Bacterial Infections Morphology Clinical Laboratory Disease Pathogenesis Manifestation Findings Macroscopic Microscopic Acute Yellow-tan exudate Meningeal arteries Heamatogenous spread Initial symptoms Lumbar puncture (the most common) This purulent exudate appeared engorged Fever Increased in Pyogenic The etiological agents covers the cerebral Neutrophilic exudate Severe ICP Meningitis is seen involving the headache spread from distant area hemispheres Abundant meninges neck of the body and lodged It usually settles at neutrophils Bacterial Prominent dilated Progression of at the CNS Along the base Elevated infection of the blood vessels disease Direct implantation of of the brain proteins Arachnoid especially the Confusion organisms Around cranial Reduced membrane Leptomeningeal Coma Trauma nerves glucose Subarachnoid vessels Seizure Congenital Openings to the Lumbar puncture is space Edema and focal Due to 4th ventricle malformation – only indicated in pts CSF inflammation ↑ICP ventricular septal defect without sign of extending into the HIE Iatrogenic Papiloedema superficial brain Toxic Lumbar puncture parenchyma Metabolic Local extension (Virchow-Robin Sinusitis space) Mastoid sinus Complications Later complications Frontal sinus Cranial nerve Infected tooth Cranial Nerves deficits and ischemic infarction deficits Osteomyelitis of the During infection, veins may inflamed and lead Ischemic Cranium to Phlebitis infarction Spine Phlebitis may disrupt blood flow, turbulance Hydrocephalus Pathophysiology may lead to formation of blood clot Blood clot may ultimately occlude smaller Vasculitis of the vessels and lead to liquefactive necrosis of the leptomeningeal arteries brain lead to an ischemic attack Hydrocephalus of the brain Purulent fibrinous exudate of infection may Hypoxic-Ischemic organize into fibrous tissue Encephalopathy (HIE) This fibrous tissue may block the exit of CSF at will then develop the 4th ventricle and lead to communicating Infection hs led to hydrocephalus disturbance in vascular Complications take to develop, sometimes it permeability of the brain develops long after the disease subsides This has led the to brain edema and leakage of protein into the CSF Ultimately, increased in ICP
Bacterial Infections Disease Pathogenesis Morphology Clinical Manifestation Laboratory Findings Macroscopic Microscopic Acute Pyogenic Meningitis Bacterial infection of the Arachnoid membrane Subarachnoid space CSF Heamatogenous spread (the most common) The etiological agents spread from distant area of the body and lodged at the CNS Direct implantation of organisms Trauma Congenital malformation – ventricular septal defect Iatrogenic Lumbar puncture Local extension Sinusitis Mastoid sinus Frontal sinus Infected tooth Osteomyelitis of the Cranium Spine Pathophysiology Vasculitis of the leptomeningeal arteries lead to an ischemic attack of the brain Hypoxic-Ischemic Encephalopathy (HIE) will then develop Infection hs led to disturbance in vascular permeability of the brain This has led the to brain edema and leakage of protein into the CSF Ultimately, increased in ICP Yellow-tan exudate This purulent exudate covers the cerebral hemispheres It usually settles at Along the base of the brain Around cranial nerves Openings to the 4th ventricle Meningeal arteries appeared engorged Neutrophilic exudate is seen involving the meninges Prominent dilated blood vessels especially the Leptomeningeal vessels Edema and focal inflammation extending into the superficial brain parenchyma (Virchow-Robin space) Initial symptoms Fever Severe headache neck Progression of disease Confusion Coma Seizure Due to ↑ICP HIE Toxic Metabolic Later complications Cranial nerve deficits Ischemic infarction Hydrocephalus Lumbar puncture Increased in ICP Abundant neutrophils Elevated proteins Reduced glucose Lumbar puncture is only indicated in pts without sign of Papiloedema Complications Cranial Nerves deficits and ischemic infarction During infection, veins may inflamed and lead to Phlebitis Phlebitis may disrupt blood flow, turbulance may lead to formation of blood clot Blood clot may ultimately occlude smaller vessels and lead to liquefactive necrosis of the brain Hydrocephalus Purulent fibrinous exudate of infection may organize into fibrous tissue This fibrous tissue may block the exit of CSF at the 4th ventricle and lead to communicating hydrocephalus Complications take to develop, sometimes it develops long after the disease subsides