A 30-year-old woman presents to the emergency department (ED) with malaise, diffusemyalgia, and a rash that has spread all over her body (see Figures 1 and 2). Her symptomsbegan the day before presentation and initially improved with ibuprofen. Her boyfriend, whohas accompanied her to the ED, adds that she has been vomiting, has appeared to be inpain with movement, and has even had intermittent confusion during the night. She hasdeveloped a headache of moderate intensity that is diffuse, radiating to her neck, andworsens with movement. She does not have any photophobia or dizziness, and she has not

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A Body-Wide Rash With Myalgia, Stiffness, Vomiting,and ConfusionLuis Soler, MD, Research, 11:57AM Mar 11, 2013

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experienced any seizures. She denies having any subjective fevers, abdominal pain,hematemesis, or diarrhea. She has not had any urinary complaints or low back pain. Shedenies having cough or shortness of breath. The patient's past medical history is onlyremarkable for trauma that occurred 3 months ago and resulted in rib fractures and bluntabdominal trauma. At that time, she underwent an exploratory laparotomy, with suture repairof liver lacerations and a right kidney laceration; she has been doing well since then. Thepatient does not have any chronic medical conditions and does not take any regularmedications. She smokes cigarettes but denies heavy alcohol use or illicit drug use.

On physical examination, she appears drowsy and uncomfortable. Her oral temperature is100.9°F (38.3°C). She is tachycardic and hypotensive, with a heart rate of 120 beats/min anda blood pressure of 80/60 mm Hg. Her respiratory rate and oxygen saturation are normal (at16 breaths/min and 99% while breathing room air, respectively). She grimaces in pain withmovement of the joints, particularly with movement of her neck, which is limited. Her pupilsare 3 mm and equally reactive. Her neurologic examination, including a cranial nerveinspection, is normal (except for her drowsy mental status). She has a nonpainful purpuricrash on her arms, trunk, and face consisting of patchy macules approximately 1-4 cm indiameter (see Figures 1 and 2). There is no cervical, axillary, or inguinal lymphadenopathy.Her lungs are clear and her heart sounds are normal, without any murmurs or gallops. Shehas a soft and nontender abdomen, with no splenomegaly. There is no midline spinaltenderness or costovertebral angle tenderness. There is no evidence of joint involvement, andno tenderness or swelling are noted. The remainder of the examination is unremarkable.

Laboratory studies show an elevated white blood cell (WBC) count of 17.6 × 103/µL (17.6 ×

109/L), a hemoglobin of 13.6 g/dL (136 g/L), and a platelet count of 54 × 103/µL (54 × 109/L).Her creatinine is 3.3 mg/dL (291.7 µmol/L) and her blood urea nitrogen (BUN) is 57 mg/dL(20.4 mmol/L). The electrolyte concentrations and hepatic studies are normal. The patient'smyoglobin and creatine kinase concentrations are elevated at 332 µg/L and 149 U/L (149units/L), respectively. The C-reactive protein (CRP) is high at 22 mg/dL. Her partialthromboplastin time (PTT) is elevated at >120 seconds, with an international normalized ratio(INR) of 2.14. The d-dimer is markedly elevated at >10 µg/mL (10 mg/L). Her serumpregnancy test is negative. An arterial blood gas shows a pH of 7.3, a lactate of 64.9 mg/dL(7.2 mmol/L), a partial pressure of carbon dioxide (pCO2) of 35.4 mm Hg, a partial pressure

of oxygen (pO2) of 318 mm Hg, and an oxygen saturation of 99.3% while using an oxygen

mask at 10 L/min. Blood cultures are drawn and sent to the laboratory.

What is the diagnosis? How would you approach this patient's treatment?

Our thanks are extended to Andrea Bianchin, MD, and Moreno Agostini, MD, for providing

the details of this case, and to Adam Perrin, MD, for reviewing this content.

See comment #47 for the diagnosis and a discussion of this condition.

More case studies, including discussions of the recognition, pathophysiology, epidemiology,and management of the featured conditions, can be foundhere: http://reference.medscape.com/index/section_10218_0.

Would you like to see more interesting and educational clinical images? Have a look at themany slideshows available from Medscapehere: http://www.medscape.com/features/slideshow.

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48 Comments

#1, Added By: chagai, MD, Family Medicine, 02:08PM Mar 11, 2013

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Number one:What her L.P. is showing.? This is meningococemia,unless proven else.

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#2, Added By: celso_miranda01, Medical Student, 03:14PM Mar 11, 2013

Meningococemia

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#3, Added By: dr.naseer84, Physician Assistant, 03:15PM Mar 11, 2013

TTP v/s HSP

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#4, Added By: mikelo90, Medical Student, 03:17PM Mar 11, 2013

Meningococcemia. Use ceftriaxone.

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#5, Added By: abirkaddar, MD, Oncology, Hematology/Oncology, 03:30PM Mar 11, 2013

DIC (septic shock) plasma transfusion Platelet transfusion if less than 50× 103/µL wide specctrum antibiotics

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#6, Added By: mikelamb777, Medical Student, 04:41PM Mar 11, 2013

Stevens-Johnson Syndrome or Meningococcemia Mimicking Stevens-Johnson Syndrome

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#7, Added By: korakot, Medical Student, 10:55PM Mar 11, 2013

auto immune disease flare

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#8, Added By: Hafomed, Medical Student, 11:20PM Mar 11, 2013

Steven Jhonson Syndrome--vs-- Bacterial Meningitis

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#9, Added By: kohatian3659, MD, Surgery, General, 12:52PM Mar 13, 2013

waterhouse friedrickson syndrome

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#10, Added By: skessdtrek, MD, Family Medicine, 07:44PM Mar 13, 2013

Looks/sounds like meningitis to me, likely meningococcal. 1st step is to get an LP (unlessit would delay antibiotic) then start antibiotic, broad spectrum that includes other possiblebacterial pathogens in coverage. Given the septic shock (renal failure, hypotensive,tachycardic in setting of infection) needs massive fluid support to start, might need platelettransfusion. May need FFP/Vit K unless supportive treatment reverses liver function withelevated INR. Assuming diagnosis is correct (which is most likely in my opinion) closecontacts will need antibiotic prophylaxis.

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#11, Added By: prv2003, Medical Student, 03:13PM Mar 19, 2013

Meningococcal septic shock as characterized by the rash. She is in DIC. Fluidresuscitation following Early Goal Directed Therapy, empiric ceftriaxone, CT head +lumbar puncture. Coagulopathy correction is also paramount....

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#12, Added By: marco.oderda, MD, Urology, 03:17PM Mar 19, 2013

It seems meningococcal meningitis to me

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#13, Added By: csctgate, MD, Ob/Gyn & Women's Health, 03:24PM Mar 19, 2013

allergic problems???it should be considered after looking for infection....

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#14, Added By: Tkay10, Medical Student, 03:26PM Mar 19, 2013

Meningococcemia

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#15, Added By: aniospic, Medical Student, 03:51PM Mar 19, 2013

Meningococcemia con meningoencefalitis, complicaciones asociadas: coagulacionintravascular diseminada (por px de inhibodor del activador del plasminogeno, por ellotiempos prolongados y trombocitopenia), purpura fulminans, compromiso suprarrenal(sindrome de Waterhouse friderichsen - hemorragias multiples causales del choque), fallarenal asociada. PLAN soportes, penicilina cristalina 1mill de unidades hora en infusioncontinua (la ceftriaxona tiene una vida media muy larga, como para esperar a quealcance niveles terapeuticos con la paciente en estas condiciones, asi que aunque labibliografia la mencione no es la mejor opcion). Ana Ospina. Hospital Militar Central. Colombia.

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#16, Added By: benket, Physician Assistant, 04:13PM Mar 19, 2013

Choc septique sur CIVD secondaire à une meningococcémie

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#17, Added By: fazdlinrahim, Medical Student, 04:24PM Mar 19, 2013

TTP

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#18, Added By: chandra.adjodah, Medical Student, 04:34PM Mar 19, 2013

Choc septique méningococcique compliqué d'une CIVD Antibiothérapie : C3G Réanimation avec amine vasopressive

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#19, Added By: yecal12, Medical Student, 04:43PM Mar 19, 2013

Sounds and looks like meningococcemia with secondary DIC. This couldn't be TTP as thiswould not affect PTT (just platelets). This patient needs fluids (LR) via two large bore

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needles, I would probably put in a triple lumen central line as this patient will need heavyduty antibiotics (ceftriaxone, vancomycin, and steroids for meningitis). Before I do this, aLP is in order, realizing that this patient may bleed extensively considering the PTT, INR,and low platelet count. To counter this, I would have some prothrobmin complex and FFPon board (Vit. K down the road as it takes several days to lower INR).

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#20, Added By: lily.aryan, Medical Student, 05:03PM Mar 19, 2013

Meningitis, Glass Test for the rash must be done and a CT and lumbar puncture must beperformed. The CSF must be tested. Once the diagnosis of meningitis is confirmed; wegive her IV Vancomycin and Ceftriaxone.

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#21, Added By: usman.gujjar, Medical Student, 05:29PM Mar 19, 2013

Meningococcemia.

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#22, Added By: edyangelo, MD, General Practice, 06:01PM Mar 19, 2013

Meningitis Meningoccic

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#23, Added By: aussiebooks, Medical Student, 07:35PM Mar 19, 2013

Meningitis

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#24, Added By: dr.gabriello, MD, General Practice, 09:36PM Mar 19, 2013

Choque séptico + Coagulación intravascular diseminada sec. meningococcemia.

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#25, Added By: chanjinei90, Medical Student, 10:40PM Mar 19, 2013

Disseminated Intravascular Coagulation (increased pTT, D-dimer) Septic shock (fever, WBC + hypotension) Since blood culture was sent, start empiric antibiotic treatment. Forward for result of lumbar puncture.

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#26, Added By: Ambra.Abate, Medical Student, 03:58AM Mar 20, 2013

dengue fever, second infection

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#27, Added By: Ambra.Abate, Medical Student, 04:44AM Mar 20, 2013

dengue hemorragic fever or rocky mountain spotted fever

Patients may need a central intravenous line for volume replacement and an arterial linefor accurate blood pressure monitoring and frequent blood tests.

Lumbar puncture : Detection of viral or Rickettsia or meningeal infection genomicsequences serum, or cerebral spinal fluid (CSF) samples via polymerase chain reaction(PCR)

The problem is the development of ipovolemic shock: Intravascular volume deficits should

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be corrected with isotonic fluids such as Ringer lactate solution. Boluses of 10-20 mL/kgshould be given over 20 minutes and may be repeated. If this fails to correct the deficit,the hematocrit value should be determined. If it is rising, limited clinical informationsuggests that a plasma expander may be administered.

wide spectrum antibiotics against opportunistic infections.

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#28, Added By: joseandres1989, Medical Student, 05:53AM Mar 20, 2013

At first I thought Meningitis (Meningoccal), the CRP is high but not very high. I don't know,so:

1)Perform a Rachicentesis, if it is clear put in dd with: Listeria, Borrelia, Leptospira or T.Pallidum, or even virus.

2)Suspect a Moskowitz or PTT, in that case perform a plasma exchange treatment!

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#29, Added By: joseandres1989, Medical Student, 05:55AM Mar 20, 2013

add: Empirical treatment: ampicillina, ceftriaxone and acycolovir in the meantime

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#30, Added By: helber_gonzalo, Medical Student, 11:54AM Mar 20, 2013

meningitis with meningococcemia, bilateral adrenal bleeding treatment: respiratory isolation in ICU, hidric reanimation, penicillin 1000000 unit/hour,ciprofloxacin 500 mg PO x 1 day, hidrocortison 100 mg ev x 1 day then 50 mg ev every 8hours, chemoprofilaxis for her boyfriend.

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#31, Added By: Smferger, Nurse, Emergency Medicine, 01:00PM Mar 20, 2013

meningococemia

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#32, Added By: drsimamoradi, Medical Student, 01:50PM Mar 20, 2013

meningococemia and DIC.

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#33, Added By: aryanzahra, Medical Student, 02:11PM Mar 20, 2013

Meningitis seem to be the answer, P/E, and Hx are in line but I think what was the reason?She had positive Hx of intensive trauma and now presented with these symptoms.Something seems to be wrong with this patient.

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#34, Added By: jw39g11, Medical Student, 03:13PM Mar 20, 2013

No electrolyte abnormalities rules out WFS, would expect hypokalaemia andhypernatraemia. Labs and sudden onset suggest meningococcaaemia over TTP thoughboth diagnoses should be chased. Antibiotics and plasmapharesis to treat.

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#35, Added By: sergio-lato, Medical Student, 04:45PM Mar 20, 2013

Meningitis meningococcica

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Shock séptico Plan: manejo en unidad cuidados intensivos, liquidos IV, penicilina G 24 millones deunidades en infusión continua.

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#36, Added By: pavidi, MD, Surgery, General, 07:57PM Mar 20, 2013

Waterhouse Friderichsen syndrome

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#37, Added By: nadia.castaldo, Medical Student, 08:09AM Mar 21, 2013

Waterhouse-Friderichsen (menincogoccemia)

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#38, Added By: daniel.bentum, Medical Student, 09:42AM Mar 21, 2013

Meningicocemia

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#39, Added By: nysrine.bennouna, Medical Student, 03:00PM Mar 21, 2013

Syndrome de Lyell sur AINS?

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#40, Added By: chrna, Medical Student, 06:20AM Mar 22, 2013

Meningitis with Meningococemia

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#41, Added By: plendor, Medical Student, 12:56AM Mar 23, 2013

autoimmune inflammatory disease ( acute stage), systemic vasculitis ? do a rapid lumbarpuncture for CSF testing against meningoccocal infection , if negative ,giveglucocorticosteriods parenteral. if negetive give broad sprectrum antibiotics first togetherwith fluid replacement, fresh frozen plasma, while checking( hemoculture and sensitivitytest) to specific antibiotics. patient should admited to ICU.

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#42, Added By: 380841854, Medical Student, 11:34AM Mar 23, 2013

dengue fever?

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#43, Added By: zenete, Medical Student, 02:59PM Mar 23, 2013

Waterhouse friderichsen

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#44, Added By: ahmadriaz229, Medical Student, 08:50AM Apr 3, 2013

sle...or meningiccoma

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#47, Added By: Luis Soler, MD, Research, 05:21PM Apr 9, 2013

From Medscape Reference:

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Waterhouse-Friderichsen syndrome is a severe complication of Neisseria meningitidisinfection. N meningitidis is a gram-negative aerobic diplococcus with a particular affinityfor the bloodstream and meninges. Infection with N meningitidis may cause clinicalconditions ranging from fever and bacteremia to life-threatening septic shock. It is acommensal bacterium in many humans that resides in the nasopharynx and colonizes upto 25% of healthy people, without causing illness. It is transmitted by aerosolizedrespiratory particles and secretions. It is not known why some people who carry invasivestrains of the bacteria become ill while others do not. A particular virulence factor may bea cause, but is not fully understood. Crowded living conditions, such as collegedormitories and military barracks, increase the risk of transmission. Other risk factorsinclude smoking and upper respiratory tract infection, as well as systemic diseases suchas multiple myeloma, nephrotic syndrome, or systemic lupus erythematosus. Immunedefects, deficiency of humoral immunity or the complement-mediated immune system,and anatomic or functional asplenia predispose patients to N meningitidis infection.Outbreaks of N meningitidis infection appear to be seasonal, occurring most often inspring and winter. The yearly incidence of the disease is about 1 case per 100,000people.

N meningitidis spreads through the inhalation of respiratory secretions transmitted by acarrier. The onset of symptoms occurs approximately 3-4 days after inoculation. Thepatient typically begins having symptoms of a respiratory illness, followed by fever,headache, and vomiting; this rapidly progresses to the development of mental statuschanges such as lethargy or confusion. Meningeal infection likely results fromhematogenous spread, as N meningitidis can be isolated via blood cultures inapproximately 75% of patients. Meningococcal sepsis with multisystem involvement,however, occurs in only one fifth of cases of meningitis caused by N meningitidis. Themortality rate of meningococcal sepsis is very high; it is even more lethal than isolatedmeningococcal meningitis. Waterhouse-Friderichsen syndrome is 1 of the most severecomplications of meningococcal infection. Although often classified by the presence ofmultiorgan dysfunction in the presence of meningococcal infection, the syndrome is morespecifically defined by the presence of hemorrhage into the adrenal glands.

A typical purpuric rash may be seen as a result of septicemia. This usually first appearson the trunk and lower extremities and subsequently spreads throughout the body surface.The development of purpura fulminans (PF), a life-threatening hemorrhagic conditioncharacterized by hypotension, disseminated intravascular coagulation (DIC), and purpura,indicates a poor prognosis. Although the presence of purpura fulminans is classic formeningococcal infection, multiple causes may be responsible and should also beconsidered. Three general categories of PF are recognized: acute infectious PF,idiopathic PF, and abnormalities of the coagulation system. In fact, the majority of PFcases are caused by coagulation abnormalities. Occasionally, meningococcal infectioncauses only focal disease, such as conjunctivitis, septic arthritis, urethritis, purulentpericarditis, or respiratory tract infection (pneumonia, epiglottitis, and otitis media).

(continued in following comment)

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#48, Added By: Luis Soler, MD, Research, 05:27PM Apr 9, 2013

(continued from previous comment)

The diagnosis of Waterhouse-Friderichsen syndrome (or of meningococcal sepsis ingeneral) must be made early and should be based on the clinical features of fever,purpuric rash, altered mental status, meningeal signs, hypotension, and septic shock.Specific testing should be used for confirmation and for guiding subsequent treatment, butit should not delay the initiation of therapy. An effort should be made to obtain bloodcultures before administering antibiotics to the patient. The results are not typicallyavailable for 12-24 hours; however, they may guide subsequent therapy. A lumbarpuncture should be performed early in the course of treatment, but it should not delay theadministration of antibiotics. Cerebrospinal fluid (CSF) analysis should include a cell countand differential, culture, Gram stain, and protein and glucose concentrations. Thepresence of meningitis is identified by leukocytosis with polymorphonuclearpredominance, an elevated protein concentration, and a low glucose concentration. Gram

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stains are often negative in meningitis. Cultures may also be obtained from synovial,pleural, or pericardial fluid, if appropriate. Methods for identifying meningococcus otherthan culture are available, such as antigen detection from biological fluids. This method israpid and can provide an exact identification of the serogroup, but it commonly producesfalse-negative results. A polymerase chain reaction (PCR) can also identify specificserogroups and does not require the presence of a live organism.

Without prompt treatment, the mortality rate of Waterhouse-Friderichsen syndromeapproaches 100%. Even with rapid and optimal medical therapy, approximately 40% ofpatients with meningococcal sepsis do not survive. When DIC is present, the mortality rateis as high as 90%. The overall mortality of meningococcal disease is 10%-20%, with thesame percentage of survivors having permanent sequelae (eg, loss of a limb, and hearingimpairment).

The most important therapeutic point for meningococcal infection is early administration ofappropriate antibiotics. Empiric antibiotics should be administered whenever there is anysuspicion of meningococcal infection because delays in therapy expose patients to highrisk of permanent disability, or death. Common antimicrobial agents are active againstNeisseria species. Penicillin G is usually the first-line antibiotic therapy, and it has a lowprevalence of resistance. In areas where penicillin-resistant strains have been identified,such as the United Kingdom or Spain, a third-generation cephalosporin can be usedinstead. Initial treatment with broad-spectrum antibiotics is recommended in any septicpatient, as antibiotic treatment can later be changed once a specific organism isidentified. Early goal-directed therapy should be initiated, with a particular focus on fluidadministration and maintenance of an adequate blood pressure. The efficacy ofcorticosteroid treatment is controversial, but it is typically recommended in cases of sepsisand meningitis. Debridement of skin and subcutaneous tissues, with subsequent skingrafting and/or limb amputation, may be necessary if septicemia results in peripheralhypoperfusion with skin and bone necrosis. In cases of fulminant meningococcemia,patients should be immediately transferred to an intensive care unit (ICU) for aggressivefluid therapy, vasopressor support, and intensive hemodynamic monitoring. Activatedprotein C may be of use in a very limited number of patients. Treatment of DIC includesthe administration of fresh frozen plasma. Additional treatments currently underinvestigation include monoclonal antibodies to inflammatory mediators, such asendotoxins, tumor necrosis factor, interleukins, and interferon-gamma.

(continued in following comment)

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#49, Added By: Luis Soler, MD, Research, 05:33PM Apr 9, 2013

(continued from previous comment)

All persons who have been in close contact with a patient with meningococcal infectionare at an elevated risk for contracting the disease. The spread of meningococci occursvia respiratory secretions, and it is quite easily transmitted to close contacts. For thisreason, all household members, classmates, medical staff, or anyone else recentlyassociated with the patient must be considered at risk for acquiring the disease. Theprobability of transmission varies with the duration and closeness of exposure; it is highestduring the first few days following the onset of disease. The risk of transmission is higherwith actions that result in direct exposure of secretions to mucous membranes, includingkissing; mouth-to-mouth resuscitation; and sharing of food, glasses, bottles, or cigarettes.People who have stayed more than 8 hours in close proximity to an infected patient or whohave had direct contact with a patient's secretions within 1 week before the onset ofsymptoms should receive prophylactic treatment. Chemoprophylaxis should be given assoon as possible, as the efficacy of prophylaxis is very low if antibiotics are not startedwithin 10-14 days after exposure. Cultures of oropharyngeal or nasopharyngeal tissue arenot useful for determining whether or not antibiotics are necessary, and waiting for theresults of these examinations can cause an inappropriate delay in the administration ofprophylactic treatment. Rifampin, ciprofloxacin, or ceftriaxone are all effective choices.The duration of chemoprophylaxis should be 1-2 days, depending on the antibiotic used.Ciprofloxacin and ceftriaxone require a single dose treatment, and rifampin may be giventwice daily for 4 doses.

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A vaccine has long been available for preventing outbreaks of N meningitidis. Thisquadrivalent polysaccharide vaccine is protective against all serogoups except B.Immunization with meningococcal conjugate vaccines is officially part of theRecommended Immunization Schedule for Persons Age 0 Through 18 Years as issued bythe Centers for Disease Control and Prevention.

The patient in this case was admitted to the ICU after early initiation of intravenousceftriaxone. The patient's blood cultures grew serogroup C N meningitidis. A few hoursafter admission, petechial lesions appeared and rapidly spread throughout her trunk, legs,back, and face. The lesions became progressively larger and hemorrhagic. Aggressivefluid therapy, vasopressor support, fresh frozen plasma, and activated protein C therapywere given. She required mechanical ventilation after developing acute respiratory failure.Renal failure soon followed and dialysis was initiated. Her hands and feet becameincreasingly cyanotic. Despite aggressive therapy, multiple organ dysfunction and DICprogressed; the patient died 4 days after admission. The post-mortem examinationconfirmed meningococcal sepsis and revealed acute purulent meningitis, adrenalapoplexy, thrombotic microangiopathy, purpura confluens, and epidermolysis bullosa;these findings are consistent with a diagnosis of Waterhouse-Friderichsen syndrome.

For more information, see the Medscape Reference article 'Meningococcemia'(http://emedicine.medscape.com/article/221473-overview).

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#50, Added By: Shjackson, Other, 01:40PM May 4, 2014

This appears to be a Staphylococcus Monoclonal Skin rash. I have studied and Researched various areas of skin diseases at site of infections. Thisalso, displays a Biochemical Immunological reaction extracted from MRSA. Clinicaloutcomes for Echinocandin Antifungals Compounds should be given to prevent Fungi Moldgrowth. Shjackson CRC, Certified Research Coordinator

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