Posted by e-Medical PPT
C.N.S infection is the most common cause of fever with S&S of C.N.S disease in children
Specific pathogen influenced by :age , immune status & epidemiology
Viral infections are more common
Clinical syndrome are similar inspite of incriminated pathogen
The common symptoms of the C.N.S infection are quite non-specific
Severity & constellation of symptoms determined by specific pathogen , host & anatomic distribution
Diagnosis depends on CSF examination
Acute bacterial meningitis beyond the neonatal period :
Associated with high rate of acute complications & risk of chronic morbidity
Meningitis in neonatal & post neonatal may overlap ( in 1-2 mo. old : GBS , strept. pn. , N.meningitidis , H.influenzae )
1) First 2 mo : maternal lora & infant enviroment (GBS , G-ve , L.monocytogenes ) , ocasionally : H.influenzae or pathogens of older infants.
2) 2-12 mo : Strept. pn. , N.meningitidis , H.influenzae
* Effects of immune deficits & anatomic ddefects.(Ps. Aerugenosa , staph. Aureus , coagulase –ve staph , Salmonella spp & L.monocytogenes )
Perivascular inflammatory infiltrate.
Inflammation of spinal nn.
Inflammation of cranial nn.
Increase of ICP :
cerebral perfusion = MAP – ICP(<50 cmH2O).
SIADH (ICP & hypotonicity).
Herniation usually does not occur.
Hydrocephalus :is uncommon acute complication.either communicating or non-communicating.
Increase CSF proteins.
Clinical manifestations :
Two patterns :1.rapidly progressive. 2.insidious
Two constellations of manifestation :1)related to non-specific systemic infection :fever which presents in 90-95%, anorexia, URTI, myalgia, arthralgia, tachycardia, hypotension & cutaneous signs. 2)related to meningeal irritation.
Other manifestation :3)younger than 18 mo. 4)increased ICP. 5)papilloedema is uncommon. 6)focal neurological signs(10-20%;30% in pneumococcus). 7)seizures(20-30%). 8)altred consciousness. 9)photophobia. 10)tachycerebrale..
Posted by e-Medical PPT
Cerebral: Bilateral strokes, Hysteria…
Cerebellar: Acute cerebellar ataxia syndromes.
Spinal: Compressive myolopathy, Transverse
Peripheral nerve: Acute inflammatory demyelinating
neuropathy, Toxic neuropathy, Diphtheria,
Neuromuscular junction: Botulism, Myasthenia Gravis…
Muscle disease: Acute myositis
Acute inflammatory myopathies
Acute Flaccid Paralysis
The sudden onset of generalized flaccid weakness in the absence of symptoms of encephalopathy implicates the motor unit.
AFP is an emergency in which management priorities are to support vital functions and reach a specific diagnosis in a timely manner with a focused history and physical examination.
It is an acute idiopathic monophasic acquired inflammatory demyelinating polyradiculoneuropathy.
GBS is the most common cause of acute flaccid paralysis in healthy infants and children.
Immune mediated disease.
There is no known genetic factors.
Two third of cases follow a respiratory or GI infection.
Campylobacter infection is the most common, but other organisms include CMV, EBV, HSV, Enteroviruses,…
Guillain-Barré syndrome has been reported to follow
The main lesions are acute inflammatory demyelinating polyradiculopathy, with acute axonal degeneration in some cases, particularly those following campylobacter infection.
Avariety of autoantibodies to gangliosides have been identified especially with axonal forms of the disease.
Usually 2 - 4 weeks following respiratory or GI infection.
The classic presentation:
Fine paresthesias in the toes and fingertips.
Lower extremity weakness: symmetric & ascending.
Inability to walk.
Respiratory muscles involvement.
Neuropathic pain… low back pain.
Facial nerve is most commonly affected, resulting in
bilateral facial weakness..
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vWD is due to an abnormality ,either quantitative ,absence or qualitative of the vWf.
vWf is a large multimeric glycoprotein that function as :
1.the factor Vlll carrier protein (vWf protect factor Vlll from degradation).
2. required for normal platelet adhesion (vWf binds on platelet to its specific receptor glycoprotein lb & acts as adhesive bridge between the platelet & damaged sub-endothelium at the site of vascular injury
vWf is composed of dimeric subunits that are linked by disulfide bonds to form complex multimers of low ,intermediate & high molecular weights .
The small multimers function mainly as carriers for factor Vlll.
High molecular weight multimers have higher numbers of platelet-binding sites & greater adhesive properties .
Each multimeric subunit has binding sites for the receptor glycoprotein lb on non-activated platelets & the receptor glycoprotein llb/llla on activated platelets,
this facilitates both platelet adhesion & aggregation
Acquired forms of vWD
1. Wilm’s tumor.
2. Congenital hear disease.
3. Systemic lupus erythmatosus.
5. Seizures disorders treated with valproate.
Aortic-valve Stenosis can be complicated by bleeding that is associated with acquired type 2A von Willebrand syndrome . However, the prevalence & cause of the haemostatic abnormality in aortic Stenosis are unknown .
We enrolled 50 consecutive patients with aortic Stenosis, who completed a standardized screening questionnaire to detect a H/O bleeding. 42 patients with sever aortic Stenosis underwent valve replacement.
Platelets function under conditions of high shear stress, vWf collagen-binding activity & Ag levels, & the multimeric structure of vWf were assessed @ base line & 1 day, 7 days, & six months post-operatively.
Skin or mucosal bleeding occurred in 21% of the patients with sever aortic Stenosis. Platelets-function abnormalities under condition of high shear stress, decreased vWf collagen-binding activity & the loss of the largest multimers, or a combination of these was present in 67 – 92 % of patients with sever aortic Stenosis & correlated significantly with the severity of valve Stenosis.
Type 2A vW Syndrome is common in patients with sever aortic Stenosis.
vWf abnormalities are directly related to the severity of aortic Stenosis & are improved by valve replacement in the absence of mismatch between patient & prosthesis.
Posted by e-Medical PPT
Emergent indications for Hemodialysis
Pulmonary edema refractory to diuretics
Non-emergent indications for Hemodialysis
Accelerated hypertension poorly responsive to antihypertensive medications
Persistent nausea and vomiting
Plasma creatinine > 12 mg/dL, or (BUN) > 100 mg/dL.
decreased cognitive tasking and depression,
severe anemia unresponsive to erythropoietin,
How to read an ABG
pH acidemia / alkalemia
Major factor metabolic / respiratory
Delta / delta
A 55-year-old woman is admitted with a complaint of severe vomiting for 5 days. Physical examination reveals postural hypotension, tachycardia, and diminished skin turgor.
A 58-year-old man with a history of chronic bronchitis developed severe diarrhea caused by pseudomembranous colitis.
Treatment of Metabolic Acidosis
The aim of therapy in metabolic acidosis is restoration of a normal extracellular pH.
The normal renal response in this setting is to markedly increase acid excretion, primarily as ammonium.
Thus, exogenous alkali may not be required if the acidemia is not severe (arterial pH >7.20), the patient is asymptomatic, and the underlying process, such as diarrhea, can be controlled