Bacterial Meningitis

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Introduction :
     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 )

Etiology :
  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 )

Pathology :
Meningeal exudate.
Ventriculitis.
Subdural effusion.
Empyema.
Perivascular inflammatory infiltrate.
Cerebral infarction.
Inflammation of spinal nn.
Inflammation of cranial nn.
Increase of ICP :
      mechanisms.
      cerebral perfusion = MAP – ICP(<50 cmH2O).
      non-localizing sign
SIADH (ICP & hypotonicity).
Herniation usually does not occur.
Hydrocephalus :is uncommon acute complication.either communicating or non-communicating.
Increase CSF proteins.
Hypoglycorrhachia.

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..

Acute Flaccid Paralysis

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Differential Diagnosis of Acute Weakness:
Cerebral: Bilateral strokes, Hysteria…
Cerebellar: Acute cerebellar ataxia syndromes.
Spinal: Compressive myolopathy, Transverse
myelitis….
Peripheral nerve: Acute inflammatory demyelinating
neuropathy, Toxic neuropathy, Diphtheria,
Tick paralysis
Neuromuscular junction: Botulism, Myasthenia Gravis…
Muscle disease: Acute myositis
Acute inflammatory myopathies
Metabolic myopathies,
Periodic paralysis…

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.
Guillain-Barré Syndrome.
Poliomyelitis.
Transverse Myelitis.

Guillain-Barré Syndrome
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.

GBS…Pathophysiology
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
vaccinations
epidural anesthesia
thrombolytic agents

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.

Clinical Features
Usually 2 - 4 weeks following respiratory or GI infection.
The classic presentation:
Fine paresthesias in the toes and fingertips.
Lower extremity weakness: symmetric & ascending.
Gait unsteadiness.
Inability to walk.
Respiratory muscles involvement.
Neuropathic pain… low back pain.
Cranial Neuropathy:
Facial nerve is most commonly affected, resulting in
bilateral facial weakness..

Von Willebrand Disease
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.
4. Angiodysplasia.
5. Seizures disorders treated with valproate.
6. Hypothyroidism.

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.

Results:
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.

Conclusions:
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.

Acid-Base Disturbances

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Renal Failure
Emergent indications for Hemodialysis
Pericarditis
Uremic encephalopathy
Bleeding Diathesis
Severe hyperkalemia
Severe acidosis
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.
 anorexia
 decreased cognitive tasking and depression,
 severe anemia unresponsive to erythropoietin,
 persistent pruritus

How to read an ABG
pH  acidemia / alkalemia
Major factor  metabolic / respiratory
Compensation
Anion gap
Delta / delta

Case 1
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.
Case 2
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

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