Definition/Description

Meningitis

The communicable disease of the central nervous system causes inflammation of the meningeal membranes (involving all three layers) surrounding the brain and spinal cord.

Before the age of antibiotics, the condition was universally fatal. Nevertheless, even with great innovations in healthcare, the condition still carries a death rate of close to 25%.

The disease is often caused by many different pathogens including bacteria, fungi, or viruses, but the very best global burden is seen with bacterial meningitis.

Despite breakthroughs in diagnosis, treatment, and vaccination, in 2015, there have been 8.7 million reported cases of meningitis worldwide, with 379,000 subsequent deaths.

Image credit: Google
The first case of meningitis associated with COVID 19 was detected in early 2020. A preliminary report warned that SARS-CoV-2 could have neuroinvasive potential because some patients present with meningitis symptoms (for example, headache, nausea, vomiting).

Etiology:

Meningitis is defined as inflammation of the meninges. The meninges are the three membranes (the dura, arachnoid mater, and pia mater) that line the spinal canal and skull enclosing the brain and spinal cord (encephalitis is inflammation of the brain itself).

Meningitis is often caused by infectious and non-infectious processes (autoimmune disorders, cancer/paraneoplastic syndromes, drug reactions).
Photo Credit: Google


The infectious etiologic agents of meningitis include bacteria, viruses, fungi, and fewer commonly parasites.

Risk factors for meningitis include:
Chronic medical disorders (renal failure, diabetes, adrenal insufficiency, cystic fibrosis); Extremes of age; Undervaccination; Immunosuppressed states (iatrogenic, transplant recipients, congenital immunodeficiencies, AIDS); Living in crowded conditions; Exposures: visit endemic areas (Southwestern U.S. for cocci; Northeastern U.S. for Lyme disease); Vectors (mosquitoes, ticks); Alcohol use disorder; Presence of ventriculoperitoneal (VP) shunt; Bacterial endocarditis; Malignancy; Dural defects; IV drug use; red blood cell anemia; Splenectomy; sinusitis, mastoiditis, and otitis.

Meningococcal meningitis is of particular importance thanks to its potential to cause large epidemics. Bacteria are transmitted from person-to-person through droplets of respiratory or throat secretions from carriers.[6] The disease can affect anyone of any age, but mainly affects babies, preschool children, and children. Untreated meningococcal meningitis is often fatal in up to 50% of cases and may result in brain damage, deafness, or disability in 10% to 20% of survivors.[6] While vaccines against meningococcal disease are available for more than 40 years, so far no universal vaccine against meningococcal disease exists.

Epidemiology:
The incidence of meningitis is 2 of 6 per 10,000 adults per annum in developed countries and is up to ten times higher in less-developed countries.

In the United States, the annual incidence of bacterial meningitis is approximately 1.38 cases/100,000 population with a case death rate of 14.3%.

The highest incidence of meningitis worldwide is in an area of sub-Saharan Africa dubbed “the meningitis belt” stretching from Ethiopia to Senegal.

The prevalence of meningitis has greatly decreased over the last fifteen years thanks to the development of vaccines.
Photo Credit: Google


Pathogens:
Most common bacterial causes of meningitis in the United States are: Streptococcus pneumoniae (incidence in 2010: 0.3/100,000); B Streptococcus; Neisseria meningitidis (incidence in 2010: 0.123/100,000); Haemophilus influenzae (incidence in 2010: 0.058/100,000); Listeria monocytogenes (video below of bacterial meningitis).

The most common viral agents of meningitis are non-polio enteroviruses (group b coxsackievirus and echovirus). Other viral causes: mumps, Parechovirus, Herpesviruses (including Epstein Barr virus also referred to as Mononucleosis, Herpes simplex virus, and Varicella-zoster virus), measles, influenza, and arboviruses (West Nile, La Crosse, Powassan, Jamestown Canyon).

Fungal meningitis typically is related to an immunocompromised host (HIV/AIDS, chronic corticosteroid therapy, and patients with cancer). Fungi causing meningitis include: Cryptococcus neoformans; Coccidioides immitis; Aspergillus; Candida; Mucormycosis (more common in patients with DM and transplant recipients; direct extension of sinus infection).
Photo Credit: Google



Pathophysiology:

Meningitis typically occurs through two routes:

Hematogenous seeding: Bacteria colonize the nasopharynx and enter the bloodstream after the mucosal invasion. Upon making their thanks to the subarachnoid space, the bacteria cross the barrier, causing an immediate inflammatory and immune-mediated reaction.

Direct contiguous spread: Organisms can enter the spinal fluid (CSF) via neighboring anatomic structures (otitis media, sinusitis), foreign objects (medical devices, penetrating trauma), or during operative procedures.

Viruses can penetrate the central system nervous (CNS) via retrograde transmission along neuronal pathways or by hematogenous seeding.

Characteristics/Clinical Presentation:
Headache, fever, vomiting, and rigidity of the neck are the foremost common symptoms that present with the onset of meningitis. Early symptoms include nausea, drowsiness, and confusion. Pain within the posterior thigh or lumbar region may also be noted. Later symptoms can include seizures, photophobia, and rapid breathing rate. additionally, a rash on the skin, scanty petechial (red or purple non-blanching macules smaller than 2mm in diameter), or a purpuric (larger than 2mm) appears on approximately 80-90% of people with bacterial meningitis.

Meningitis causes inflammation of the meningeal membranes; as a result, nerve roots may endure tension as they undergo these inflamed membranes. Passive ROM of the neck into flexion will gradually become painful and limited. Also, neck extension and rotation could also be painful as well, but to not the extent of flexion. In severe cases, Brudzinki’s sign ( caused by passive neck flexion producing flexion of the hips or knees) or Kernig’s sign presents. In cases when meningitis isn't treated immediately (especially bacterial meningitis), the parenchyma within the brain could also be involved. As a result, individuals may present with lethargy, vomiting, seizures, papilledema, confusion, coma, focal deficits, and nerve palsies.
Photo Credit: Google


Treatment

  •  Antibiotics and probative care are critical in all cases of bacterial meningitis.

  •  Managing the airway, maintaining oxygenation, and giving sufficient intravenous fluids while furnishing fever control is a corridor of the foundation of meningitis operation. 

  •  The type of antibiotic is grounded on the presumed organism causing the infection. The clinician must take into account case demographics and once medical history in order to give the stylish antimicrobial content. 

  •  Steroid remedy There's inadequate substantiation to support the wide use of steroids in bacterial meningitis. 

  •  Increased Intracranial Pressure If the case develops clinical signs of increased intracranial pressure( altered internal status, neurologic poverties,non-reactive pupils, bradycardia), interventions to maintain cerebral perfusion include 

  •  Elevating the head of the bed to 30 degrees 
  •  persuading mild hyperventilation in the intubated case 
  •  Bibulous diuretics similar to 25 mannitol or 3 saline.
  • Chemoprophylaxis is Indicated for close connections of a case diagnosed with meningitidis and H. influenzae type B meningitis. near connections include housemates, significant others, those who have participated in implements, and health care providers in propinquity to concealment( furnishing mouth-to-mouth reanimation, intubating without a facemask)

Tests
Meningitis is diagnosed through cerebrospinal fluid( CSF) analysis, which includes white blood cell count, glucose, protein, culture, and in some cases, polymerase chain response( PCR). CSF is attained via a lumbar perforation( LP), and the opening pressure can be measured. 

fresh testing should be performed acclimatized on suspected etiology Viral Multiplex and specific PCRs; Fungal CSF fungal culture, India essay stain for Cryptococcus; Mycobacterial CSF Acid-fast bacilli smear and culture; Syphilis CSF VDRL; Lyme complaint CSF burgdorferi antibody.

Complications 
The median threat of sequelaepost-discharge was19.9( 2010 meta-analysis). The most common organism insulated wasH. influenzae, followed by S.pneumoniae. The most common sequelae were hearing loss( 6), followed by behavioral(2.6) and cognitive difficulties(2.2), motor deficiency(2.3), seizure complaint(1.6) and visual impairment(0.9).

Other complications include

Increased intracranial pressure from cerebral edema is caused by increased intracellular fluid in the brain. Several factors are involved in the development of cerebral edema increased in blood-brain hedge permeability, cytotoxicity from cytokines, vulnerable cells, and bacteria. 
  •  Hydrocephalus 
  •  Cerebrovascular complications 
  • Focal neurologic poverties

Physical Therapy Management 
  •  According to the American Physical Therapy Association's companion to Physical Therapist Practice contagious diseases of the central nervous system fall under the following favored practice patterns; 5D disabled Motor Function and sensitive Integrity Associated with Nonprogressive diseases of the Central Nervous System- Acquired in Adulthood or Adolescence and 5I disabled Arousal, Range of Motion, and Motor Control Associated with Coma, Near Coma, or Vegetative State. 
 
  •  generally, physical remedy treatment is initiated in the ferocious care unit. While initiating a plan of care, it's pivotal to keep in mind a case’s map information or contraindications to remedy similar as intracranial pressure, cerebral perfusion pressure, and other lab values that determine recuperation guidelines. Meningitis may present with analogous symptoms to brain injuries, neurological complications, immunological insufficiency, vascular concession, and fresh secondary impairments. 

  •  Also understanding the colorful stages of knowledge or behavioral changes a case with secondary complications may go through can guide the approach to treatment. The therapist should produce a terrain that would ease the case’s acuity to sensitive input similar to light or sound, therefore, creating a structured terrain to exclude behavioral outbursts. Close monitoring of the vital signs will allow the therapist to gauge the case's receptiveness to remedy. The therapist should be familiar with the Glasgow Coma Scale and cover the case’s progression through the situations of knowledge. 
 
  •  Proper positioning and range of stir exercise should be initiated as soon as safely possible in the acute phase. Proper positioning with pillows and apkins will cover the skin integrity and forestallment contractures. Maintaining mobility of the box and neck is important to sustain functional mobility. Before a remedy is initiated with a case, the chances of secondary impairments are dropped allowing for a better prognostic. 

  • A primary crucial element to treating a case recovering from bacterial meningitis is proper education not only to the case but for the family and caregivers as well. furnishing the case and family with education on the complaint, stages of the complaint, secondary complications, advising signs, and coffers can encourage the case and family to come more involved in the treatment. It's veritably important to educate on the goods of different systemic involvement and how the timeline of recovery may vary.
 
 
 Differential opinion 
  • Stroke 
  •  Subdural hematoma 
  •  Subarachnoid hemorrhage 
  •  Metastatic brain complaint 
  •  Brain abscess( might attend with meningitis)

  1. Jump up to: