cultured from skin lesions (as reported in four cases). Five children developed the Waterhouse-Friderichsen Syndrome, two of whom died. This severe, highly fatal course, characterized by rapid cardiovascular deterioration, is associated with meningococcal infections but can also be caused by other gram-negative and gram-positive organisms. Pathogenesis includes endotoxin triggering of the inflammatory cascade leading to damage and thrombi of microvessels and DIC with severe impairment of the adrenal function due to cell death and/or hemorrhage. Why do some individuals respond with such a fulminant course and others do not? Current investigation suggests that individuals with polymorphisms in genes associated with TNF-a, plasminogen, and/or neutrophil receptors may be predisposed to a more severe clinical course. Further studies focused more on the host than the microorganism can be envisioned for this and other infectious diseases in the future. The article details a case of a child admitted with meningitis and shock who responded rapidly to therapy that included norepinephrine and steroids. Whether the child survived because of the treatment, an individual response to infection, or both, is an open question. This and the other two children that survived had meningeal involvement, a clinical feature that has been associated with a more favorable outcome. In any case, this represents one of a series of initial reports from the early 1950s describing survival of fulminant meningitis associated with the use of adrenergic drugs and steroids. The significant advances in cardiovascular and respiratory support and fluid management during these 50 years have certainly saved many lives of both children and adults with meningococcal infections. Meningococcal infections will be controlled with the development and delivery of effective vaccines. The polysaccharide meningococcal vaccines developed in the 1970s perform poorly in young children. Newly-released conjugate vaccines have been highly efficacious against N meningitidis C in young children and adolescents. The challenge remains for conjugate vaccines against serogroup A responsible for the large pandemic outbreaks and the majority of disease in sub-Saharan Africa. Serogroup B antigens are poorly immunogenic and for this serogroup a vaccine different than a polysaccharidebased antigen will most likely be required. Miguel O’Ryan, MD Microbiology and Mycology Program, Institute of Biomedical Sciences Faculty of Medicine, University of Chile Santiago, Chile YMPD1011 10.1016/j.jpeds.2004.06.020
234
Serwint
The Journal of Pediatrics August 2004
25. Ahrens WR, Hard RG. Emergency physicians’ experience with pediatric death. Am J Emerg Med 1997;15:642-3. 26. Mitchell JT, Everly GS. Critical incident stress debriefing: an operations manual for CISD: defusing and other group crisis interventions services. 3rd ed. Ellicott City (MD): Chevron Publishing Corporation; 1997. 27. Scurry MT, Bruhn JG, Bunce H. The house officer and the dying patient: attitudes, experiences, and needs. Gen Hosp Psychiatry 1979;4: 301-5. 28. McCue JD. The naturalness of dying. JAMA 1995;273:1039-43.
50 Years Ago in The Journal of Pediatrics MENINGOCOCCAL INFECTIONS: WITH PARTICULAR REFERENCE TO FULMINANT MENINGOCOCCEMIA (WATERHOUSE-FRIDERICHSEN SYNDROME) TREATED WITH CORTISONE AND NOREPINEPHRINE
Grifn JW, Daeschner CW. J Pediatr 1954;45:264-72 Neisseria meningitidis remains one of the leading causes of bacterial meningitis and sepsis worldwide. In this case series the authors describe 32 patients with documented or presumed meningococcal infections. Two aspects that are worth remembering from this description are the significant risk of intrafamilial transmission (as documented by one family that had four members affected) and that the microorganism can be cultured from skin lesions (as reported in four cases). Five children developed the Waterhouse-Friderichsen Syndrome, two of whom died. This severe, highly fatal course, characterized by rapid cardiovascular deterioration, is associated with meningococcal infections but can also be caused by other gram-negative and gram-positive organisms. Pathogenesis includes endotoxin triggering of the inflammatory cascade leading to damage and thrombi of microvessels and DIC with severe impairment of the adrenal function due to cell death and/or hemorrhage. Why do some individuals respond with such a fulminant course and others do not? Current investigation suggests that individuals with polymorphisms in genes associated with TNF-a, plasminogen, and/or neutrophil receptors may be predisposed to a more severe clinical course. Further studies focused more on the host than the microorganism can be envisioned for this and other infectious diseases in the future. The article details a case of a child admitted with meningitis and shock who responded rapidly to therapy that included norepinephrine and steroids. Whether the child survived because of the treatment, an individual response to infection, or both, is an open question. This and the other two children that survived had meningeal involvement, a clinical feature that has been associated with a more favorable outcome. In any case, this represents one of a series of initial reports from the early 1950s describing survival of fulminant meningitis associated with the use of adrenergic drugs and steroids. The significant advances in cardiovascular and respiratory support and fluid management during these 50 years have certainly saved many lives of both children and adults with meningococcal infections. Meningococcal infections will be controlled with the development and delivery of effective vaccines. The polysaccharide meningococcal vaccines developed in the 1970s perform poorly in young children. Newly-released conjugate vaccines have been highly efficacious against N meningitidis C in young children and adolescents. The challenge remains for conjugate vaccines against serogroup A responsible for the large pandemic outbreaks and the majority of disease in sub-Saharan Africa. Serogroup B antigens are poorly immunogenic and for this serogroup a vaccine different than a polysaccharidebased antigen will most likely be required. Miguel O’Ryan, MD Microbiology and Mycology Program, Institute of Biomedical Sciences Faculty of Medicine, University of Chile Santiago, Chile YMPD1011 10.1016/j.jpeds.2004.06.020
234
Serwint
The Journal of Pediatrics August 2004