Meningitis and Sepsis: Causes, Diagnosis and Management PDF

Here is the transcription of the image into markdown format ### Meningitis and Sepsis Stephen Ritchie [email protected] The image shows a diagram of the layers of meninges and the skull. - Skull - Dura mater - Arachnoid mater - Pla mater - Brain The image shows a diagram comparing normal m...

Here is the transcription of the image into markdown format ### Meningitis and Sepsis Stephen Ritchie [email protected] The image shows a diagram of the layers of meninges and the skull. - Skull - Dura mater - Arachnoid mater - Pla mater - Brain The image shows a diagram comparing normal meninges to meningitis. In the normal configuration: The cerebrospinal fluid is clear. In meningitis: The cerebrospinal fluid contains bacteria, white blood cells, inflammatory proteins, and cell debris. Inflammation of the subarachnoid space extends to the surface of the brain. ### Meningitis is caused by: | Cause | Description | |--------------|--------------------------------------------------------------------------------------| | Viruses | common, mild, spontaneously improves: enteroviruses, influenza, HSV2 | | Bacteria | common, serious, medical emergency: N. meningitidis, streptococcus pneumoniae Rare: Haemophilus influenzae, Listeria monocytogenes, mycobacterium tuberculosis| | Fungi | rare, AIDS or cancer: Cryptococcus neoformans | | Protozoa | rare, accidental ingestion of worm eggs or larvae, Angiostrongylus cantonensis- not in NZ| | Other | common: drugs, trauma, neurosurgery, cancer | The image shows a diagram of the systemic effects of inflammation and meningitis. Inflammation of the meninges leads to headache, photophobia, neck stiffness and drowsiness. Systemic inflammatory response causes fever, drowsiness, septic shock and in some cases rash (Neisseria meningitidis) ### Bacterial Meningitis Illness is preceded by nasopharyngeal colonisation. 10-20% of young adults are colonised with N. meningitidis. Bacteria enter subarachnoid space and propogate ### Diagnosis of meningitis *Clinical suspicion* Symptoms can be vague early in the illness and signs of meningitis appear late in the illness. Samples include cerebrospinal fluid, blood cultures, throat swab, and blood to detect bacterial DNA by PCR. A diagram shows how to test for meningitis using Kernig's sign. Kernig's sign: lift the legs slowly Meningitis: Sore Hamstrings. The image shows a diagram of spinal tap for extracting cerebrospinal fluid. ### Cerebrospinal Fluid Obtained by lumbar puncture. | | Bacterial Meningitis | Viral Meningitis | |---------------------|----------------------|------------------| | Glucose | ↓ | Normal | | Protein | ↑ | ↑ or Normal | | White Blood Cells | ↑ | ↑ | | Cells | Neutrophils | Lymphocytes | | Gram Stain | + / - | - | | Culture | ++ / - | - | ### Meningococcal disease: *Neisseria meningitidis* The frequency of this disease has changed over time. The epidemic occurred during the 1990’s. The cases often occur in winter. It is a deadly disease commonly effecting Maori and Pacific children. The image illustrates Meningococcal disease cases and influenza isolates by month, 2001-2007 The image illustrates Meningococcal disease rates by age group and ethnicity, 2007 The image illustrates Meningococcal disease case-fatality rates, 2007-2011 The image illustrates effects of Meningococcal disease. ### Management of Bacterial Meningitis GIVE IV antibiotics (penicillin). Resuscitate. Take blood cultures when IV line sited. Transfer to hospital. Investigations, pain relief, fluids, IV antibiotics. DROPLET precautions ### Management of Viral Meningitis DROPLET precautions Reassurance. Analgesia. Can usually recover at home ### Sepsis How do infections (e.g. N. meningitidis or appendicitis) kill people? The bacterial cell wall contains lipopolysaccharide - a substance foreign to the human body Lipopolysaccharide and other bacterial components interact with human cells e.g. endothelial cells Platelets white blood cells. Upon activation, phagocytes engulf and kill bacteria. Once human cells have been triggered by bacterial components they release cytokines, for example interferon, tumour necrosis factor, interleukin -2, IL-6 etc. Cytokines induce changes in neighbouring vessels and immune cells follow the chemical gradient to get to the infection (chemotaxis). Gaps open between endothelial cells as endothelial cells express proteins which makes them more sticky. Neutrophils bounce along the sticky epithelium then squeeze through the gaps between epithelial cells (diapedis) and then move towards the site of infection (chemotaxis). At the same time antibodies bind to bacterial sugars and proteins which also stimulate human immune cells. Complement cascade - a biochemical cascade is triggered by: Antibody bound to bacterial components. Bacterial sugars bound to an immune protein called mannose binding lectin (MBL). * Complement forms spontaneously on the surface of bacteria. * Complement can make holes in bacterial cell wall to kill the bacteria. * Complement binds to bacteria (opsonisation) to increase recognition by immune cells. * Complement enhances chemotaxis. During Serious bacterial infection blood vessels open up (vasodilation) to increase blood flow to the site of infection, to provide oxygen nutrients and more immune cells If infection worsens and immune response increases further vasodilation occurs (and in non-infected parts of the body) In rare circumstances this can lead to shock - reduced blood pressure, tachycardia and reduced perfusion of organs. * The image provides a list of symptoms including: * tachycardia * low blood pressure * skin grey and clammy * aching pains * reduced urine output During bacterial infections neutrophils release DNA into small blood vessels where the DNA is sticky and traps bacteria, red blood cells, and platelets. The small blood vessels in organs become clogged, reducing blood flow and oxygenation. ### Management of Septic Shock It is an emergency - in mild cases the mortality rate is 10-15%. Once organ failure has occurred the mortality rate increases to 40-50%. The goals of treatment are to maintain organ function and resolve the cause of infection. Early recognition is essential