Bacterial meningitis (infection): Difference between revisions
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==Types of purulent meningitis== | ==Types of purulent meningitis== | ||
===Pneumococcal purulent meningitis=== | ===Pneumococcal purulent meningitis=== | ||
Pneumococcal purulent meningitis occurs at any age, usually of secondary etiology. | |||
'''Patogenní''' jsou '''opouzdřené kmeny'''. | '''Patogenní''' jsou '''opouzdřené kmeny'''. | ||
Nejtěžší průběh má u oslabených osob (alkoholici, cirhotici) a u splenektomovaných osob (fulminantní průběh). | Nejtěžší průběh má u oslabených osob (alkoholici, cirhotici) a u splenektomovaných osob (fulminantní průběh). |
Revision as of 20:50, 10 February 2022
Bacterial meningitis is one of the most serious acute diseases. Its progress is very fast. It leaves permanent consequences or ends in death. It is an acute infection of the subarachnoid spaces and meninges characterized by the presence of polymorphonuclear cells in liquor.
Characteristics
It is an urgent condition in neurology accompanied by encephalitis. Typical manifestations are acute meningeal syndrome, cefalea, vomiting, fever with photophobia and mental changes.
Etiology
According to the method of origin:
- primary – infection occurs Hematogenous
- secondary – transition from surrounding deposit (middle ear, petrosis axis, paranasal sinuses)
- throwing in infective endocarditis
- predisposing factors - head injuries, subdural barrier disorder, etc.
The bacterial spectrum differs significantly in newborns, children and adults:
- newborns: G- rods: E. coli, Klebsiella, Haemophilus influenzae
- children: Haemophilus influenzae, pneumococcus, meningococcus
- adults: pneumococcus, meningococcus
The causative agents are diverse - they include: Listeria monocytogenes, Streptococcus pyogenes, Staphylococcus aureus, mycotic agents or amoebae (rarely).
Risk factors: ethylism, diabetes mellitus, hyposplenism, AIDS.
Pathogenesis
Bacteria penetrate the meninges hematogenously (usually from a distant site of inflammation), or porogenically from surrounding inflammation (otitis, sinusitis, etc.). Another mechanism of occurrence is trauma with disruption of the dura mater - communication between the external and intracranial space is created. Rarely, the source of infection is iatrogenic (lumbar puncture, infected shunt).
Pathological-anatomical picture
- Congestion of meninges with polymorphonuclear infiltration;
- blood-brain barrier breached;
- purulent exudate from basal cisterns into convex sulks;
- arteriitis and venous thromboflebitis of subarachnoid vessels;
- brain is not affected by itself (intact pia mater prevents the formation of abscesses);
- edema and ischemia of the brain;
- the condition can be complicated by thrombosis and subsequent infarcts of the brain;
- cerebral ventricles dilated, involvement of cranial nerves in cisterns common (oculomotor, n. VII, n. VIII);
- Healing is accompanied by scarring, with hydrocephalus.
Diagnosis
Diagnosis should be made as quickly as possible; after admission to hospital, diagnosis should be made and treatment started within 30 min-1 h. In secondary , a history - repeated inflammation of the middle ear or sinuses will help.
- blood collection for hemoculture;
- Inflammatory cerebrospinalfluid at lumbar puncture (intracranial hypertension must be excluded before !);
- fluid stained greenish yellow on lumbar puncture, cells is 100–10 000/mm3 (80-90 % polymorphonuclear cells), sugars decreased (0.3 g/l), protein increased (0.5 g/l), lactate dehydrogenase increased, chloride normal;
- Gram-stained sediment is examined microscopically;
- Serological + immunological tests determine immunoelectrophoretically the capsular antigen in cerebrospinal fluid;
- a latex-agglutination test is also performed at the bedside - detection of antibodies in the fluid (quick orientation about the causative agent);
- the aim of the examination of the collected fluid is the identification of the infectious agent directly or by culturing according to the sensitivity to use the optimal treatment, the cultivation is negative in 10–20%;
- we choose a suitable ATB according to: age, severity, result of samples.
Clinical course
thumb|Symptomy meningitidy Primary purulent meningitis manifests itself in a very rapid deterioration of the condition, in contrast to secondary, which has a more prolonged course. From full health, it progresses to a typical image within 24-36 hours. The patient is hyperpathic, has severe headache, is photophobic, rising temperature. There are meningeal symptoms, confusion and reluctance. Accompanying disorder of consciousness occur in about 90% of patients, bradycardia is seen in edema of the brain. Cerebral symptoms include hemiparesis and epileptic seizures. The cranial nerves, mainly the oculomotor nerves and n. VII and VIII, are affected. Other complications include septic ones (pyogenic arthritis, acute bacterial endocarditis), within a few hours, vital signs may fail, shock and disseminated intravascular coagulation (DIC) may develop. Development is so rapid that it may resemble stroke, aggression and disorientation may occur. In meningococcal and haemophilic meningitis, petechiae and suffusion are found on the skin. Newly formed petechiae, larger than 2 mm, confluent and located on the thighs and abdomen, are typical of meningococcal disease. Differentiation from ordinary urticaria is possible by pressure (exanthema at pressure below the petechiae persist ('slide method')) [1].
Complications
The complications of purulent meningitis are numerous. Acute stage may be accompanied by brain edema which may cause visual or hearing impairment or central palsy. In the recovery phase, parainfectious arthritis, myocarditis, headache and fatigue occur. Children may then have psychomotor retardation or hydrocephalus.
Prognosis
Symptoms usually subside on the 3rd-5th day of treatment and the patient gradually improves. Early diagnosis, adequate therapy and resistance of the organism are crucial. In practice, the disease has a dual course:
- mild: insignificant symptoms, rapid correction of findings in the liquor
- difficult: patient in coma from the beginning, death can occur within 24 hours under the picture of shock, a frequent complication of adrenal haemorrhage (Waterhouse-Fridrichsen) or DIC
Differential diagnosis
- if history is absent and consciousness disorder progresses → rule out stroke, subarachnoid haemorrhage, metabolic comatose states (DM), poisoning, etc.
- other meningitis (serous, tuberculous, mycotic), brain abscess, epidural empyema/abscesses (intracranial or spinal), subdural empyema, infective endocarditis with CNS embolizations, thrombophlebitis of the sinus, rupture of dermoid cyst, brain tumours
- the diagnosis is determined by examination of the cerebrospinal fluid
Treatment
- causal: antibiotics
- symptomatic: antiemetics, analgesics, antiedema preparations, infusion
- early treatment with ATB (RIGHT AWAY!, control CSF in 1-2 days)
- a doctor can save a life by administering penicillin before transport to hospital
- Optimal today are Generation III cephalosporins (e.g. cefotaxime, ceftriaxone)
- the selected ATB must cross the blood-brain barrier well (not tetracycline, partially aminoglycosides), dosing in children is guided by weight and age
- chloramphenicol may rarely lead to aplastic anaemia, also unsuitable for children under 5 years of age
- the source of meningitis may be another inflammatory deposit in the body = secondary meningitis: early treatment and search for a possible cause
- correction of the internal environment with respect to ADH secretion
- we correct possible brain edema, administer vitamins and other symptomatic therapy
- We discontinue ATB no earlier than 10-14 days after temperature normalization
- meningococcal meningitis is contagious (vaccination, prophylaxis in family members)
Types of purulent meningitis
Pneumococcal purulent meningitis
Pneumococcal purulent meningitis occurs at any age, usually of secondary etiology. Patogenní jsou opouzdřené kmeny. Nejtěžší průběh má u oslabených osob (alkoholici, cirhotici) a u splenektomovaných osob (fulminantní průběh). Primárně se může přenášet vzduchem (hlavně v zimě), avšak nejčastěji vzniká sekundárně. Infekční agens se množí se v dýchacích cestách, odtud se šíří krví do mozku. Do mozku se může též dostat přestupem z dutin či ucha. Není vzácností ani vznik abscesu. V CSF je typický obraz pro purulentní meningitidu, nutná je mikrobiologie.
Meningokoková meningitida a sepse
Meningokoková meningitida je spojena s projevy systémové odpovědi organismu. U nás způsobují onemocnění převážně sérotypy: B,C,A,Y, přenáší se vzdušně. Vzniká často po vyčerpání (sport, diskotéka, probdělá noc atd.). Projevy:
- někdy zpočátku 1–2 dny příznaky faryngitidy, únavnost a bolesti břicha
- následně horečka, zvracení, poruchy vědomí
- na kůži se objevují petéchie a sufúze
- rozvoj DIC a šoku – multiorgánové postižení
Nejtěžší případy končí během několika hodin pod obrazem Waterhouse-Friderichsenova syndromu (krvácení do nadledvin).
Sepse má větší úmrtnost než meningitida. Při sepsi je nález v likvoru normální.
Shuntová meningitis
Shuntová meningitis se vyskytuje u dětí, které mají při hydrocefalu zavedené spojky pro odvod moku (může dojít k infekci).
Jiná neurologická poškození
Jedním z možných poškození mohou být obrny hlavových nervů či motorické poruchy (např. hemiparéza či kvadruparéza, ataxie). Dále se může vyskytnout mozková ischémie, diencefalohypofyzární syndrom či SIADH (syndrome of inappropriate secretion of antidiuretic hormone), který se projeví oligurií a CSWS (cerebral salt wasting syndrome) projevující se polyurií.
Odkazy
Související články
- Meningitida • Meningitida (pediatrie)
- Virová meningitida • Serózní meningitidy a meningoencefalitidy • Herpetická meningoencefalitida
- Hnisavá meningitida • Hnisavá meningitida (pediatrie) • Hemofilová meningitida • Tuberkulózní meningitida
- Infekční onemocnění mozku • Neuroinfekce, záněty CNS/PGS • Encefalitida
- Meningokoková meningitida
Zdroj
Použitá literatura
Kategorie:Neurologie
Kategorie:Mikrobiologie
Kategorie:Infekční lékařství
Kategorie:Neurochirurgie
Kategorie:Patologie