- Define meningitis, meninges and the layers that make up the meninges.
- Explain the modes of infiltration bacteria use to enter the meningeal space.
- Recognize the four major symptoms of bacterial meningitis.
Hopefully, your detailed history and exam have lead you to the correct diagnosis, because I’m talking about infections of the central nervous system (CNS)——specifically bacterial meningitis. Meningitis is inflammation of the fluid-filled spaces in the brain: notably the meninges and cerebral ventricles. Although its occurrence is fairly rare, these patients’ ultimate survival and recovery demand your attention to this disease’s possible presence.
- Cerebrospinal fluid: The fluid that surrounds the central nervous system, provides nutrient/waste product transport to the brain, and acts as the medium for bacteria growth in bacterial meningitis.
- Leptomeninges: The collective term for the arachnoid and pia maters, two of the three meningeal layers.
- Meninges: The three layers of tissue that form the covering to the central nervous system.
- Meningitis: Inflammation of the leptomeninges that ultimately leads to the symptoms associated with the disease process.
- Nuchal rigidity: Stiffness in the neck that prevents the chin from being flexed into the chest due to the inflammation of the central nervous system in patients with meningitis.
A non-transporting paramedic unit is dispatched along with a BLS ambulance to a university for a 20-yearold student in the campus infirmary with an altered mental status. The paramedic and two EMTs find him sitting upright but slumped over in a chair. The patient appears obviously toxic, but aside from his mental status, is in no acute distress. He’s only responsive to loud verbal stimuli and speaks incoherently when asked questions.
The infirmary staff report he had a oneweek history of a viral sinus infection that seemed to be clearing up. However, within the last 24 hours, the patient developed a modest fever (102 degrees Fahrenheit) that wasn’t responding to oral antipyretics. The campus physician diagnosed him about six hours ago with post-viral, sub-clinical pneumonia that had developed following a viral upper respiratory infection. The patient received one dose of oral antibiotics and was sent back to his dorm.
The patient’s roommates brought him back to the infirmary where the university’s providers immediately noted the patient’s obvious deterioration in clinical status. His fever had surged to 104.9 degrees Fahrenheit, his mental status had declined, and his heart rate went from normal to 120 bpm. Blood sugar as tested by the staff was found to be 278 mg/dL. A urinalysis done just prior to EMS arrival showed very concentrated urine indicating dehydration and no signs of urinary tract infection. 9-1-1 was activated because it’s believed the patient is now pneumoseptic and needs ICU-level care.
With the exception of pale, hot and clammy skin, the initial physical exam reveals no significant findings. Most notably, the lungs are clear and equal with only minimal diminishment in the bases. Pupils are normal and reactive. Abdomen is soft and non-tender. There’s no evidence of any trauma.
A cursory review of the patient’s medical record reveals no significant past medical history, no known drug allergies and no routine medications.
The EMTs place the patient on low-flow oxygen via cannula and obtain a complete set of vitals: heart rate is 126, respirations are at 28, blood pressure is 104/82, SpO2 is 92% and body temperature (tympanic) is 105.3 degrees Fahrenheit. The patient is placed on the heart monitor and has a rhythm of sinus tachycardia.
The paramedic begins to search for IV access to begin fluid resuscitation, believing that the patient is indeed quite septic from a subclinical pneumonia based on the sending staff ‘s report. However, due to the patient’s fluid status and sepsis, his peripheral vascular wasn’t able to be visualized or palpated. The paramedic then decides to place an external jugular IV to obtain access. As the paramedic begins to manipulate the patient’s head and neck searching for a site, the paramedic notices that when the patient’s head is rotated, he suddenly arouses and yells, “Ow, ow, ow!”
After quickly replaying the last 10 minutes in his head, the paramedic suddenly realizes this patient’s diagnosis has been wrong. The paramedic takes the fingertips of his right hand and places them under the patient’s occiput. He then lifts the patient’s entire upper half of his body off of the stretcher with the only spinal flexion taking place at the patient’s hips. The impaired neck flexion, likely due to nuchal rigidity, makes the diagnosis crystal clear: bacterial meningitis!
Recognition and early treatment of severe infections and sepsis has become a mainstay in emergency medicine over the past decade. From physicians to nurses to first responders, the need for early recognition of these disease processes is paramount and a foundation of our practices.1 As specialists at harnessing the ability to quickly discern immediate and delayed life threats in our patients, prehospital emergency medicine providers become very good at recognizing the common features and causes of sepsis.
I make it a point to obtain a body temperature in nearly all of my medical patients. In any patient with an altered mental status and a normal blood glucose, obtaining a body temperature is crucial and subsequently drives my therapy. This practice is imperative because a large portion of prehospital patients fall into the spectrum of sepsis, truly making this best practice.
After making a diagnosis of sepsis, most providers usually direct the history and physical exam toward locating the site of the infection. For patients with community-acquired infections who will ultimately develop some degree of sepsis, the most common site of the pathogen is pulmonary with an occurrence of about 50%.2 The other common sites are intraabdominal, bloodstream and renal/urinary, with incidences of 20%, 15% and 14%, respectively.3
But what happens when you encounter a patient who looks incredibly toxic and their appearance screams sepsis, yet you can’t definitively locate a source of infection? What if this patient stands an incredibly high likelihood of dying from the disease if untreated? And if the patient does survive, what if they stand a good chance of suffering from permanent disability following this infection? And even more still, of those infected, what if many are likely to be around your age? Where do you look for clues regarding this patient’s illness?
Make no mistake, our ability to put the whole picture together could dramatically increase this patient’s chances at survival and a meaningful recovery.1
In a normal, healthy individual, the brain and other components of the CNS are well protected from the attack of outside organisms. The skull and surrounding tissue and skin create the foundation of protection by preventing easy access to the inside of the skull. The same is true of the vertebral column in regard to the spinal cord. Within the confines of the CNS’s bony structures lies an extremely tough membrane that covers nearly the entire surface of the CNS. This membrane is comprised of three distinct layers and is collectively referred to as the “meninges”; hence the term “meningitis.” (See Figure 1.)
The most superficial layer of the meninges is the dura mater, also referred to as “the dura.” This membrane is the thickest and most durable of the three layers. It offers support and structure to the brain and protection from some of the skull’s more rough or sharp topography. It also provides some structure and anchoring for the larger blood vessels within the CNS, as this is the only layer of the meninges that’s anchored to and directly communicates with the skull.
Directly inside the sack that’s created by the dura lies the arachnoid mater. This layer is essentially invisible to the naked eye. This structure very much resembles that of spider webbing, lending to the name “arachnoid.” In particular, this layer provides cushion to the organs of the CNS during movement and acts as a watertight, physical barrier between the cerebrospinal fluid (CSF) housed within the subarachnoid space and the blood circulating within the dura.
Deep in the arachnoid mater lies the pia mater. This layer acts as the fragile envelope to the brain’s outer surfaces. Unlike the outer two layers of the meninges that form sacks around the CNS, the pia mater communicates directly with the solid organs of the CNS and follows their shape. The pia mater is where the capillaries that supply the blood flow to the CNS deliver their nutrients and remove waste. Blood actually doesn’t directly communicate with the parenchyma of the CNS; rather, all of the exchange happens at the capillary level between the intravascular blood and the extravascular CSF. The CSF then delivers or removes the materials needed or wasted by the CNS tissues.
Since the arachnoid layer is somewhat anchored and connected to the pia mater by way of some spider webbing that comprises the arachnoid mater, they can often be grouped together via nomenclature and referred to as the “leptomeninges.” This is important because bacterial meningitis in its most basic of descriptions is known as an inflammatory disease process of the leptomeninges.
Providing additional protection to the brain is a physiologic barrier that surrounds all of the blood vessels that supply the CNS. This grouping of cells that provide a surrounding barrier are collectively known as the bloodbrain barrier. Although this barrier doesn’t provide much physical protection, it does act as a gatekeeper between the CSF and circulating blood volume, selectively determining what chemicals and materials are allowed in and out of the CNS, including bacterial pathogens.4
Despite these and other protective mechanisms, bacterial inoculation of the CNS still occurs usually via a specific but unknown point of entry.5 There are three basic modes that allow for the bacterial pathogen to invade the CNS and colonize within the CSF:
- Upper respiratory illness. Many patients who suffer from bacterial meningitis often originally present with symptoms consistent with upper respiratory infections (URI). Following the initial colonization of the pathogen within the upper respiratory tract, patients can develop meningitis after bacteria successfully enters the bloodstream or gains physical access to the meningeal space via small defects or malformations in the skull.
- Bacteremia. When a patient’s blood becomes inoculated with bacteria, they’re said to have bacteremia and are labeled as bacteremic. The patients are almost always actively ill, as the bacteria are alive, multiplying and causing disease from within the patient’s normally sterile bloodstream. Should the bacteria be able to make it to the capillary beds within the pia mater, the bacteria are able to force their way across the vessel wall and through the blood-brain barrier.
- Direct inoculation. Bacteria can also enter the meningeal space directly——through traumatic injury, surgical contamination or implanted device colonization, for example——without any other infectious means such as URI or bacteremia.
Once in the CSF, the bacteria are able to grow nearly unchecked at a very high rate of reproduction.6 This is able to occur because the CSF is extremely low in white blood cells and disease-fighting chemicals needed to control and eradicate the bacteria’s disease process.
At this point, the disease rapidly progresses. Patients often present to a medical provider or activate 9-1-1 in a few hours to just a day or two following the onset of symptoms.7 The rapid nature of disease progression is often one of the tip-offs in the patient’s medical history that bacterial meningitis may be the cause. Once the pathogen begins multiplying and causing disease within the confines of the leptomeninges, the patient’s deterioration is extremely rapid.
The symptomatology of the disease is typically secondary to the destruction caused by the actual bacteria itself as their toxins and waste products incite an extreme inflammatory response by the affected tissues. The subsequent inflammatory cascade quickly leads to dramatic inflammation and irritation of neural tissue, high fever, cerebral edema, altered sensorium and unconsciousness. If left untreated, death usually occurs due to sepsis and cardiovascular collapse or cerebral herniation.
Bacterial meningitis will typically present to you very soon after the onset of symptoms. You’ll want to be on the lookout for patients or bystanders who report an extremely fast deterioration in clinical status, not progression of symptoms like in influenza. These patients may start with a headache in the morning, and by the afternoon are unconscious and extremely febrile.
Patients also often present with headache that’s general and global in nature, and progressively worsening. The patient will likely tell you this isn’t their normal headache and that it’s severe, but don’t confuse this severe headache with that of an aneurysm’s telltale thunderclap.
You’ll also want to be on the lookout for patients who report they recently had a cold or sinus infection. Some patients may even report they had just gotten over a URI, but are now getting sick again.
Special attention to the patient’s history and demographics will also provide you with clues. Patients who are immuno-compromised (HIV positive, organ transplant recipient, chemotherapy patient), in extremes of age, living in communal settings (e.g., jail or college dorm), or recently exposed to other bacterial meningitis patients have a greater risk for developing the disease.
After a focused but thorough history, your exam should be able to solidify a bacterial meningitis diagnosis.
First, be on the lookout for fever. Fever is present in 95% of patients with bacterial meningitis.8 The fever is often quite high (> 38 degrees Celsius), very fast in its progression, unyielding and unrelenting. Following its onset, the fever will persist for the entirety of the untreated disease period and well after treatment has been initiated. It can also be difficult to control when antipyretics are used alone without aggressive antibiotic administration.
Nuchal Rigidity is also a probable exam finding in these patients. A nuchal rigidity is considered positive when a patient’s neck is found to be stiff or immobile with passive flexion (typically in unconscious patients) or if the patient is unable to flex their neck by bringing their chin to the chest; 88% of patients will present with this finding.8
The next hallmark is altered mental status. Nearly 80% of patients with confirmed bacterial meningitis will present with some form of an altered mental status. Most altered patients present with only lethargy and/or altered sensorium. However, over 20% have been found to only respond to pain, and almost 6% will present completely unresponsive, warranting immediate airway control.8
When a patient has fever, nuchal rigidity and altered mental status, they’re said to have the “triad of bacterial meningitis.” Not all patients will have the triad——only about 50% actually have all three9–although patients with all three are considered clinically positive for bacterial meningitis. Patients without any of the triad’s symptoms are considered negative for the disease. If you add headache to the triad, nearly all bacterial meningitis patients (95%) will have at least two of the four symptoms.9
Other signs and symptoms can include a bizarre rash pattern, arthritis/joint/muscle pain, focal neuro deficits, seizure, photophobia, nausea, and vomiting; however, most of these are fairly unreliable as a diagnostic or prognostic indicator when compared to fever, nuchal rigidity, altered mental status and headache.
TREATMENT & TRANSPORT
Treatment of these patients is fairly straightforward. Manage your ABCs (airway, breathing and circulation) appropriately and be on the lookout for severe unconsciousness warranting advanced airway management. These patients can also present with severe sepsis and septic shock. Be sure to administer volume resusciation as indicated by the patient’s clinical status and local protocols.
Upon your initial suspicion of bacterial meningitis and pending the patient doesn’t require airway control or oxygen, the patient should be masked for droplet protection. If you’re unable to mask the patient, you should wear one yourself. Certain causative agents of bacterial meningitis are extremely contageous and warrant vigilant isolation and contact precautions.
The best thing we can do for these patients is recognize the disease early, promptly consulting medical command and transporting the patient to a definitive care facility with infectious disease and neurology services. The greater the delay in care and the initiation of antimicrobial therapy (and we’re talking only hours), the more devastating this disease is.
In ideal situations, your conversation with medical command should illicit a waiting bed in the receiving ED as well as a care team standing by to perform a lumbar puncture to confirm the diagnosis and culture the pathogen.
It’s also worth nothing that meningitis can be elicited from sources other than bacteria. Viruses, funguses, protists, parasites and even certain chemical agents can cause irritation and inflammation of the leptomeninges, producing symptomatology similar to that of bacterial meningitis. In fact, viral meningitis can produce a very similar sequela to bacterial meningitis and has an incidence of 25:1 when compared to bacterial meningitis.10 However, viral meningitis is almost always not as severe or life-threatening, and is usually self-limiting over 7—10 days without any hospitalization or treatment.10 Fungal meningitis, on the other hand, has an extremely high mortality rate; however, it usually affects severely immuno-compromised patients, especially those with advanced AIDS. The progression of fungal meningitis is usually much slower than bacterial and is one of the distinguishing characteristics from other forms. The other causes of meningitis are extremely rare and variable in their epidemiology and pathogenesis, and most prehospital providers would likely never encounter them during their career.
The patient is immediately masked for droplet precautions.
The paramedic calls medical command at the receiving ED and tells the physician the entire story with an emphasis on symptom progression and current exam findings. Ten minutes later, the doctor, a nurse and an ED tech meet the ambulance upon its arrival to the hospital. The crew wheels the patient toward the exam room while the ED attending performs a quick physical exam and gains other pertinent information from the paramedic.
Upon reaching the exam room, there’s a sterile table with supplies and an IV bag of antibiotics hanging on a bedside poll. The ED attending asks that the patient is rolled onto his side as he’s transferred, with his knees brought up to his chest. The prehospital crew is quite perplexed, but do as asked. Only moments later, the ED attending——now gowned, masked and wearing sterile gloves——picks up a large needle off the sterile table and asks that the crew stay in the room to help hold the patient and keep him from moving during the lumbar puncture. The supplies in the room and patient’s position upon transfer suddenly made sense.
The patient is held in this lateral position, and just seconds later, the ED attending pops up from behind the patient with a small test tube full of a yellowish-white, cloudy and soupy liquid. She explains this is the patient’s CSF and it’s supposed to be a clear, thin liquid with only a slightly yellow tint. This confirms fulminant bacterial meningitis and antibiotics are started immediately. Within two hours, the patient is transported to the ICU. The patient spends 18 days in the hospital, makes a complete recovery, and is later discharged without any lasting effects of the infection.
As the crew prepares to leave, the ED attending thanks them and says that had they not done such a thorough job conveying this patient’s grave situation so clearly in the pre-arrival report, the patient would have likely waited much longer for the definitive treatment he received within just minutes of entering the ED.
Early recognition and communication are critical when encountering these types of patients. Although the paramedic may have accidentally stumbled across this patient’s nuchal rigidity, it was his ability to quickly put the pieces together and build a trusting rapport with the physician on the phone by giving a detailed but concise report that ultimately lead to this patient’s great outcome. Despite the limited options EMS has to treat these patients, providers still play a large role in advocating for and seeing that these patients get the timely and definitive care they need.
1. Studnek JR, Artho MR, Garner CL Jr, et al. The impact of emergency medical services on the ED care of severe sepsis. Am J Emerg Med. 2012;30(1):51—56.
2. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(21):2063
3. Vincent JL, Rello J, Marshall J, et al. International study of the prevalence and outcomes of infection in intensive care units. JAMA. 2009;302(21):2323—2329.
4. van Sorge NM, Doran KS. Defense at the border: The bloodbrain barrier versus bacterial foreigners.Future Microbiol. 2012;7(3):383—394.
5. Parkkinen J, Korhonen TK, Pere A, et al. Binding sites in the rat brain for Escherichia coli S fimbriae associated with neonatal meningitis. J Clin Invest. 1988;81(3):860—865.
6. Small PM, Täuber MG, Hackbarth CJ, et al. Influence of body temperature on bacterial growth rates in experimental pneumococcal meningitis in rabbits. Infect Immun. 1986;52(2):484—487.
7. de Gans J, van de Beek D; European Dexamethasone in Adulthood Bacterial Meningitis Study Investigators. Dexamethasone in adults with bacterial meningitis. N Engl J Med. 2002;347(20):1549—1456.
8. Durand ML, Calderwood SB, Weber DJ, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med. 1993;328(1):21—28.
9. van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004;351(18):1849—1859.
10. Mohseni MM, Wilde JA. Viral meningitis: Which patients can be discharged from the emergency department? J Emerg Med. 2012:43(6):1181—1187.