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

Learning Objectives
Understand the pathophysiology of TOS
Learn the provocative maneuvers to diagnose TOS
Understand treatment options for TOS

Case Presentation
EB is a 30 year old white female who presents with left upper extremity swelling and pain, which began while she was watching a movie in a theater. She says that when she left the movie, a couple of hours after the symptoms initially began, she noted that the swelling of her left arm was worse and there was pain in her shoulder region. She also could not get her ring off of her finger and her left hand was dusky. She did not have any shortness of breath or pleuritic chest pain. A few days before that the patient had been shoveling snow during a heavy snow storm and the day after that developed upper respiratory symptoms including sore throat, sharp chest pain, a sensation of her ears being plugged and swollen glands in her neck.
The patient had a Doppler evaluation which revealed clot in the subclavian and axillary veins. A CT scan of the chest revealed no evidence of pulmonary embolism. She had a hypercoagulable workup which was negative. She was treated with heparin and then started on Coumadin and consideration was given a couple of times to giving thrombolytics but this was not done. She was taken off her OCP.
Ultrasound of the left upper extremity was performed about 15 days after the onset of symptoms and revealed interval partial recanalization of the left subclavian vein and slight increase in flow within the left axillary vein in a patient with previous occlusive thrombus in these vessels.
MRI of the left upper extremity was performed to look for a compressive component to her vasculature in the left upper extremity as a cause for the DVT.

TOS – Differential Diagnosis
Cervical disc disease
Cervical facet disease
Malignancies (Pancoast/local tumors, spinal cord tumors)
Peripheral nerve entrapments (ulnar or median nerve)
Brachial plexitis
Rotator cuff injuries
Fibromyalgia, muscle spasm
Neurologic disorders (MS)
Chest pain, angina
Vasculitis
Vasospastic disorder (Raynaud’s)
Neuropathic syndromes of upper extremity

Stroke:An Introduction

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What is a Stroke? (Brain Attack)
Disruption of blood flow to part of the brain caused by:
Occlusion of a blood vessel (ischemic stroke)
OR
Rupture of a blood vessel (hemorrhagic stroke)

What happens with cutoff of blood supply?
Oxygen deprivation to nerve cells in the affected area of the brain -->
 Nerve cells injured and die -->
 The part of the body controlled by those nerve cells cannot function.

What happens with rupture of a blood vessel?
Oxygen deprivation to nerve cells in the affected area of the brain and local destruction of nerve cells-->
 Nerve cells injured and die -->
 The part of the body controlled by those nerve cells cannot function.

Stroke Impact
750,000 strokes per year
Third leading cause of death
(1st: heart disease, 2nd: all cancers)
Over 160,000 deaths per year
Over 4 million stroke survivors

Stroke Diagnosis
Symptoms of Stroke
Sudden numbness or weakness of face, arm or leg, especially on one side of the body
Sudden confusion, trouble speaking or understanding
Sudden trouble seeing from one or both eyes
Sudden unsteadiness, dizziness, loss of balance or coordination
Sudden severe headache with no known cause

Common Stroke Patterns
Left (Dominant) Hemisphere:
Aphasia
Right hemiparesis
Right hemisensory loss
Right visual field defect
Left gaze preference
Dysarthria
Difficulty reading, writing, or calculating

Right (Nondominant) Hemisphere:
Left hemiparesis
Left hemisensory loss
Left neglect
Left visual field defect
Right gaze preference
Dysarthria

Brainstem/Cerebellum/Posterior Circulation
Motor or sensory loss in all 4 limbs
Crossed signs (face vs. body)
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Cortical blindness

Spinal Cord lesions

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Anatomy
Spinal cord lies within protective covering of vertebral column.
Begins just below foramen magnum of the skull.
Ends opposite 2nd lumbar vertebra.
Below L2 continue as a leash of nerve roots known as cauda equina.
Prolongation of the pia matter forms filum terminale.

Spinal cord structure
The spinal cord consists of central core of grey matter containing nerve cell bodies, and outer layer of white matter of nerve fibers.
Within the grey matter, the dorsal horn contains sensory neurons, the ventral horn contains motor neurons and the lateral horn contains preganglionic sympathetic neurons.
Within the white matter run ascending and descending nerve fiber tracts, which link the spinal cord to the brain.
The principle ascending tracts are the spinothalamic tracts, spinocerebellar tracts and dorsal columns. The coticospinal tracts is an important descending tract.
The spinal cord receives information from, and controls the trunk and limbs.
This is achieved through 31 pairs of spinal nerves which join the cord at intervals along its length and contain afferent and efferent nerve fibers connecting with the structures at the periphery.

Causes of spinal cord lesions
congenital; spinal stenosis.
Infection; TB ,abscess.
Trauma; vertebral body fracture or facet joint dislocation.
Inflammatory; Rheumatoid arthritis.
Disc and vertebral lesion.
Vascular;  epidural and subdural hemorrhage.
Tumors.

Congenital spinal stenosis
The patient is born with a narrow spinal canal due to abnormally formed parts of the spine.
This condition is most common in patients with a short stature, such as achondroplastic dwarves.

Other causes of spinal stenosis
aging process (most common cause )
herniated discs
bone and joint enlargement
spondylolisthesis
bone spurs

Spine surgery:
  used when conservative treatment failed.
 -laminectomy (removing bone behind the spinal cord).
 -foramenotomy (removing bone around the spinal nerve).
 -discectomy (removing the spinal disc to relieve pressure).

Complications:
   Dural tears.
   Infections.
   Instability of the spine

Oligomenorrhoea:
“ the occurrence of menses on only five or fewer occasions per year”
2ry Amenorrhoea:
“ the absence of menses for 6 months ( or greater than three times the previous cycle intervals) in a woman who has menstruated before”
Rule out PREGNANCY

Hypo-estrogenic 2ry Am’rrhoea
Hypothalamic-pituitary dysfunction
Premature ovarian failure
Hyperprolctinemia

Hypothalamic-pituitary dysfunction:
Eating disorders e.g, Anorexia nervosa, extensive dieting or exercise. A loss of >10 kg … a’hoea… estrogen lllow …osteoporosis
Hypothalamic lesions
Nonsecreting pituitary adenomas
Other CNS system neoplasms
Sheehan’s syndrome

Premature ovarian failure:
Causes:
Chromosomal abnormalities. Amenorrhoea < 35 years of age
47 XXY ….. High risk of malignancy… gonadectomy
Turner’s syndrome mosaic (XX/XO)

Resistant ovarian syndrome. May be due to auto antibodies against ovaries or gonadotropin receptors. Could be part of disease involving thyroid, adrenal and acid receptors in stomach
If  present in younger age <35 years check auto antibodies

Premature menopause. < 45 mainly familial
High FSH & LH Low Estradiol, chromosomal analysis / ovarian biopsy

Hyperprolactinemia
Causes
Prolactin secreting tumours. 40-50% of cases; most are “micro-adenomas” (,10mm diameter). Macro adenoma levels >2500-3000 mU/l
Idiopathic. 40% levels are usually <2500 mIU/L
Other tumours compressing the the pituitary stalk. Rare, e.g. cranio- pahryngioma.
Primary hypothyroidism (3-5%).
Drugs (1-2%).  Metochlopramide and phenothiazides are the commonest + cimetidine, haloperidol, methyl dopa and reserpine
Systemic problems.
Acromegaly
Acute or chronic renal failure
Herpes zoster of the breast dermatomes

Investigation
Slight to moderate elevation. Repeat the test, if still high, screen for gross abnormality by lateral skull X-ray. If it shows enlargement of the pituitary fossa or erosion of the clinoid process …. CT scan to detect macro-adenoma.
Marked elevation… repeat the test + arrange CT scan ASAP. Specially urgent when headache or visual field defect present

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