WATERHOUSE-FRIDERICHSEN SYNDROME IN AN ADULT PATIENT WITH MENINGOCOCCAL MENINGITIS
Description
● Introduction:
➣Meningococcal infection is still a major source of morbidity and death even with the advent of better antibiotics. It can manifest as meningitis, meningitis with antibiotics.
septic shock, or meningococcemia.
➣A uncommon yet serious consequence, Waterhouse-Friderichsen syndrome (WFS) is caused by a meningococcal infection and shock from bilateral adrenal haemorrhage.
➣ The reported instance included a male adult who died.
● Case Study:
➣ Patient: male, age 29.
➣History:
• Severe fever, chills, and vomiting for seven days.
• Two days of hemorrhagic rash throughout the trunk and belly.
➣ Examination:
• Feverish, cyanosed, and unstable.
• Shock: BP 70 mmHg, pulse 90/min.
• Meningitis symptoms, or positive Kernig's and Brudzinski's signs.
• Generalised hemorrhagic/purpuric rash, mostly on the trunk and abdomen.
➣Investigations
• CSF: 9400 cells/mm³ (86% polymorphs), protein ↑ (309 mg%), and sugar ↑ (20 mg%).
• Gramme stain: intracellular and extracellular Gram-negative diplococci with pus cells.
Neisseria meningitidis produces transparent colonies on chocolate and blood agar in a CSF culture.
•Adrenal haemorrhage verified by CT scan: a WFS diagnosis.
• Sensitivity: susceptible to TMP-SMX, penicillin, ceftriaxone, and chloramphenicol.
➣ IV ceftriaxone with steroids were used as treatment.
➣Result: On the third day after admission, the patient died after deteriorating and experiencing refractory shock.
●Discussion
➣Epidemiology (Asia/India): Delhi outbreaks (1966–1985).
• 2005 outbreak: 429 cases, primarily in young adults aged 16 to 30; young adults died at the greatest rate.
➣Rash and WFS pathogenesis:
• Rashes are characteristic because they are caused by endothelial injury, vasculitis, and microthrombi.
•Initiated by neutrophil activation (Sanarelli–Schwartzman response), cytokines, and meningococcal endotoxin.
Adrenal haemorrhage (WFS) is caused by both overwhelming sepsis and DIC.
➣Diagnosis:
• Gramme stain = quick and practical.
• Culture is the gold standard (blood, CSF, and skin lesions).
• In this instance, blood was not tested, but CSF was positive.
➣ Microbiology in India:
• Many isolates are resistant to ciprofloxacin;
• Current case isolate: susceptible to all medications;
• Usually sensitive to ampicillin, ceftriaxone, and penicillin.
●Discussion
➣Epidemiology (Asia/India): Delhi outbreaks (1966–1985).
• 2005 outbreak: 429 cases, primarily in young adults aged 16 to 30; young adults died at the greatest rate.
➣Rash and WFS pathogenesis:
• Rashes are characteristic because they are caused by endothelial injury, vasculitis, and microthrombi.
•Initiated by neutrophil activation (Sanarelli–Schwartzman response), cytokines, and meningococcal endotoxin.
Adrenal haemorrhage (WFS) is caused by both overwhelming sepsis and DIC.
➣Diagnosis:
• Gramme stain = quick and practical.
• Culture is the gold standard (blood, CSF, and skin lesions).
• In this instance, blood was not tested, but CSF was positive.
➣ Microbiology in India:
• Many isolates are resistant to ciprofloxacin;
• Current case isolate: susceptible to all medications;
• Usually sensitive to ampicillin, ceftriaxone, and penicillin.
●Discussion
➣Epidemiology (Asia/India): Delhi outbreaks (1966–1985).
• 2005 outbreak: 429 cases, primarily in young adults aged 16 to 30; young adults died at the greatest rate.
➣Rash and WFS pathogenesis:
• Rashes are characteristic because they are caused by endothelial injury, vasculitis, and microthrombi.
•Initiated by neutrophil activation (Sanarelli–Schwartzman response), cytokines, and meningococcal endotoxin.
Adrenal haemorrhage (WFS) is caused by both overwhelming sepsis and DIC.
➣Diagnosis:
• Gramme stain = quick and practical.
• Culture is the gold standard (blood, CSF, and skin lesions).
• In this instance, blood was not tested, but CSF was positive.
➣ Microbiology in India:
• Many isolates are resistant to ciprofloxacin;
• Current case isolate: susceptible to all medications;
• Usually sensitive to ampicillin, ceftriaxone, and penicillin.
●Discussion
➣Epidemiology (Asia/India): Delhi outbreaks (1966–1985).
• 2005 outbreak: 429 cases, primarily in young adults aged 16 to 30; young adults died at the greatest rate.
➣Rash and WFS pathogenesis: • Rashes are characteristic because they are caused by endothelial injury, vasculitis, and microthrombi.
•Initiated by neutrophil activation (Sanarelli–Schwartzman response), cytokines, and meningococcal endotoxin.
Adrenal haemorrhage (WFS) is caused by both overwhelming sepsis and DIC.
➣Diagnosis: Gramme stain = quick and practical.
• Culture is the gold standard (blood, CSF, and skin lesions).
• In this instance, blood was not tested, but CSF was positive.
➣ Microbiology in India:
• Many isolates are resistant to ciprofloxacin;
• Current case isolate: susceptible to all medications;
• Usually sensitive to ampicillin, ceftriaxone, and penicillin.
➣ Antibiotics and sensitivity notwithstanding, mortality from shock or adrenal failure results.
➣History: Rupert Waterhouse wrote the first description in 1911.
Fever, purpuric rash, DIC, coagulopathy, and shock are among the symptoms.
➣Etiology:
• Mostly N. meningitidis, but also S. pneumoniae, group A strep, S. aureus, N. gonorrhoeae, E. coli, H. influenzae, Klebsiella, and Pasteurella.
• Noninfectious reasons include trauma, antiphospholipid syndrome, anticoagulants, and post-adrenal haemorrhage.
➣Prognosis: Overall mortality of about 20%.
Up to 50% of patients die if they are in shock.
Protocol
●Management & Key Takeaways:
➣Delayed diagnosis of WFS results in a significant death rate.
➣ Antibiotic treatment: Ceftriaxone and penicillin work well; begin right away.
• Hydrocortisone 100 mg IV/IM immediately (life-saving) is an example of steroid treatment.
•Dexamethasone can lessen inflammation caused by bacterial lysis before antibiotics are administered.
➣Vasopressors, fluids, and critical care are examples of supportive treatment.
➣Rapid adrenal failure and shock cause a high death rate even with good antibiotics. More instances may go undiagnosed, resulting in an underreported illness.
● Common Issues:
➣ Patients with dermatological disorders such atopic dermatitis and acne vulgaris face many difficulties, such as physical discomfort, mental anguish, and social stigma.
• Prolonged itching and inflammation that damages skin and increases the risk of subsequent infections.
•Depression, anxiety, and sleep difficulties are among the major effects on quality of life.
• The absence of strong standards and standardised procedures for management in environments with limited resources makes diagnosis and follow-up difficult.
● Nursing Interventions: When it comes to managing and improving patient outcomes with dermatological disorders, nursing interventions are essential. The tactics are designed to address long-term management as well as problem mitigation:
➣Evaluation and Surveillance
• A thorough evaluation of the skin to determine the kind, location, severity, and infection risk of a lesion.
• Consistent vital sign and skin integrity monitoring to track the course of the illness and the effectiveness of therapy.
➣Patient education
• includes instruction on how to take care of your skin, how to avoid triggers (such as harsh cleansers), and how important it is to take your medications as prescribed.
• Training on topical application methods and subsequent infection warning indicators.
➣Psychosocial Support
•Counseling to minimise anxiety and stigma and help patients cope with the psychological impact of chronic skin conditions.
• Facilitating family support or support groups to promote continued care and mental health.
➣ Administration of Medicines
• Administer systemic or topical medications as directed, including retinoids, corticosteroids, antibiotics, and antihistamines; keep an eye out for adverse effects.
•Keeping an eye out for drug side effects and assisting with timely medical intervention as necessary.
➣ Symptom Management
• Using comfort measures, such as cold compresses, to ease discomfort and itching.
• When necessary, use sedatives as directed to ease pain and, in extreme situations, lower intracranial pressure.
➣ Changes to the Environment and Lifestyle
• Advice on modifying the environment to lessen dermatitis flare-ups, such as avoiding allergens and controlling humidity.
• Promotion of lifestyle modifications, such as stress reduction, regular exercise, and dietary guidance.
➣Continuous Monitoring
• Arranged follow-up appointments for ongoing monitoring of side effects and evaluation of treatment effectiveness, particularly with extended use of corticosteroids.
• Keeping records to track the progression of the disease and its response to therapy over time.
➣ Management Difficulties and Their Resolutions
• Accurate diagnosis is challenging since skin disorders might show differently.
Individualised care, education, and ongoing support are the main goals of nursing management in order to meet both medical symptoms and psychological needs.
•Working with interdisciplinary teams to provide complete treatment and, where necessary, send moderate-to-severe patients to dermatological experts.
Notes
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