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Meningowhatal? … Meningococcal disease in the emergency department
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Meningowhatal? ... Meningococcal Disease in the Emergency Department
Donna Malone), Clinical Nurse Specialist, Emergency Department Wyong Hospital, Central Coast NSWAustralia ABSTRACT
The unpredictable environment of an emergency department can often seem daunting to the newly experienced emergency nurse - a role I felt I was "mastering" very well with 18 months experience up my sleeve. The year was 2001 and I was nearing the end of my Graduate Certificate in Emergency Nursing, pleased with the rate to which I was acquiring knowledge and my skill of applying it to practice. I felt confident in the fact that I could assess and prioritise the care of patients at triage, recognise the patient experiencing an acute myocardial infarct, interpret a electrocardiograph, put in a intravenous cannula and efficiently perform in the resuscitation room as part of the trauma team, just to name a few. However, lurking in the subconsciousness of my mind was a disease that I recall I had heard the name of, listened to the lectures on the topic, and knew that it was a disease that had been highlighted recently in the press and which most people feared they may contract. Nothing however prepared me for the day that I came face to face with the deadly disease whilst caring for a patient. The aim of this experiential paper is to discuss the epidemiology of meningococcal disease in Australia and in particular the Central Coast of New South Wales (NSW), its modes of transmission and describe the associated signs and symptoms. The investigations used to diagnose the disease and the subsequent treatment and management will also be discussed. Finally, prevention techniques through the use of chemoprophylaxis and vaccination will be addressed. KEY WORDS Meningococcal, Meningitis, Meningococcaemia, Neisseria Meningitidis, Petechiae, Rash, DIC
Introduction
Why meningococcaldisease? In order to set the scene, I will outline my day as a new staffmember within an emergencydepartment on the central coast of NSW. The staffing that day consisted of a senior in charge registered nurse (myself, with 18 months emergency experience) and one junior triage nurse. The day commencedwith a paediatric pedestrian hit by a car travelling at high speed, the incidentwitnessed by his brother and the occupants of a school bus. The management of this patient consisted of bilateral chest drains, CPR, defibrillation and multiple other resuscitative adjuncts, however, some 40 minutes later the child was pronounced dead. After cleaning the patient, dealing with the parents and siblings, hearing the mothers distinct shrieking cry (a sound that I knew would linger in my ears for a long time to come), we headed off for a debriefing session. The next patient to be placed on the resuscitation bed was a teenage girl brought in by ambulance at 1300hrs following a collapse at home, although her Glascow Coma Score on arrival what 15. The ambulance officers state that she was discovered by her family unconscious, with a spotted bluish rash on her legs. There was no previous history of disease, no evidence of drug ingestion and she had been healthy and active although she had woken that morning feeling unwell with flu like symptoms of headache, sore throat, temperature and vomiting. A short time after arrival her condition deteriorated rapidly and the speed at which it did so surprised me beyond belief. She became confused, restless and agitated, crying due to excruciating leg and joint pain and for the fear of death, constantly asking "Nurse, am I dying?" The rash spread in front of my eyes and she developed acute respiratory distress
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syndrome (ARDS), was intubated and transported to the Intensive Care Unit (ICU) of a larger hospital at 1430hrs. This true scenario typifies the presentation and rapid progression of meningococcal disease. From this day I became aware that my knowledge of meningococcal disease was no more than that of the lay person, I had no idea of the pathophysiology of the disease, its mode of transmission, the recommended treatment and management of the disease, nor the chemoprophylaxis. As a registered nurse I felt my input into the resuscitation, and being able to anticipate future needs could have been greatly enhanced had I understood the physiological basis of the disease. I was much more disturbed by this patient than the tragic death of the child which occurred a few hours earlier. I was paranoid about contracting the disease myself due to a messy intubation and as a result required chemoprophylaxis. This time there was no debriefing, the "witching hour" had arrived, and at the end of the shift we all headed offto the pub.
What Is Meningococcal Disease? Neisseria Meningitidisis an invasivebacterium responsible for meningococcal disease. Meningococcal disease includes two patterns of illness, meningitis or
septicaemia (meningococcaemia), or a combination of both (Bowler, 1998). Infectionwith Neisseriamem'ngitidis most frequently presents as meningococcaemia which may progress rapidly to overwhelming shock (Waterhouse-Friderichsen syndrome) (Rosen et al, 1999). The most characteristic feature of the disease is the non-blanching petechial rash which often starts as clusters of pinpoint spots at the axillae, wrists and ankles, progressing rapidly to any body part. The face, palms of the hands and soles of the feet are less affected. As the disease progresses these dusters go on to form larger petechial spots and eventually maylead to purpura fulminans, the severest form of the disease, evidenced by large ecchymotic lesions. Neisseria meningitidis has 13 serogroups consisting of A, B, C, D, 29E, H, I, K, L, W135, X, Y and Z. Serogroups B and C are responsible for more than 90% of meningo-coccal disease in Australia (Leaver, 1998; CDNA, 2001).
Australian Incidence The incidence of meningococcal disease varies from 1 to 3/100,000 in Australia (Kumar, 2000). Highest incident rates occur during winter and early spring. Seasonal influence is thought to be related to an increase in indoor activities, which increases overcrowding, poor ventilation and close personal
Table 1. Yearly incidence of meningococcal notifications in Australia, NSW and the Central Coast from 1991 to 2002 800
700 Total Cases •
600
621
NSW
• ~' Central Coast 500
424•J
400 E
~-337 3OO
380
383
1994
1995
496
481
1997
1998
~ " ~ 8 0 304
200
1O0
0-~ 1991
1992
1993
1996
1999
2000
2001
Year
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contact. It can occur at any age, but is mostly seen in children and young adults (NSW Health, 2000a). A higher proportion of serogroup B disease occurs in children younger than two years, whereas serogroup C disease is relatively more common in older children, adolescents and adults. Across Australia there are on average 460 notifications per year, with almost half of these occurring in NSW and approximately 10 cases per year on the Central Coast, the area this author lives and works (CCAHS Public Health Unit, 2000). Most of these cases are reportedly unrelated. It is important to bear in mind that the true incidence ofmeningococcal disease is not known, as in NSW under reporting has been estimated at between 20 and 55% (Patel, 1997) and similar results could be expected in other states and territories. Table 1 highlights the yearlyincidenceofmeningococcal notifications in Australia, NSW and the Central Coast from 1991 to July 2001 (Central Coast Public Health Unit, 2000 and CDNA, 2001).
Modes of Transmission The Neisseria rneningitidis bacteria are passed from person to person through prolonged close contact and transmitted via airborne droplets such as coughing and sneezing, oral secretions such as sharing drinks or kissing (Delrosa, 1999). The nasopharynx is the natural reservoir (Smillova andWalker, 2000) and the organism is unique only to humans (Pierson, 1997). Even if bacteria are passed to another person, very few will develop the invasive disease. Carriage rates have been estimated to be as high as 25 % of the population without any manifestation of the disease in these carriers, and this aids in natural immunity (Leaver, 1998). The mechanism for invasive meningococcal disease is thought to be transport of the bacteria across the mucosal cells of the nasopharynx within phagocytic vacuoles (Smillova and Walker, 2000). The incubation period from initial infection to dissemination via the bloodstream ranges from two to ten days. In the vascular compartment the invading meningococci may
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be killed by the combined actions of serum antibodies, complement and phagocytic cells, or may multiply, initiating the bacteraemic stage (Solberg, 1998). It is at this stage that the related disease may be termed meningococcaemia. In meningococcal meningitis, bacteria are localised primarily to the meningeal compartment, whereas in meningococcaemia, the bacteria and their products are found primarily in the systemic circulation (Smillova and Walker, 2000).
Signs and Symptoms There are a multitude of signs and symptoms that are indicative ofmeningococcal disease - fever, vomiting, headache, decreased oral intake, to name a few. The problem being that these presentations to the ED especially among the paediatric population are so frequent. So how are we to know which person has the potentially fatal disease? While fulminant meningococcal disease with the distinct rash is not difficult to miss, it is the hidden disease lurking behind the runny nose or headache that is of concern. It has been well documented that the key in surviving this disease is prompt recognition of the signs and symptoms and early treatment. It is therefore imperative that registered nurses are able to recognise these signs in addition to the history and our level of suspicion, as we are the first line of contact. More importantly, we have the responsibility of triaging these patients which ultimately results in the time they wait to see a medical practitioner. It is also important to be aware of the importance of reassessment as meningococcal disease can progress at avery rapid rate. Smillova and Walker (2000) document the signs and symptoms ofmeningococcaldiseaseinto two categories: onset and progression. The onset phase is usually abrupt without specific signs or symptoms. It has been documented that signs and symptoms of upper respiratory tract infection may be present several days prior to presentation, such as a cough, runny nose and lethargy (Smillova and Walker, 2000). It is thought that this is the incubation period.
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The next phase, progression, is thought to be when the bacteria are transported across the mucosal cells of the nasopharynx within phagocytic vacuoles as described earlier (Smillova and Walker, 2000). Once the bacteria are in the blood, signs and symptoms of fever, vomiting, diarrhoea, headache, drowsiness, abdominal pain, cold extremities and petechial rash may occur. This infection in its fulminant form eventually leads to the clinical signs of shock. The signs shown during this stage may include seizures, tachycardia, hypotension, decreased cardiac output, leftventricular failure,vasomotor collapse, and later coagulopathy, disseminated intravascular coagulation (DIC), respiratory and/or metabolic failure and ARDS. Obviously, if we can recognise the early signs and symptoms and commence treatment it may delay or prevent the progression to the worst form of meningococcal disease. When the worst form of the disease develops, fulminant meningococcaemia, patients experience signs of clinical shock which may rapidly progress to hemodynamic collapse, DIC and multisystem failure (Smillova and Walker, 2000). The distinct rash involving the flanks, wrists and ankles is present in 75% of patients with the fulminant form. Widespread eruptions of the purpuric ecchymoses or tiny red/purple pinprick spots suggest fulminating disease. These can develop to look like fresh bruises or blotches on the skin. This rash will not normally disappear when pressed, and is a distinct sign of meningococcal disease (Delrosa, 1999). Figure 1, Figure 2 and Figure 3 demonstrate the three types of petechial rash characteristic of this disease. In 40-60% of cases, death is due to circulatory collapse caused by intravascularvolumedepletion, capillaryleak,vasodilation and myocardial failure (Smillova and Walker, 2000).
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Figure 1. Example of Purpura Fulminans (AENJ, 34:1997)
Figure 2. Typical petichial rash (AENJ, 35:1997)
Pathophysiology Understanding the pathophysiology behind the signs and symptoms can be complex. SmiUova and Walker (2000) and Mehta and Levin (2000) explain that meningococcaemia is a result of interplay between microbial products and host mediator systems. Microbial products include the lipid A component and
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Figure 3. cluster of petichial lesions (AENJ, 35:1997)
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gram-negative lipopolysaccharides. Host factors include complement, kinin, coagulation systems and factors released from stimulated cells. Once the Neisseria meningitidis bacteria invade beyond the nasopharynx and are not adequately contained by the immune response, they multiply and release endotoxin (lipopolysaccharide). The circulating endotoxin triggers a cascade of events, resulting in altered immune response, circulatory collapseand DIC. Lipopolysaccharide activates complement via the alternative pathway resulting in vasodilation, loss of vasomotor tone and capillary leak which is the cause of the purpuric rash. As a result of capillary leak, hypotension and tachycardia occur. The lipopolysaccharides go onto cause more havoc, binding to certain proteins. The complex interacts with monocytes, macrophages and neutrophils, stimulating these cells to release cytotoxic enzymes, cytokines and inflammatory mediators. Cytokines alter the normal functioning oflymphocytes and neutrophils and as a result cause endothelial injury resulting in further loss of vasomotor tone, induce myocardial dysfunction resulting in circulatory collapse, stimulation of the extrinsic coagulation pathway, contribute to the procoagulant state and activation of the fibrinolytic and kinin systems. Activation of the kinin system leads to the release ofbradykinin, causing vasodilation, increased vascular permeability, smooth muscle contractions, pain and increased gastrointestinal motility (Smillova and Walker, 2000). It is for this reason that many patients with meningococcal disease complain of excruciating joint and limb pain. The pathophysiology behind the altered immune response as outlined is by no means complete, as it is an intensely complex system. It does however provide a moderate scope in understanding the pathophysiology of the disease and the resulting signs and symptoms.
Diagnostic Investigations Establishing a diagnosis for meningococcal disease is not always easy. Kumar (2000) states that the diagnosis of meningococcal disease is based on a high index of
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suspicion in the initial stages. Cultures from the cerebrospinal fluid (CSF) or blood generally take more than 24 hours, and with such rapid progression of meningococcal disease it would be too late to wait for positive cultures before commencing antibiotics. Once the rash appears however it cannot be missed. Kumar (2000) also states diagnosis can be confirmed by a positive blood culture and/or a positive lumbar puncture, however, McCormack (1998) notes that when CSF is used it is useful in the diagnosis of bacterial meningitis but is not specific for meningococci. Schaad (1998) however, states that the importance of lumbar puncture should be stressed, and withheld only in patients with signs of raised intracranial pressure, cardiorespiratory compromise,coagulopathy, or infection at the site of lumbar puncture. Various antigen tests are widely used (latex agglutination, co-agglutination and countercurrent immunoelectrophoresis), but all have a false negativity rate of up to 50%. Gram-staining and culture of skin lesions, aspirates or biopsies are advocated by some clinicians, but these procedures are not widely used (McCormack, 1998). Isolation of the meningococci from the nasopharynx alone is not diagnostic, because as previously mentioned, carriage rates can be as high as 25% in some areas (Kumar, 2000). In essence, as aptly stated by Kumar (2000), "although there are many ways of confirming the diagnosis, it is always better to over-treat than to under-treat in these circumstances, because treatment can always be stopped if the results are negative". The recommendations are that the diagnosis of meningococcal disease be made on the basis of the clinical picture. Antibiotics must be commenced if there is reasonable suspicion and after the drawing of blood cultures, diagnosis can be confirmed at a later time when results return. Cultures may also be taken of skin lesions if present, depending on the treating doctor's preference (Reed, 2001).
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Treatment
Meningococcal disease can be highly unpredictable and the associated morbidity and mortality devastatingly high. It is for this reason that Solberg (1998) states that all patients with invasive meningococcal infection, whatever their clinical condition, should be observed for 48hours, with monitoring of blood pressure, pulse, perfusion, urine output, and core and peripheral temperature. Many patients will deteriorate within hours with the development of severe shock and profound DIC. Patients however may have already reached this stage when they arrive at the ED and require urgent intervention. Initial assessment must commence with the ABC's. Careful attention to the airway, breathing and circulation is essential. Assessment of whether the patient can protect their own airway is the first priority. Smillova and Walker (2000) advocate early endotracheal intubation stating that "even in patients who are alert and breathing adequately, early intubation ensures a patent airway, reduces the work of breathing, and allows continued oxygenation, ventilation and improved cerebral perfusion." Assessment of breathing follows. The primary pulmonary feature in meningococcaemiais pulmonary oedema caused by capillary leak. Patients experience increased work of breathing and decreased pulmonary compliance and often develop ARDS. Assessment of arterial blood gases (ABG), respiratory effort and oxygen saturation monitoring will determine respiratory function. Supplementary oxygen therapy should be commenced if the patient is not ventilated. Circulatory support involves fluid resuscitation after intravenous (IV) access is obtained by insertion of two large bore cannulae. Blood cultures should be obtained and urgent administration of antibiotics commenced. Venous access is often difficult due to the shocked state. Intraosseous access may be used in children to avoid delay in volume resuscitation. Strategies to reverse circulatory failure as a result of the severe capillary leak
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and myocardial dysfunction include optimising preload, decreasing afterload and improving myocardial contractility (Solberg, 1998). Fluid resuscitation together with inotropic support with dobutamine should be started immediately and titrated accordingly to reverse this failure. Solberg (1998) states that in the adult patient with marked tissue oedema eight to ten litres of fluid may be necessary during the first 24 hour period. Colloids are initially used to fill the intravascular compartment. The effectiveness of fluid resuscitation can be assessedby monitoring heart rate, blood pressure, central venous pressure, urine output and metabolic status (Mehta and Levin, 2000). Peripheral indicators such as capillary refill may also offer guidance. Patients with severe meningococcaemia require close monitoring of serum electrolytes, acid-base balance and metabolism. Metabolic acidosis results from poor tissue perfusion where there is an increase of lactic acid as a result of tissue hypoxia (Hillman and Bishop, 1996; Mehta and Levin, 2000). Profound metabolic derangements such as hypoglycaemia, hypokalemia, hypomagnesaemia, hypocalcaemia contribute to myocardial dysfunction. The toxic effect ofendotoxin on the myocardium potentiates cardiac demands imposed by intravascular hypovolaemia (Mehta and Levin, 2000). It is therefore essential to monitor for heart failure and arrhythmias. Regular electrocardiographs and careful titration of fluids and inotrope are necessary. Acute renal failure is frequently present, requiring supportive therapy such as dialysis. Dialysis is highly effective in reducing extravascular fluid accumulation and correcting electrolyte and metabolic imbalances and should be commenced early in patients with severe meningococcaemia. While this may not be appropriate in the ED, it is hoped that by this stage the patient will have been transported to ICU. It should also be noted that since meningococcal disease may present simultaneously as meningitis and septicaemia, all patients should be monitored for signs of increased intracranial pressure (Mehta and Levin, 2000).
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Disseminated intravascular coagulation can result in the patient with meningococcaemia as a result of endotoxic shock. There is also evidence ofcoagulopathy and thrombocytopenia. For the treatment of DIC, flesh-frozen plasma (FFP), cryoprecipitate and vitamin K can be administered if the prothrombin time is two to three times above normal or if active bleeding occurs. Platelets are administered if the platelet count is low while packed red blood cells are given to maintain an adequate haemoglobin level to ensure adequate oxygen delivery (Smillova and Walker, 2000).
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Figure 4. Nursing and medical management of patients with meningococcaemia, (adapted from Smillova & Walker, 2000, Figure 4)
Smillova and Walker (2000) and Solberg (1998) document that routine heparinisation of patients with DIC has failed to improve prognosis and is not recommended. However, patients with impending peripheral gangrene and severe coagulopathy, administration of low dose heparin together with FFP may be tried. According to a recent study discussed by Smillova and Walker (2000), heparin may limit thrombosis and necrosis of the digits and extremities. Arguments against the use of heparin are based on the potential for haemorrhage associated with the use of this drug. Steroids have been used in the treatment ofmeningococcaemia, however their effectiveness remains controversial. Smillova and Walker (2000) explain that corticosteroids are used to treat adrenal insufficiency or haemorrhage and for reducing inflammation. They go on to say that while the occurrence of adrenal insufficiency in patients with meningococcaemia is rare, and no evidence supports routine use of steroids in these patients, that because some patients with the infection die of untreated adrenal insufficiency, treatment with corticosteroids might be considered. Singer (2000) however, explains that steroids have been found to improve audiological and neurological outcome and improves the survival from meningococcaemia. Singer (2000) also states that dexamethasone reduces white cell count, tumour necrosis factor and meningeal inflammation in the CSF. Figure 4 from Smillova and Walker (2000) is an excellent guide to the nursing and medical management of patients with meningococcaemia. August 2002, Volume 5 Number 2 - Australian Emergency Nursing Journal
Suspicion of meningococcaemia
Respiratory isolation... obtain specimens of blood and CSFfor culturing Administer antibiotics Transport to intensive care unit (of tertiary care facility if feasible)
Continuous monitoring of vital signs and neurological status... Monitor for shock (depressed mental status, tachycardia, base deficit, delayed capillary refill) Assess airway and acid-base status Administer oxygen Mechanically intubate if indicated Replace fluids
If patient's status has not improved (hypotension, tachycardia, depressed mental status)... Establish central venous access and insert an arterial cannula Start inotropic agents: dopamine and adrenaline Continue fluid replacement Administer fresh-frozen plasma, cryoprecipitate, platelets, vitamin K as indicated for disseminated intravascular coagulation Consider inserting a pulmonary artery catheter
If no improvement in patient's status... Consider treatment with steroids (hydrocortisone 2mg/kg) Consider further inotropic, vasoconstrictor, or vasodilator therapy (milrinone, noradrenaline, nitroprusside)
If no improvement in patient's status... Consider experimental therapy as available Consider heparin therapy for disseminated intravascular coagulation and to limit necrosis of skin, digits and extremities
Administer chemoprophylax~to close contacts within 24 hours
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The role of the nurse in the ED as well as delivering patient care, extends to emotional support to the patient's family. Many families and parents are shocked bywhat has happened, particularly because of the rapid onset of the disease and reactions of other people. Anxiety and fear are associated with any hospital admission and especially when the condition is lifethreatening. The environment is unfamiliar, painful procedures are performed, and the monitoring and equipment can be overwhelming for both the patient and their family. It is important for emergency nurses to keep this in mind, listen carefully to families, explain procedures, the disease process, and prognosis and encourage questions, thoughts and feelings (Smillova and Walker, 2000). Antibiotics Any febrile patient with a petechial rash should be considered to have meningococcal infection and given antibiotics until proven otherwise. Blood cultures should be taken immediately and treatment begun without awaiting confirmation. It has been well documented that early treatment with antibiotics reduces the morbidity and mortality of the disease. In the prehospital setting antibiotics must be commenced and the drug of choice is benzylpenicillin G intramuscularly if unable to give intravenously. In the hospital setting benzylpenicillin G is also the drug of choice for meningococcal disease, but should be given intraveneously (McCormack, 1998; MIMMS 2001).
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Third generation cephalosporins such as ceftriaxone or cefotaxime are given in addition to benzylpenicillin G (MIMMS 2001). Table 2 outlines the recommended doses of these antibiotics for children and adults. The cephalosporins provide coverage for some penicillin-resistant meningococci bacteria and are excellent in penetrating into the cerebral spinal fluid and lack toxicity. Reed (2001) stated treatment with benzylpenicillin G and ceftriaxone is reasonable for any patient suspected of having the disease.Additionally, if unsure or in the event that gram positive cocci are present on staining, vancomycin should be given. Duration of the antibiotic therapy should continue in high doses for seven to ten days (McCormack, 1998), Solberg 0998) adds that these doses should not be tapered over this period. Prevention Chemoprophylaxis Current recommendations for the use of chemoprophylaxis are that household members, day-care centre contacts and persons exposed to the oral secretions, such as performing mouth to mouth or a "messy" intubation of a patient with meningococcaemiashould receive prophylaxis. There is controversy concerning the efficacy ofchemoprophylaxis in preventing further cases of meningococcal disease, however the aim is to reduce the risk of infection to other susceptible individuals (CDNA, 2001).
Table 2. Antibiotics used in the management of meningococcal disease (Adapted from CDNA, 2001) Antibiotic
Prehospital or on admission Antibiotics
Early hospital treatment where N. meningitides is the agent
Benzylpenicillin
< I year: 300mg IV/IM single dose
Child: 60mg/kg (up to 1.8g IV 4 hourly for 7-10 days
I-9 years: 600mg IV/IM single dose Adult or child (10 years or more): 1.2g IV/IM single dose Ceftriaxone
50mg/kg (up to 2g) IV daily (all ages)
Adult: 1.8g IV 4 hourly for 7-I0 days
Child: 100mg/kg (up to 4g) IV daily in 1 or 2 divided doses for 7-10 days Adult: 4g IV daily in 1 or 2 divided for 7-10 days
Cefotaxime
Child: 50mg/kg (up to 2g) IV 6 hourly for 5-7 days Adult: 2g IV 6 hourly for 5-7 days
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Susceptible individuals such as other household contacts exposed to patients with meningococcal disease have an increased risk rate of 500-1,000 times greater of contracting the disease (Mehta and Levin, 2000; McCormack, 1998; Williams, 1999). Conversely, the National Health and Medical Research Council (NHMRC) (1996) state that the only published study to support the use of chemoprophylaxis was an unblinded observational study that failed to reach statistical significance. However, due to ethical objections it would be virtually impossible to conduct such studies now given prophylaxis would need to be withheld from a control group (CDNA, 2001). Although evidence is lacking from randomised trials, there is evidence which suggests microbial clearance of meningococci following the administration of chemoprophylaxis (NHMRC, 1996). There are three antibiotics currently used for chemoprophylaxis ofmeningococcal disease, each has advantages and disadvantages, and each is preferred in specific circumstances. Ceftriaxone
Ceftriaxone is a single intramuscular injection, and is well tolerated with no adverse reactions to note. Ceftriaxone should be dissolved in 1% lignocaine to reduce pain at the injection site. Ceftriaxone is 97% effective in eradicating pharyngeal meningococci from carriers. The recommended doses for chemoprophylaxis are 250mg for adults and 125mg for children younger than 12 years of age. It is recommended that ceftriaxone not be given to infants in their first 4 weeks. Ceftriaxone is the preferred chemoprophylaxis for pregnant women. Further, because compliance is likely to be good and as it is readily available, it should be considered as the preferred agent when required in rural and remote communities, especially in Indigenous communities. Although ceftriaxone is not registered for chemoprophylaxis of meningococcal disease in Australia, it is recommendedby the Meningococcal Disease Guidelines Working Party for that purpose (Benenson, 2000; CDNA, 2001).
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Ciprofloxacin Ciprofloxacin is given as a single oral dose of 500mg, and has been shown to be 97% effective in eradicating pharyngeal meningococci. It is the drug of choice for women on the contraceptive pill, but is recommended it not be given to children or pregnant women (CDNA, 2001; McCormack, 1998). While allergic reactions are very uncommon, they have been reported, and it is for this reason recipients should be observed for 30 minutes post ingestion if possible (Benenson, 2000; CDNA, 2001).
Rifampicin The regime ofrifampicin for those over twelve years of age is 600mg orally every 12 hours for 2 days (McCormack, 1998). It has been shown to eradicate nasopharyngeal meningococci in 75-95% of carriers (Benenson, 2000; CDNA, 2001). Side effects include headache, dizziness, gastrointestinal symptoms and orange discolouration of urine, tears and soft contact lenses (CDNA, 2001;NSW Health, 2000). Rifampicin also interferes with the oral contraceptive pill and is contraindicated in pregnancy, alcoholism and severe liver disease (NHMRC, 1996; Benenson, 2000; CDNA, 2001). Vaccination
Vaccines are available in Australia for four serogroups, A, C, W-135 and Y (Smillova and Walker, 2000) for use in epidemics and high risk populations. Unfortunately no vaccine is effective against serogroup B, which is the predominate serogroup causing sparodic disease in Australia (NHMRC, 1996). The efficacy rate of a single dose of serogroup C vaccine is at least 90% and is recommended to travellers to areas where the disease is epidemic, such as parts of Africa, and also to people with specific health conditions such as splenic dysfunctions (NSW Health, 2000). This vaccine however produces poor immune responses in children less than two years of age who unfortunately comprise the highest risk age-group for meningococcal disease. Serogroup C in particular is poorly immunogenic in young children. Further, it takes at least two weeks to
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induce an optimal immune response even in older people, and does not induce long-term immunity (NHMRC, 1996; Mehta and Levin, 2000). Research is ongoing to develop a vaccine that will be effective against all strains of meningococci, induce long term immunity and be incorporated into a childhood immunisation program (Smillova and Walker, 2000; Mehta and Levin, 2000).
Conclusion Meningococcal disease appears to be on the increase and whilst it presents as an alarming contributor to morbidity and mortality, epidemic disease in Australia has not occured for many years and endemic disease rates remain low (CDNA, 2000). Until a vaccine is developed for all serogroups, successful treatment of the disease depends on early recognition and initiation of antibiotic therapy. Initial signs and symptoms may be non-speciflc, however delays in treatment may have devastating consequences. Knowledge of the cause, progression and current treatment modalities may assist nurses in the early detection and prompt treatment ofmeningococcal disease and thereby, improve patient outcomes. Editors Footnote This paper was submitted and accepted for publication in December 2001. Since that time a new proteinconj ugatedgroup C meningococcalvaccine (Meningitec ®) has been developed. For further information on this vaccine or meningococcal disease please visit the CDNA website at: htrp://www.health.gov.au/pubhlth/cdi/cdna/ press/pr4_Ol.htmor contact the Meningitis Foundation on their 24 hour free phone Australian helpline: 1800 129 068 Meningitis Foundation: (02) 9960 0055. Reference List Abramson, J.S., Baker, C.J., Fisher, M.C., Gerber, M.A., et al (2000) Meningococcal Disease prevention and control strategies for practice-based physicians. Pediatrics, 106, 1500-1504 Benenson, A. (2000) Control of communicable disease manual. New York: American Public Health Association Bowler, S. (1998) Meningococcal disease. Nursing Standards, 13, 49-56
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Central Coast Area Health Service Public Health Unit (2000) Information sheet for contacts ofmeningococcalinfection. Public Health Unit CCAHS, Gosford Communicable Disease NetworkAustralia (2001) Guidelinesfor
the early clinicaland public health management of meningococcal disease in Australia. Canberra: Commonwealth Department of Health and Aged Care. Available: http://www.health.gov.au/ pubhlth/cdi/pubs/pdflmening_guide.pdf Delrosa, A.M. (1999) Meningitis: the facts. Nursing Times, 95, 17 HiUman, K. and Bishop, G. (1996) Clinical Intensive Care. Cambridge: University Press Kumar, K. (2000) Meningococcal infections and meningitis: what is new? AustralianJournal of RuralHealth, 8, 318-321 Leaver, M. (1998) Meningococcal disease inAustralia. Collegian, 5, 44-45 McCormack, J. (1998) The treatment of meningococcal disease. Anti-Bacterial Chronicle, 12, 1-2 Mehta, N. and Levin, M. (2000) Management and prevention of meningococcal disease. Hospital Practice:Advances in Medicine for primary care physicians, 35, 75. Available: http://www.
hosppract,com/issues/2OOO/O8/cemehta.htm New South Wales Health Department (2000) NSW Health DiseasesManual. NSW Health Department, Sydney. Patel, M. (1997) Meningococcal disease in Australia: looking at the past, thinking of the future. CommunicableDiseasesIntelligence,
21,233-236.Available: http://www.mja.com.au/public/issues/jun2/ patel/patel.html Pierson, D. M. (1997) Case study of fulminant meningococcal septicemia diagnosed in a twenty-year-old woman with bulimia nervosa. Heart and Lung, 26, 492-500 Reed (2001) (pers conversation) Emergency Physician and Staff Specialist Emergency Department, Wyong Hospital: Gosford, NSW Australia Rosen, P., Barkin, R.M., Hayden, S.R. et al (1999) The5 minute emergency medicine consult. Sydney: Hppincott Williams and Wilkins Schaad, U.B. (1998). Bacterialmeningitis. Anti-BacterialChronicle, 12, 3-4 Singer, A. (2000) Meningitis. In Cameron, P., Jelinek, G., Kelly, A., Murray, L. and Heyworth, J. (ed) TextbookofAdult Emergency Medicine. Churchill Livingstone, London. Smillova, A. and Walker, E. (2000) Meningococcemia: a critical care emergency. Critical Care Nurse, 20, 28-37 Solberg, C.O. (1998) Meningococcal infections. In A.S. Fauci, E. Braunwald, K.J. Isselbacher, J.D. Wilson, et al (Eds.). Harrison's principles of internal medicine. (14th ed) New York: McGrawHill Williams, G. (1999) Meningococcal meningitis.AustralianDoctor, 1-2
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Meningowhatal? ... Meningococcal Disease in the Emergency Department
Donna Malone), Clinical Nurse Specialist, Emergency Department Wyong Hospital, Central Coast NSWAustralia ABSTRACT
The unpredictable environment of an emergency department can often seem daunting to the newly experienced emergency nurse - a role I felt I was "mastering" very well with 18 months experience up my sleeve. The year was 2001 and I was nearing the end of my Graduate Certificate in Emergency Nursing, pleased with the rate to which I was acquiring knowledge and my skill of applying it to practice. I felt confident in the fact that I could assess and prioritise the care of patients at triage, recognise the patient experiencing an acute myocardial infarct, interpret a electrocardiograph, put in a intravenous cannula and efficiently perform in the resuscitation room as part of the trauma team, just to name a few. However, lurking in the subconsciousness of my mind was a disease that I recall I had heard the name of, listened to the lectures on the topic, and knew that it was a disease that had been highlighted recently in the press and which most people feared they may contract. Nothing however prepared me for the day that I came face to face with the deadly disease whilst caring for a patient. The aim of this experiential paper is to discuss the epidemiology of meningococcal disease in Australia and in particular the Central Coast of New South Wales (NSW), its modes of transmission and describe the associated signs and symptoms. The investigations used to diagnose the disease and the subsequent treatment and management will also be discussed. Finally, prevention techniques through the use of chemoprophylaxis and vaccination will be addressed. KEY WORDS Meningococcal, Meningitis, Meningococcaemia, Neisseria Meningitidis, Petechiae, Rash, DIC
Introduction
Why meningococcaldisease? In order to set the scene, I will outline my day as a new staffmember within an emergencydepartment on the central coast of NSW. The staffing that day consisted of a senior in charge registered nurse (myself, with 18 months emergency experience) and one junior triage nurse. The day commencedwith a paediatric pedestrian hit by a car travelling at high speed, the incidentwitnessed by his brother and the occupants of a school bus. The management of this patient consisted of bilateral chest drains, CPR, defibrillation and multiple other resuscitative adjuncts, however, some 40 minutes later the child was pronounced dead. After cleaning the patient, dealing with the parents and siblings, hearing the mothers distinct shrieking cry (a sound that I knew would linger in my ears for a long time to come), we headed off for a debriefing session. The next patient to be placed on the resuscitation bed was a teenage girl brought in by ambulance at 1300hrs following a collapse at home, although her Glascow Coma Score on arrival what 15. The ambulance officers state that she was discovered by her family unconscious, with a spotted bluish rash on her legs. There was no previous history of disease, no evidence of drug ingestion and she had been healthy and active although she had woken that morning feeling unwell with flu like symptoms of headache, sore throat, temperature and vomiting. A short time after arrival her condition deteriorated rapidly and the speed at which it did so surprised me beyond belief. She became confused, restless and agitated, crying due to excruciating leg and joint pain and for the fear of death, constantly asking "Nurse, am I dying?" The rash spread in front of my eyes and she developed acute respiratory distress
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syndrome (ARDS), was intubated and transported to the Intensive Care Unit (ICU) of a larger hospital at 1430hrs. This true scenario typifies the presentation and rapid progression of meningococcal disease. From this day I became aware that my knowledge of meningococcal disease was no more than that of the lay person, I had no idea of the pathophysiology of the disease, its mode of transmission, the recommended treatment and management of the disease, nor the chemoprophylaxis. As a registered nurse I felt my input into the resuscitation, and being able to anticipate future needs could have been greatly enhanced had I understood the physiological basis of the disease. I was much more disturbed by this patient than the tragic death of the child which occurred a few hours earlier. I was paranoid about contracting the disease myself due to a messy intubation and as a result required chemoprophylaxis. This time there was no debriefing, the "witching hour" had arrived, and at the end of the shift we all headed offto the pub.
What Is Meningococcal Disease? Neisseria Meningitidisis an invasivebacterium responsible for meningococcal disease. Meningococcal disease includes two patterns of illness, meningitis or
septicaemia (meningococcaemia), or a combination of both (Bowler, 1998). Infectionwith Neisseriamem'ngitidis most frequently presents as meningococcaemia which may progress rapidly to overwhelming shock (Waterhouse-Friderichsen syndrome) (Rosen et al, 1999). The most characteristic feature of the disease is the non-blanching petechial rash which often starts as clusters of pinpoint spots at the axillae, wrists and ankles, progressing rapidly to any body part. The face, palms of the hands and soles of the feet are less affected. As the disease progresses these dusters go on to form larger petechial spots and eventually maylead to purpura fulminans, the severest form of the disease, evidenced by large ecchymotic lesions. Neisseria meningitidis has 13 serogroups consisting of A, B, C, D, 29E, H, I, K, L, W135, X, Y and Z. Serogroups B and C are responsible for more than 90% of meningo-coccal disease in Australia (Leaver, 1998; CDNA, 2001).
Australian Incidence The incidence of meningococcal disease varies from 1 to 3/100,000 in Australia (Kumar, 2000). Highest incident rates occur during winter and early spring. Seasonal influence is thought to be related to an increase in indoor activities, which increases overcrowding, poor ventilation and close personal
Table 1. Yearly incidence of meningococcal notifications in Australia, NSW and the Central Coast from 1991 to 2002 800
700 Total Cases •
600
621
NSW
• ~' Central Coast 500
424•J
400 E
~-337 3OO
380
383
1994
1995
496
481
1997
1998
~ " ~ 8 0 304
200
1O0
0-~ 1991
1992
1993
1996
1999
2000
2001
Year
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contact. It can occur at any age, but is mostly seen in children and young adults (NSW Health, 2000a). A higher proportion of serogroup B disease occurs in children younger than two years, whereas serogroup C disease is relatively more common in older children, adolescents and adults. Across Australia there are on average 460 notifications per year, with almost half of these occurring in NSW and approximately 10 cases per year on the Central Coast, the area this author lives and works (CCAHS Public Health Unit, 2000). Most of these cases are reportedly unrelated. It is important to bear in mind that the true incidence ofmeningococcal disease is not known, as in NSW under reporting has been estimated at between 20 and 55% (Patel, 1997) and similar results could be expected in other states and territories. Table 1 highlights the yearlyincidenceofmeningococcal notifications in Australia, NSW and the Central Coast from 1991 to July 2001 (Central Coast Public Health Unit, 2000 and CDNA, 2001).
Modes of Transmission The Neisseria rneningitidis bacteria are passed from person to person through prolonged close contact and transmitted via airborne droplets such as coughing and sneezing, oral secretions such as sharing drinks or kissing (Delrosa, 1999). The nasopharynx is the natural reservoir (Smillova andWalker, 2000) and the organism is unique only to humans (Pierson, 1997). Even if bacteria are passed to another person, very few will develop the invasive disease. Carriage rates have been estimated to be as high as 25 % of the population without any manifestation of the disease in these carriers, and this aids in natural immunity (Leaver, 1998). The mechanism for invasive meningococcal disease is thought to be transport of the bacteria across the mucosal cells of the nasopharynx within phagocytic vacuoles (Smillova and Walker, 2000). The incubation period from initial infection to dissemination via the bloodstream ranges from two to ten days. In the vascular compartment the invading meningococci may
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be killed by the combined actions of serum antibodies, complement and phagocytic cells, or may multiply, initiating the bacteraemic stage (Solberg, 1998). It is at this stage that the related disease may be termed meningococcaemia. In meningococcal meningitis, bacteria are localised primarily to the meningeal compartment, whereas in meningococcaemia, the bacteria and their products are found primarily in the systemic circulation (Smillova and Walker, 2000).
Signs and Symptoms There are a multitude of signs and symptoms that are indicative ofmeningococcal disease - fever, vomiting, headache, decreased oral intake, to name a few. The problem being that these presentations to the ED especially among the paediatric population are so frequent. So how are we to know which person has the potentially fatal disease? While fulminant meningococcal disease with the distinct rash is not difficult to miss, it is the hidden disease lurking behind the runny nose or headache that is of concern. It has been well documented that the key in surviving this disease is prompt recognition of the signs and symptoms and early treatment. It is therefore imperative that registered nurses are able to recognise these signs in addition to the history and our level of suspicion, as we are the first line of contact. More importantly, we have the responsibility of triaging these patients which ultimately results in the time they wait to see a medical practitioner. It is also important to be aware of the importance of reassessment as meningococcal disease can progress at avery rapid rate. Smillova and Walker (2000) document the signs and symptoms ofmeningococcaldiseaseinto two categories: onset and progression. The onset phase is usually abrupt without specific signs or symptoms. It has been documented that signs and symptoms of upper respiratory tract infection may be present several days prior to presentation, such as a cough, runny nose and lethargy (Smillova and Walker, 2000). It is thought that this is the incubation period.
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The next phase, progression, is thought to be when the bacteria are transported across the mucosal cells of the nasopharynx within phagocytic vacuoles as described earlier (Smillova and Walker, 2000). Once the bacteria are in the blood, signs and symptoms of fever, vomiting, diarrhoea, headache, drowsiness, abdominal pain, cold extremities and petechial rash may occur. This infection in its fulminant form eventually leads to the clinical signs of shock. The signs shown during this stage may include seizures, tachycardia, hypotension, decreased cardiac output, leftventricular failure,vasomotor collapse, and later coagulopathy, disseminated intravascular coagulation (DIC), respiratory and/or metabolic failure and ARDS. Obviously, if we can recognise the early signs and symptoms and commence treatment it may delay or prevent the progression to the worst form of meningococcal disease. When the worst form of the disease develops, fulminant meningococcaemia, patients experience signs of clinical shock which may rapidly progress to hemodynamic collapse, DIC and multisystem failure (Smillova and Walker, 2000). The distinct rash involving the flanks, wrists and ankles is present in 75% of patients with the fulminant form. Widespread eruptions of the purpuric ecchymoses or tiny red/purple pinprick spots suggest fulminating disease. These can develop to look like fresh bruises or blotches on the skin. This rash will not normally disappear when pressed, and is a distinct sign of meningococcal disease (Delrosa, 1999). Figure 1, Figure 2 and Figure 3 demonstrate the three types of petechial rash characteristic of this disease. In 40-60% of cases, death is due to circulatory collapse caused by intravascularvolumedepletion, capillaryleak,vasodilation and myocardial failure (Smillova and Walker, 2000).
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Figure 1. Example of Purpura Fulminans (AENJ, 34:1997)
Figure 2. Typical petichial rash (AENJ, 35:1997)
Pathophysiology Understanding the pathophysiology behind the signs and symptoms can be complex. SmiUova and Walker (2000) and Mehta and Levin (2000) explain that meningococcaemia is a result of interplay between microbial products and host mediator systems. Microbial products include the lipid A component and
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Figure 3. cluster of petichial lesions (AENJ, 35:1997)
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gram-negative lipopolysaccharides. Host factors include complement, kinin, coagulation systems and factors released from stimulated cells. Once the Neisseria meningitidis bacteria invade beyond the nasopharynx and are not adequately contained by the immune response, they multiply and release endotoxin (lipopolysaccharide). The circulating endotoxin triggers a cascade of events, resulting in altered immune response, circulatory collapseand DIC. Lipopolysaccharide activates complement via the alternative pathway resulting in vasodilation, loss of vasomotor tone and capillary leak which is the cause of the purpuric rash. As a result of capillary leak, hypotension and tachycardia occur. The lipopolysaccharides go onto cause more havoc, binding to certain proteins. The complex interacts with monocytes, macrophages and neutrophils, stimulating these cells to release cytotoxic enzymes, cytokines and inflammatory mediators. Cytokines alter the normal functioning oflymphocytes and neutrophils and as a result cause endothelial injury resulting in further loss of vasomotor tone, induce myocardial dysfunction resulting in circulatory collapse, stimulation of the extrinsic coagulation pathway, contribute to the procoagulant state and activation of the fibrinolytic and kinin systems. Activation of the kinin system leads to the release ofbradykinin, causing vasodilation, increased vascular permeability, smooth muscle contractions, pain and increased gastrointestinal motility (Smillova and Walker, 2000). It is for this reason that many patients with meningococcal disease complain of excruciating joint and limb pain. The pathophysiology behind the altered immune response as outlined is by no means complete, as it is an intensely complex system. It does however provide a moderate scope in understanding the pathophysiology of the disease and the resulting signs and symptoms.
Diagnostic Investigations Establishing a diagnosis for meningococcal disease is not always easy. Kumar (2000) states that the diagnosis of meningococcal disease is based on a high index of
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suspicion in the initial stages. Cultures from the cerebrospinal fluid (CSF) or blood generally take more than 24 hours, and with such rapid progression of meningococcal disease it would be too late to wait for positive cultures before commencing antibiotics. Once the rash appears however it cannot be missed. Kumar (2000) also states diagnosis can be confirmed by a positive blood culture and/or a positive lumbar puncture, however, McCormack (1998) notes that when CSF is used it is useful in the diagnosis of bacterial meningitis but is not specific for meningococci. Schaad (1998) however, states that the importance of lumbar puncture should be stressed, and withheld only in patients with signs of raised intracranial pressure, cardiorespiratory compromise,coagulopathy, or infection at the site of lumbar puncture. Various antigen tests are widely used (latex agglutination, co-agglutination and countercurrent immunoelectrophoresis), but all have a false negativity rate of up to 50%. Gram-staining and culture of skin lesions, aspirates or biopsies are advocated by some clinicians, but these procedures are not widely used (McCormack, 1998). Isolation of the meningococci from the nasopharynx alone is not diagnostic, because as previously mentioned, carriage rates can be as high as 25% in some areas (Kumar, 2000). In essence, as aptly stated by Kumar (2000), "although there are many ways of confirming the diagnosis, it is always better to over-treat than to under-treat in these circumstances, because treatment can always be stopped if the results are negative". The recommendations are that the diagnosis of meningococcal disease be made on the basis of the clinical picture. Antibiotics must be commenced if there is reasonable suspicion and after the drawing of blood cultures, diagnosis can be confirmed at a later time when results return. Cultures may also be taken of skin lesions if present, depending on the treating doctor's preference (Reed, 2001).
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Treatment
Meningococcal disease can be highly unpredictable and the associated morbidity and mortality devastatingly high. It is for this reason that Solberg (1998) states that all patients with invasive meningococcal infection, whatever their clinical condition, should be observed for 48hours, with monitoring of blood pressure, pulse, perfusion, urine output, and core and peripheral temperature. Many patients will deteriorate within hours with the development of severe shock and profound DIC. Patients however may have already reached this stage when they arrive at the ED and require urgent intervention. Initial assessment must commence with the ABC's. Careful attention to the airway, breathing and circulation is essential. Assessment of whether the patient can protect their own airway is the first priority. Smillova and Walker (2000) advocate early endotracheal intubation stating that "even in patients who are alert and breathing adequately, early intubation ensures a patent airway, reduces the work of breathing, and allows continued oxygenation, ventilation and improved cerebral perfusion." Assessment of breathing follows. The primary pulmonary feature in meningococcaemiais pulmonary oedema caused by capillary leak. Patients experience increased work of breathing and decreased pulmonary compliance and often develop ARDS. Assessment of arterial blood gases (ABG), respiratory effort and oxygen saturation monitoring will determine respiratory function. Supplementary oxygen therapy should be commenced if the patient is not ventilated. Circulatory support involves fluid resuscitation after intravenous (IV) access is obtained by insertion of two large bore cannulae. Blood cultures should be obtained and urgent administration of antibiotics commenced. Venous access is often difficult due to the shocked state. Intraosseous access may be used in children to avoid delay in volume resuscitation. Strategies to reverse circulatory failure as a result of the severe capillary leak
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and myocardial dysfunction include optimising preload, decreasing afterload and improving myocardial contractility (Solberg, 1998). Fluid resuscitation together with inotropic support with dobutamine should be started immediately and titrated accordingly to reverse this failure. Solberg (1998) states that in the adult patient with marked tissue oedema eight to ten litres of fluid may be necessary during the first 24 hour period. Colloids are initially used to fill the intravascular compartment. The effectiveness of fluid resuscitation can be assessedby monitoring heart rate, blood pressure, central venous pressure, urine output and metabolic status (Mehta and Levin, 2000). Peripheral indicators such as capillary refill may also offer guidance. Patients with severe meningococcaemia require close monitoring of serum electrolytes, acid-base balance and metabolism. Metabolic acidosis results from poor tissue perfusion where there is an increase of lactic acid as a result of tissue hypoxia (Hillman and Bishop, 1996; Mehta and Levin, 2000). Profound metabolic derangements such as hypoglycaemia, hypokalemia, hypomagnesaemia, hypocalcaemia contribute to myocardial dysfunction. The toxic effect ofendotoxin on the myocardium potentiates cardiac demands imposed by intravascular hypovolaemia (Mehta and Levin, 2000). It is therefore essential to monitor for heart failure and arrhythmias. Regular electrocardiographs and careful titration of fluids and inotrope are necessary. Acute renal failure is frequently present, requiring supportive therapy such as dialysis. Dialysis is highly effective in reducing extravascular fluid accumulation and correcting electrolyte and metabolic imbalances and should be commenced early in patients with severe meningococcaemia. While this may not be appropriate in the ED, it is hoped that by this stage the patient will have been transported to ICU. It should also be noted that since meningococcal disease may present simultaneously as meningitis and septicaemia, all patients should be monitored for signs of increased intracranial pressure (Mehta and Levin, 2000).
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Disseminated intravascular coagulation can result in the patient with meningococcaemia as a result of endotoxic shock. There is also evidence ofcoagulopathy and thrombocytopenia. For the treatment of DIC, flesh-frozen plasma (FFP), cryoprecipitate and vitamin K can be administered if the prothrombin time is two to three times above normal or if active bleeding occurs. Platelets are administered if the platelet count is low while packed red blood cells are given to maintain an adequate haemoglobin level to ensure adequate oxygen delivery (Smillova and Walker, 2000).
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Figure 4. Nursing and medical management of patients with meningococcaemia, (adapted from Smillova & Walker, 2000, Figure 4)
Smillova and Walker (2000) and Solberg (1998) document that routine heparinisation of patients with DIC has failed to improve prognosis and is not recommended. However, patients with impending peripheral gangrene and severe coagulopathy, administration of low dose heparin together with FFP may be tried. According to a recent study discussed by Smillova and Walker (2000), heparin may limit thrombosis and necrosis of the digits and extremities. Arguments against the use of heparin are based on the potential for haemorrhage associated with the use of this drug. Steroids have been used in the treatment ofmeningococcaemia, however their effectiveness remains controversial. Smillova and Walker (2000) explain that corticosteroids are used to treat adrenal insufficiency or haemorrhage and for reducing inflammation. They go on to say that while the occurrence of adrenal insufficiency in patients with meningococcaemia is rare, and no evidence supports routine use of steroids in these patients, that because some patients with the infection die of untreated adrenal insufficiency, treatment with corticosteroids might be considered. Singer (2000) however, explains that steroids have been found to improve audiological and neurological outcome and improves the survival from meningococcaemia. Singer (2000) also states that dexamethasone reduces white cell count, tumour necrosis factor and meningeal inflammation in the CSF. Figure 4 from Smillova and Walker (2000) is an excellent guide to the nursing and medical management of patients with meningococcaemia. August 2002, Volume 5 Number 2 - Australian Emergency Nursing Journal
Suspicion of meningococcaemia
Respiratory isolation... obtain specimens of blood and CSFfor culturing Administer antibiotics Transport to intensive care unit (of tertiary care facility if feasible)
Continuous monitoring of vital signs and neurological status... Monitor for shock (depressed mental status, tachycardia, base deficit, delayed capillary refill) Assess airway and acid-base status Administer oxygen Mechanically intubate if indicated Replace fluids
If patient's status has not improved (hypotension, tachycardia, depressed mental status)... Establish central venous access and insert an arterial cannula Start inotropic agents: dopamine and adrenaline Continue fluid replacement Administer fresh-frozen plasma, cryoprecipitate, platelets, vitamin K as indicated for disseminated intravascular coagulation Consider inserting a pulmonary artery catheter
If no improvement in patient's status... Consider treatment with steroids (hydrocortisone 2mg/kg) Consider further inotropic, vasoconstrictor, or vasodilator therapy (milrinone, noradrenaline, nitroprusside)
If no improvement in patient's status... Consider experimental therapy as available Consider heparin therapy for disseminated intravascular coagulation and to limit necrosis of skin, digits and extremities
Administer chemoprophylax~to close contacts within 24 hours
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The role of the nurse in the ED as well as delivering patient care, extends to emotional support to the patient's family. Many families and parents are shocked bywhat has happened, particularly because of the rapid onset of the disease and reactions of other people. Anxiety and fear are associated with any hospital admission and especially when the condition is lifethreatening. The environment is unfamiliar, painful procedures are performed, and the monitoring and equipment can be overwhelming for both the patient and their family. It is important for emergency nurses to keep this in mind, listen carefully to families, explain procedures, the disease process, and prognosis and encourage questions, thoughts and feelings (Smillova and Walker, 2000). Antibiotics Any febrile patient with a petechial rash should be considered to have meningococcal infection and given antibiotics until proven otherwise. Blood cultures should be taken immediately and treatment begun without awaiting confirmation. It has been well documented that early treatment with antibiotics reduces the morbidity and mortality of the disease. In the prehospital setting antibiotics must be commenced and the drug of choice is benzylpenicillin G intramuscularly if unable to give intravenously. In the hospital setting benzylpenicillin G is also the drug of choice for meningococcal disease, but should be given intraveneously (McCormack, 1998; MIMMS 2001).
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Third generation cephalosporins such as ceftriaxone or cefotaxime are given in addition to benzylpenicillin G (MIMMS 2001). Table 2 outlines the recommended doses of these antibiotics for children and adults. The cephalosporins provide coverage for some penicillin-resistant meningococci bacteria and are excellent in penetrating into the cerebral spinal fluid and lack toxicity. Reed (2001) stated treatment with benzylpenicillin G and ceftriaxone is reasonable for any patient suspected of having the disease.Additionally, if unsure or in the event that gram positive cocci are present on staining, vancomycin should be given. Duration of the antibiotic therapy should continue in high doses for seven to ten days (McCormack, 1998), Solberg 0998) adds that these doses should not be tapered over this period. Prevention Chemoprophylaxis Current recommendations for the use of chemoprophylaxis are that household members, day-care centre contacts and persons exposed to the oral secretions, such as performing mouth to mouth or a "messy" intubation of a patient with meningococcaemiashould receive prophylaxis. There is controversy concerning the efficacy ofchemoprophylaxis in preventing further cases of meningococcal disease, however the aim is to reduce the risk of infection to other susceptible individuals (CDNA, 2001).
Table 2. Antibiotics used in the management of meningococcal disease (Adapted from CDNA, 2001) Antibiotic
Prehospital or on admission Antibiotics
Early hospital treatment where N. meningitides is the agent
Benzylpenicillin
< I year: 300mg IV/IM single dose
Child: 60mg/kg (up to 1.8g IV 4 hourly for 7-10 days
I-9 years: 600mg IV/IM single dose Adult or child (10 years or more): 1.2g IV/IM single dose Ceftriaxone
50mg/kg (up to 2g) IV daily (all ages)
Adult: 1.8g IV 4 hourly for 7-I0 days
Child: 100mg/kg (up to 4g) IV daily in 1 or 2 divided doses for 7-10 days Adult: 4g IV daily in 1 or 2 divided for 7-10 days
Cefotaxime
Child: 50mg/kg (up to 2g) IV 6 hourly for 5-7 days Adult: 2g IV 6 hourly for 5-7 days
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Susceptible individuals such as other household contacts exposed to patients with meningococcal disease have an increased risk rate of 500-1,000 times greater of contracting the disease (Mehta and Levin, 2000; McCormack, 1998; Williams, 1999). Conversely, the National Health and Medical Research Council (NHMRC) (1996) state that the only published study to support the use of chemoprophylaxis was an unblinded observational study that failed to reach statistical significance. However, due to ethical objections it would be virtually impossible to conduct such studies now given prophylaxis would need to be withheld from a control group (CDNA, 2001). Although evidence is lacking from randomised trials, there is evidence which suggests microbial clearance of meningococci following the administration of chemoprophylaxis (NHMRC, 1996). There are three antibiotics currently used for chemoprophylaxis ofmeningococcal disease, each has advantages and disadvantages, and each is preferred in specific circumstances. Ceftriaxone
Ceftriaxone is a single intramuscular injection, and is well tolerated with no adverse reactions to note. Ceftriaxone should be dissolved in 1% lignocaine to reduce pain at the injection site. Ceftriaxone is 97% effective in eradicating pharyngeal meningococci from carriers. The recommended doses for chemoprophylaxis are 250mg for adults and 125mg for children younger than 12 years of age. It is recommended that ceftriaxone not be given to infants in their first 4 weeks. Ceftriaxone is the preferred chemoprophylaxis for pregnant women. Further, because compliance is likely to be good and as it is readily available, it should be considered as the preferred agent when required in rural and remote communities, especially in Indigenous communities. Although ceftriaxone is not registered for chemoprophylaxis of meningococcal disease in Australia, it is recommendedby the Meningococcal Disease Guidelines Working Party for that purpose (Benenson, 2000; CDNA, 2001).
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Ciprofloxacin Ciprofloxacin is given as a single oral dose of 500mg, and has been shown to be 97% effective in eradicating pharyngeal meningococci. It is the drug of choice for women on the contraceptive pill, but is recommended it not be given to children or pregnant women (CDNA, 2001; McCormack, 1998). While allergic reactions are very uncommon, they have been reported, and it is for this reason recipients should be observed for 30 minutes post ingestion if possible (Benenson, 2000; CDNA, 2001).
Rifampicin The regime ofrifampicin for those over twelve years of age is 600mg orally every 12 hours for 2 days (McCormack, 1998). It has been shown to eradicate nasopharyngeal meningococci in 75-95% of carriers (Benenson, 2000; CDNA, 2001). Side effects include headache, dizziness, gastrointestinal symptoms and orange discolouration of urine, tears and soft contact lenses (CDNA, 2001;NSW Health, 2000). Rifampicin also interferes with the oral contraceptive pill and is contraindicated in pregnancy, alcoholism and severe liver disease (NHMRC, 1996; Benenson, 2000; CDNA, 2001). Vaccination
Vaccines are available in Australia for four serogroups, A, C, W-135 and Y (Smillova and Walker, 2000) for use in epidemics and high risk populations. Unfortunately no vaccine is effective against serogroup B, which is the predominate serogroup causing sparodic disease in Australia (NHMRC, 1996). The efficacy rate of a single dose of serogroup C vaccine is at least 90% and is recommended to travellers to areas where the disease is epidemic, such as parts of Africa, and also to people with specific health conditions such as splenic dysfunctions (NSW Health, 2000). This vaccine however produces poor immune responses in children less than two years of age who unfortunately comprise the highest risk age-group for meningococcal disease. Serogroup C in particular is poorly immunogenic in young children. Further, it takes at least two weeks to
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induce an optimal immune response even in older people, and does not induce long-term immunity (NHMRC, 1996; Mehta and Levin, 2000). Research is ongoing to develop a vaccine that will be effective against all strains of meningococci, induce long term immunity and be incorporated into a childhood immunisation program (Smillova and Walker, 2000; Mehta and Levin, 2000).
Conclusion Meningococcal disease appears to be on the increase and whilst it presents as an alarming contributor to morbidity and mortality, epidemic disease in Australia has not occured for many years and endemic disease rates remain low (CDNA, 2000). Until a vaccine is developed for all serogroups, successful treatment of the disease depends on early recognition and initiation of antibiotic therapy. Initial signs and symptoms may be non-speciflc, however delays in treatment may have devastating consequences. Knowledge of the cause, progression and current treatment modalities may assist nurses in the early detection and prompt treatment ofmeningococcal disease and thereby, improve patient outcomes. Editors Footnote This paper was submitted and accepted for publication in December 2001. Since that time a new proteinconj ugatedgroup C meningococcalvaccine (Meningitec ®) has been developed. For further information on this vaccine or meningococcal disease please visit the CDNA website at: htrp://www.health.gov.au/pubhlth/cdi/cdna/ press/pr4_Ol.htmor contact the Meningitis Foundation on their 24 hour free phone Australian helpline: 1800 129 068 Meningitis Foundation: (02) 9960 0055. Reference List Abramson, J.S., Baker, C.J., Fisher, M.C., Gerber, M.A., et al (2000) Meningococcal Disease prevention and control strategies for practice-based physicians. Pediatrics, 106, 1500-1504 Benenson, A. (2000) Control of communicable disease manual. New York: American Public Health Association Bowler, S. (1998) Meningococcal disease. Nursing Standards, 13, 49-56
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Central Coast Area Health Service Public Health Unit (2000) Information sheet for contacts ofmeningococcalinfection. Public Health Unit CCAHS, Gosford Communicable Disease NetworkAustralia (2001) Guidelinesfor
the early clinicaland public health management of meningococcal disease in Australia. Canberra: Commonwealth Department of Health and Aged Care. Available: http://www.health.gov.au/ pubhlth/cdi/pubs/pdflmening_guide.pdf Delrosa, A.M. (1999) Meningitis: the facts. Nursing Times, 95, 17 HiUman, K. and Bishop, G. (1996) Clinical Intensive Care. Cambridge: University Press Kumar, K. (2000) Meningococcal infections and meningitis: what is new? AustralianJournal of RuralHealth, 8, 318-321 Leaver, M. (1998) Meningococcal disease inAustralia. Collegian, 5, 44-45 McCormack, J. (1998) The treatment of meningococcal disease. Anti-Bacterial Chronicle, 12, 1-2 Mehta, N. and Levin, M. (2000) Management and prevention of meningococcal disease. Hospital Practice:Advances in Medicine for primary care physicians, 35, 75. Available: http://www.
hosppract,com/issues/2OOO/O8/cemehta.htm New South Wales Health Department (2000) NSW Health DiseasesManual. NSW Health Department, Sydney. Patel, M. (1997) Meningococcal disease in Australia: looking at the past, thinking of the future. CommunicableDiseasesIntelligence,
21,233-236.Available: http://www.mja.com.au/public/issues/jun2/ patel/patel.html Pierson, D. M. (1997) Case study of fulminant meningococcal septicemia diagnosed in a twenty-year-old woman with bulimia nervosa. Heart and Lung, 26, 492-500 Reed (2001) (pers conversation) Emergency Physician and Staff Specialist Emergency Department, Wyong Hospital: Gosford, NSW Australia Rosen, P., Barkin, R.M., Hayden, S.R. et al (1999) The5 minute emergency medicine consult. Sydney: Hppincott Williams and Wilkins Schaad, U.B. (1998). Bacterialmeningitis. Anti-BacterialChronicle, 12, 3-4 Singer, A. (2000) Meningitis. In Cameron, P., Jelinek, G., Kelly, A., Murray, L. and Heyworth, J. (ed) TextbookofAdult Emergency Medicine. Churchill Livingstone, London. Smillova, A. and Walker, E. (2000) Meningococcemia: a critical care emergency. Critical Care Nurse, 20, 28-37 Solberg, C.O. (1998) Meningococcal infections. In A.S. Fauci, E. Braunwald, K.J. Isselbacher, J.D. Wilson, et al (Eds.). Harrison's principles of internal medicine. (14th ed) New York: McGrawHill Williams, G. (1999) Meningococcal meningitis.AustralianDoctor, 1-2
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