Meningitis Flashcards

Question

### Key Takeaways for Your Exam: - Understand the difference in symptoms and signs between patients **with and without meningitis**. - Know how to elicit **Kernig's** and **Brudzinski's signs**, which are used to diagnose meningitis. - **CSF analysis** is crucial in determining the cause of meningitis (bacterial vs. viral) and how to treat it. - Recognize when a **CT scan** is necessary before a lumbar puncture to avoid complications like **cerebral herniation**. These points cover the essentials for understanding meningitis and the diagnostic process, which will be important for your exam. Let me know if you need further clarification on any points!

Answer 1

### Typical Cerebrospinal Fluid (CSF) Findings in Infectious Meningitis: 1. **Viral Meningitis**: - **WBC Count**: 50-1000 cells/mm³ - **Predominant Cell Type**: Mononuclear (may be neutrophilic early in the course) - **CSF:Serum Glucose Ratio**: ≥0.5 - **Protein Level**: 0.4-0.8 g/L 2. **Bacterial Meningitis**: - **WBC Count**: 100-500 cells/mm³ - **Predominant Cell Type**: Neutrophilic (may become mononuclear after antibiotics) - **CSF:Serum Glucose Ratio**: ≤0.5 - **Protein Level**: 0.5-2.0 g/L 3. **Tuberculous Meningitis**: - **WBC Count**: 50-300 cells/mm³ - **Predominant Cell Type**: Mononuclear - **CSF:Serum Glucose Ratio**: ≤0.3 - **Protein Level**: 0.5-3.0 g/L 4. **Cryptococcal Meningitis**: - **WBC Count**: 20-500 cells/mm³ - **Predominant Cell Type**: Mononuclear - **CSF:Serum Glucose Ratio**: ≤0.5 - **Protein Level**: 0.5-3.0 g/L

Answer 2

### **Bacterial Meningitis Management** **Bacterial meningitis** is considered a **medical emergency**, and the goal is to diagnose and treat it as early as possible to avoid complications. Here's how the management is structured: 1. **Early diagnosis**: Prompt identification of bacterial meningitis is essential because delay in treatment increases the risk of severe complications or death. 2. **Immediate optimum treatment**: Once bacterial meningitis is suspected, the patient must receive immediate, appropriate therapy, which includes antibiotics and supportive care. 3. **Intensive supportive therapy**: Patients may need intensive care for monitoring and managing vital functions, such as breathing, heart function, and blood pressure. 4. **Rehabilitation**: Some patients may experience neurological damage or other complications that require rehabilitation to recover normal function. 5. **Prophylaxis to family**: Close contacts of the patient (such as family members) should receive prophylactic antibiotics to prevent the spread of the infection, especially for certain types of meningitis like meningococcal meningitis. 6. **Notification to General Practitioner (GP) and Public Health**: Meningitis is a notifiable disease, meaning it needs to be reported to public health authorities to manage outbreaks and protect the community. ### **ABC Management** In any medical emergency, the **ABC approach** stands for: - **Airway**: Ensuring the patient's airway is clear and open. - **Breathing**: Ensuring the patient is breathing adequately. If needed, supplemental oxygen or ventilation may be provided. - **Circulation**: Managing the patient's blood pressure and perfusion. ### **Fluid Management**: - **Aggressive resuscitation** with IV fluids is critical, especially if the patient is in shock or has low blood pressure due to infection. ### **Dexamethasone**: - This **steroid** is used mainly in **pneumococcal** and **Haemophilus influenzae type B (HiB)** meningitis to reduce inflammation and prevent long-term neurological damage. - It must be given **before or with the first dose of antibiotics**. Once bacterial meningitis is confirmed, dexamethasone is continued for 4 days. ### **Inotropes**: - Inotropes are medications used to **increase blood pressure** (especially diastolic pressure) and **improve heart function** in patients with severe infection (septic shock). ### **Treat what you expect!** This phrase emphasizes the need for **empiric antibiotic treatment**—starting broad-spectrum antibiotics based on the most likely organisms before the exact pathogen is identified. - **Empiric antibiotic treatment** is based on: - **Epidemiology**: Common causes of bacterial meningitis in the patient’s location. - **Risk factors**: Specific conditions that make a patient more susceptible (e.g., age, immunosuppression). - **Local resistance patterns**: The presence of antibiotic-resistant bacteria in the area, which will guide antibiotic choice.

Answer 3

### **Empiric Antibiotic Treatment** 1. **IV ceftriaxone 2g twice daily (BD)** or **cefotaxime 2g four times daily (QDS)**: These are broad-spectrum antibiotics effective against the most common causes of bacterial meningitis. 2. **Dexamethasone 0.15mg/kg four times daily (QDS)** for 4 days: It’s started with the first dose of antibiotics (especially for suspected pneumococcal meningitis) and stopped if it turns out to be a non-bacterial cause. 3. **IV ampicillin 2g every 4 hours**: This is added if **Listeria monocytogenes** is suspected, particularly in: - Patients aged over 55 years. - Immunosuppressed patients (due to medications or conditions like HIV). 4. **Consult with Microbiology**: - This is necessary if the patient is a **returning traveler** from an area with potential antibiotic resistance, or if they are **immunocompromised**.

Answer 4

The use of **dexamethasone** for **all patients** with suspected bacterial meningitis is still debated. However, it is commonly used, especially for **pneumococcal** meningitis, as it reduces the risk of hearing loss and other neurological complications. But if the infection is found to be non-bacterial, the dexamethasone treatment is usually discontinued.

Answer 5

1. **Septic shock**: This is a severe drop in blood pressure due to overwhelming infection, which can lead to **disseminated intravascular coagulation (DIC)**. In DIC, the body's blood clotting mechanisms are disrupted, leading to both excessive clotting and bleeding, which can cause organ damage. 2. **Cerebral edema**: Swelling of the brain due to inflammation. This is dangerous as it increases intracranial pressure and can lead to brain damage. 3. **Seizures**: Meningitis can cause seizures, which are sudden, uncontrolled electrical disturbances in the brain. Seizures may result from direct infection or secondary to swelling and inflammation. 4. **Arteritis/Venous thrombosis**: Inflammation of the arteries (**arteritis**) or the formation of blood clots in the veins (**venous thrombosis**) can impair blood flow to the brain, potentially leading to strokes. 5. **Subdural effusions**: Fluid may collect between the layers of tissue surrounding the brain, creating pressure and potentially worsening brain inflammation. 6. **Hydrocephalus**: An abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased intracranial pressure and brain swelling. 7. **Brain abscess**: Pockets of pus can form within the brain tissue, which can be life-threatening and may require surgical drainage. 8. **Deafness**: Hearing loss, especially affecting cranial nerve VIII, is a common long-term complication of meningitis, particularly in bacterial cases. 9. **Partially treated meningitis**: This refers to cases where antibiotics have been administered before a formal diagnosis, altering typical findings in bacterial meningitis: - **CSF** may appear mainly **lymphocytic** rather than neutrophil-dominated. - **Normal glucose** levels may still be present. - Positive **culture** results are reduced by 30%. - **Gram stain** sensitivity is also reduced by 20%. **Complications:** Headache, seizures, cerebral edema, hydrocephalus, **syndrome of inappropriate antidiuretic hormone secretion (SIADH),** residual neurological deficits (especially affecting cranial nerve VIII), and deafness are common. Some patients may also experience permanent **brain damage** or death.

Answer 6

Mortality rates: - Streptococcus pneumoniae: ~25% - Neisseria meningitidis: 5-10% - Haemophilus influenzae: ~5% Certain factors increase the likelihood of a worse prognosis: - Extremes of age: Both very young children and the elderly are more vulnerable. - Delays in diagnosis and treatment. - Severe symptoms such as stupor, coma, seizures, or focal neurological signs. Septic shock.

Answer 7

Prevention of Meningitis **Immunization:** Vaccination is the most effective method of preventing bacterial meningitis. Safe and affordable vaccines for organisms like Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae provide long-lasting protection. **Management of sick patients and their contacts**: Once a case is identified, close contacts should receive chemoprophylaxis (preventive antibiotics) to reduce the risk of spread. **Environmental control:** Reducing airborne infections, particularly in hospital settings, is crucial. This may involve isolation procedures or improved ventilation. **Surveillance**: Regular monitoring for meningitis outbreaks, particularly in areas like sub-Saharan Africa, is important for early detection and containment of epidemics.

Answer 8

Answer: Bacterial meningitis begins with infection of the upper respiratory tract or mucosal surfaces, such as the nasopharynx, followed by invasion into the bloodstream (bacteremia). Bacteria, like Neisseria meningitidis, then penetrate the blood-brain barrier, seeding the meninges and causing inflammation. This inflammatory response triggers the release of cytokines and other immune mediators, leading to: Cerebral edema: Swelling of the brain due to increased permeability of the blood-brain barrier, which raises intracranial pressure. Increased intracranial pressure (ICP): This results from both cerebral edema and increased CSF production or blocked absorption, contributing to symptoms like headaches, seizures, and vomiting. Vascular inflammation (arteritis or venous thrombosis): Inflammation can lead to strokes or venous clots, reducing blood supply to brain tissue. Subdural effusions: Fluid can accumulate between the meninges, causing pressure on the brain. Hydrocephalus: CSF flow is disrupted, leading to excessive accumulation and further increasing ICP. Seizures: Direct irritation of the brain by the infection or secondary to raised ICP. Neurological complications arise due to the increased pressure, reduced blood supply, and the direct inflammatory effects on brain tissue, which can lead to permanent brain damage, hearing loss, and cognitive deficits.

Answer 9

Answer: The clinical presentation of bacterial meningitis often includes:

Answer 10

**Answer:** The pathogenesis of bacterial meningitis typically follows three key steps: 1. **Infection of the Upper Respiratory Tract**: Bacteria like *Neisseria meningitidis*, *Streptococcus pneumoniae*, or *Haemophilus influenzae* often colonize the nasopharynx, the back of the throat, without causing immediate illness. These pathogens are commensals in the nasopharynx of healthy individuals but can become pathogenic under certain conditions. 2. **Invasion of the Bloodstream (Bacteremia)**: Under certain conditions, the bacteria invade the bloodstream, bypassing the body's immune defenses. This can happen due to immune suppression, anatomical defects in the meningeal structures, or breaches like sinusitis or head trauma. Once in the bloodstream, the bacteria multiply and evade immune clearance due to virulence factors such as polysaccharide capsules. 3. **Seeding and Inflammation of the Meninges**: Once the bacteria cross the blood-brain barrier (BBB), they invade the cerebrospinal fluid (CSF) and seed the meninges, leading to inflammation. The immune system responds by sending white blood cells, especially neutrophils, into the CSF, which releases inflammatory cytokines and enzymes. This inflammatory response increases the permeability of the BBB, leading to cerebral edema, increased intracranial pressure, and damage to the brain and spinal cord.

Answer 11

**Answer:** Differentiating bacterial, viral, and fungal meningitis is largely based on the findings in the cerebrospinal fluid (CSF) analysis: 1. **Bacterial Meningitis**: - **Appearance**: Turbid or cloudy CSF. - **Glucose**: Significantly **low** (<40 mg/dL), as bacteria consume glucose. - **Protein**: Elevated levels (>100 mg/dL) due to increased permeability of the blood-brain barrier. - **WBC Count**: Elevated with **neutrophilic predominance** (>1000 cells/µL). - **Culture/Gram Stain**: Positive for bacteria in most cases. 2. **Viral (Aseptic) Meningitis**: - **Appearance**: Clear to slightly turbid CSF. - **Glucose**: Normal, as viruses do not consume glucose in the same way. - **Protein**: Mildly elevated or normal (50-100 mg/dL). - **WBC Count**: Elevated with **lymphocytic predominance** (10-500 cells/µL). - **Culture/Gram Stain**: Negative for bacteria; PCR may be positive for viruses. 3. **Fungal Meningitis**: - **Appearance**: Clear to slightly cloudy CSF. - **Glucose**: Decreased but less dramatically than in bacterial meningitis. - **Protein**: Elevated but less than in bacterial meningitis (50-150 mg/dL). - **WBC Count**: Elevated with **lymphocytic predominance**. - **Culture/Smear**: Positive for fungi; **India ink stain** may show *Cryptococcus*.

Answer 12

**Answer:** Key clinical signs of meningitis include: - **Headache** (severe, typically frontal). - **Fever** (>38°C). - **Neck stiffness** (nuchal rigidity). - **Nausea and vomiting**. - **Photophobia** (sensitivity to light). - **Seizures** (focal or generalized). - **Altered mental status** (ranging from confusion to coma). **Kernig’s Sign**: - To elicit Kernig’s sign, the patient is placed in a supine position with their hips and knees flexed to 90°. The examiner then attempts to extend the patient’s knee. A **positive Kernig’s sign** is when the patient experiences pain or resistance to knee extension, indicating meningeal irritation. **Brudzinski’s Sign**: - To elicit Brudzinski’s sign, the patient is again in a supine position. The examiner gently flexes the patient’s neck towards the chest. A **positive Brudzinski’s sign** is when this movement causes **involuntary flexion of the hips and knees**, which also suggests meningeal irritation.

Answer 13

**Answer:** The management of bacterial meningitis involves **early diagnosis and immediate initiation of treatment**, as the condition is a medical emergency. The key aspects of management include: 1. **Empiric Antibiotic Treatment**: - **IV Ceftriaxone (2g twice daily)** or **Cefotaxime (2g four times daily)** is the first-line treatment for most cases of bacterial meningitis. - **IV Ampicillin (2g every 4 hours)** is added if *Listeria monocytogenes* is suspected, particularly in patients >55 years of age, those with immunosuppression, or those with a history of consumption of unpasteurized dairy. - For patients with recent travel to endemic areas or a history of immunocompromised status, consultation with microbiology is essential for considering potential penicillin-resistant pathogens or unusual organisms. 2. **Corticosteroids (Dexamethasone)**: - **Dexamethasone** (0.15 mg/kg every 6 hours) is given for **4 days** in suspected cases of **pneumococcal meningitis**. It is administered **before** or with the first dose of antibiotics. - The rationale is that corticosteroids reduce inflammation, particularly in **pneumococcal** and **Haemophilus influenzae** meningitis, which helps reduce complications like cerebral edema and hearing loss. - Dexamethasone should be discontinued if a non-bacterial cause of meningitis is identified. 3. **Supportive Care**: - **Aggressive fluid resuscitation** to maintain adequate perfusion. - **Inotropes** to increase aortic diastolic pressure and improve myocardial contractility if septic shock is present. - **Prophylaxis** for close contacts, usually with rifampicin or ciprofloxacin, to prevent spread of the infection.

Answer 14

**Answer:** Common complications of meningitis include: 1. **Septic Shock**: This can lead to **multi-organ failure** and DIC, significantly increasing mortality risk. 2. **Cerebral Edema**: Swelling in the brain can lead to increased intracranial pressure, brain herniation, and brain damage. 3. **Seizures**: Common in meningitis, particularly in bacterial forms, and can cause long-term neurological damage. 4. **Hydrocephalus**: Accumulation of CSF in the brain, leading to increased pressure and potential for brain damage. 5. **Hearing Loss**: Damage to the auditory nerves, especially cranial nerve VIII, is a common long-term complication. 6. **Neurological Deficits**: Patients may suffer from residual motor or cognitive deficits after recovery, particularly in cases with **delayed treatment** or complications like **cerebral infarctions**. 7. **Mortality**: Mortality varies by pathogen: - **Streptococcus pneumoniae**: ~25%. - **Neisseria meningitidis**: 5-10%. - **Haemophilus influenzae**: ~5%. The prognosis is worse in patients with **extremes of age** (very young or elderly), those who experience **delays in treatment**, and those presenting with **coma, seizures, or septic shock**.

Answer 15

. **Mechanisms Leading to Increased ICP in Meningitis** 1. **Interstitial Edema**: - This occurs when the normal flow of **cerebrospinal fluid (CSF)** is obstructed, often due to **hydrocephalus** (an accumulation of CSF in the ventricles of the brain). In meningitis, inflammation can block CSF drainage, leading to an abnormal buildup of fluid. - The fluid accumulation increases pressure inside the skull, which compresses brain tissue. 2. **Cytotoxic Edema**: - In cytotoxic edema, there is **swelling of the brain cells** themselves. This swelling is triggered by toxic factors released by bacteria and the immune system's response to the infection, primarily via **neutrophils** (a type of white blood cell that fights infection). - The infected cells lose their ability to regulate water and sodium, leading to excess water retention in the cells, contributing to brain swelling. 3. **Vasogenic Edema**: - This type of edema arises from damage to the **blood-brain barrier (BBB)**, which normally prevents harmful substances from crossing into the brain. In meningitis, inflammation increases the permeability of the BBB, allowing fluids and plasma proteins to leak into the brain tissue, leading to swelling.

Answer 16

The combined effect of interstitial, cytotoxic, and vasogenic edema leads to a **vicious cycle**: - **Obstructed CSF flow** and swelling cause increased **intracranial pressure (ICP)**. - **Worsening cerebral edema** further compromises the **cerebral blood flow (CBF)**. - As ICP rises, it compresses the **brain tissue and blood vessels**, reducing the brain's access to oxygen and nutrients. - This can lead to **ischemia** (insufficient blood supply) and **cell death** if left untreated. If medical intervention is delayed or inadequate, the rising ICP will continue unchecked. Eventually, this will result in **endothelial injury**, **vasospasm** (sudden narrowing of blood vessels), and **thrombosis** (blood clots), worsening the situation by blocking both blood flow and CSF flow further.

Answer 17

In addition to the effects in the brain, **systemic hypotension** (low blood pressure) from **septic shock** can reduce cerebral perfusion, depriving the brain of the oxygen it needs, thus worsening the brain’s condition. This systemic and cerebral damage can lead to **diffuse central nervous system (CNS) ischemia**—a reduction of blood flow throughout the brain—eventually causing death due to brain herniation or other systemic complications.

Answer 18

- **Increased CSF viscosity**: Due to plasma components entering the subarachnoid space (the space where CSF flows), the CSF becomes thicker. This reduces **venous outflow**, contributing to interstitial edema. - **Accumulation of bacterial debris** and **immune cells** like neutrophils leads to cytotoxic edema, as mentioned earlier. - These forms of edema increase **intracranial hypertension**, which reduces **cerebral blood flow**. Without proper blood flow, brain cells switch to **anaerobic metabolism**, producing **lactate** (a byproduct of oxygen-deprived metabolism) and causing **lactic acidosis**. ### **Hypoglycorrhachia** Hypoglycorrhachia refers to low glucose levels in the CSF. In meningitis: - **Anaerobic metabolism** increases lactate levels in the brain. - At the same time, **glucose transport** into the CSF is impaired due to inflammation and damage to the blood-brain barrier. - This depletion of glucose in the brain leads to neuronal dysfunction, as brain cells rely on glucose for energy. ### **Outcomes Without Intervention** If left untreated: - **Neuronal injury** begins as a result of poor oxygenation, reduced glucose availability, and lactate accumulation. - This injury can range from **transient dysfunction** (temporary and reversible) to **permanent neuronal damage** and death of brain cells, resulting in cognitive and neurological deficits.

Meningitis Flashcards

(44 cards)