A Potpourri of Neurological Disorders

A Potpourri of Neurological Disorders
By:Stephanie Rodriguez MS RN

Chronic Neurological Problems
Headaches
* Classified based on characteristics of the headache
* Functional vs. Organic type
* May have more than one type of headache
* History & neurologic exam diagnostic keys

Not always chronic…be careful
Pattern
Tension
Migraine
Cluster
Site
Bilateral, basilar, band-like
Unilateral, anterior
Unilateral, occular
Quality
Squeezing, constant
Throbbing
Severe
Pattern
Cycles, years
Periodic, years
Remitting, relapsing
Duration
Days, weeks, months
Hours, days
30-90 min
Onset
Anytime
Prodrome, starts in AM
Nocturnal
Assoc. Sx
Stiff neck
N&V, photo/phono-phobia
Horner syndrome
ONSET: Not reliable or diagnostic

Horner’s Syndrome
HA: Essential History
* Onset this particular headache
* Character of pain, severity and duration
* Associated symptoms
* Prior history, pattern
* Original onset: prior testing, treatment
* Exertional aspects
* Other therapeutic regimens

Physical Exam
* Neurologic examination
* Inspect for local infections, nuchal rigidity
* Palpation for tenderness, bony swellings
* Auscultation for bruits over major arteries

Organic vs. Traumatic vs. Functional: Diagnostics
* CBC: underlying illness, anemia
* Chem panel: if associated vomiting, dehydrated
* U/A
* CT scan: for focal neurological signs, sinuses
* SED rate: if recent onset, > 50 yrs (temporal arteritis)
* No LP for suspected ICP; ↑ association with brain herniation (question from last time: ARTICLE

Don’t Miss It
* Caused by subarachnoid hemorrhage from an aneurysm or head injury
* “Worse headache of my life”
* Changes in LOC, focal neurological signs
* Highly correlated with CVA
* Untreated, 50 % mortality

Headache Teaching Guide
* Keep a calendar/diary
* Avoid triggers
* Medications (purpose, side effects)
o Imitrex: take med at 1st sign of HA, ↓blood flow to brain
* Stress reduction
o Dark quiet room, exercise, relaxation
* Regular exercise
* When to contact PCP

Multiple Sclerosis
Definition
MS is a chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination of the nerve fibers of the brain and spinal cord.

Multiple Sclerosis
Etiology
* Cause is unknown.
o Possibly related to viral, immunologic, and genetic factors.
* Susceptibility appears to be inherited with 1st, 2nd, and 3rd degree relatives at slight increased risk.

Pathophysiology
* MS is characterized by chronic inflammation, demyelination, and gliosis in the CNS.
* Autoimmune process is orchestrated by autoreactive T cells (lymphocytes)
* Activated T cells migrate to CNS causing blood-brain barrier disruption.
* Subsequent antigen-antibody reaction within the CNS activates the inflammatory response leading to demyelination of axons, with plaque formation.

A: Normal Nerve Cell
B: Normal Axon
C: Myelin Breakdown
D:Myelin completely disrupted

U-tube: animation
* http://www.youtube.com/watch?v=eE_Y3KMYC0g

Disease Process: Early
* Myelin sheaths of neurons in the brain and spinal cord are initially attacked.
* Myelin sheath is damaged but nerve fiber still intact.
* Nerve impulses are still transmitted but patient may complain of weakness.
* Remission occurs if inflammatory process stops and myelin regenerates.

Disease Process: Late
* If remission does not occur, myelin disruption continues and axon is affected.
* Myelin is replaced by glial scar tissue which forms plaques in the CNS.
* Lacking myelin, nerve impulses slow, axons are destroyed, resulting in permanent loss of function.`

Symptoms
* Initially insidious with symptoms evolving over months to years.
* Systems affected depend on distribution of lesions.
* Disease process may be chronic and progressive or have periods of remission and exacerbation.
* Even in relapsing disease, overall trend is progressive deterioration of neurologic function.

Symptoms: Motor
* Weakness
* Paralysis of limbs, trunk or head.
* Diplopia
* Scanning speech
* Muscle spasticity

Symptoms: Sensory
* Numbness, tingling, parathesia.
* Scotomas (patchy blindness)
* Blurred vision
* Vertigo
* Tinnitus, decreased hearing
* Neuropathic pain
* Radicular pain

Symptoms: Cerebellar
* Nystagmus
* Ataxia
* Dysarthia
* Dysphagia

Symptoms: Emotional
* Emotional stability may be affected
* Depression common co morbidity
* Range of emotions include anger to euphoria.
* Cognitive function usually not affected.
* Emotional lability may negatively affect progress of disease.

Symptoms: Bowel & Bladder
* Symptoms depend on where sclerotic plaque is located.
* Spastic bladder indicates lesion above S2 resulting in small capacity. This yields frequency, urgency, dribbling or incontinence.
* Flaccid bladder results form disruption of reflex arc resulting in loss of sensation or desire to void.
o Crede Method
* Bowel symptoms are usually constipation.

Multiple Sclerosis Drug Therapy
Agent
Corticosteroid (ACTH, Prednisone)
Immunomodulators (B-interferon,Betaseron, Copaxone)
Immunosuppresants (Novantrone)
Cholinergics (Urecholine, Prostigmin)
Anticholinergics (Pro-bathine, Ditropan)
Muscle Relaxants (Valium, baclofen, Zanaflex)

Target Symptom
Exacerbations
Urinary retention; flaccid bladder
Urinary freq. and urgency; spastic bladder
Spasticity

Nursing Care Planning
* Impaired physical mobility
* Self-care deficit
* Impaired skin integrity; risk/actual
* Impaired elimination; urinary, bowel
* Sexual dysfunction
* Interrupted family process

Myasthenia Gravis
Definition & Pathophysiology
* Autoimmune disease of the neuromuscular junction in which antibodies attack acetylcholine (ACh) receptors.
* ACh is prevented from attaching and stimulating muscle contraction
* 90% of patients have ocular manifestations (ocular myasthenia)
* Generalized myasthenia affecting trunk and limbs less common.
* 15% of patients have abnormal thymus glands.
* No other neural disorders accompany MG.
o no sensory loss, reflexes are normal, atrophy is rare.

Myasthenic Crisis
An acute exacerbation of muscle weakness
o triggered by infection, surgery, stress, overdose or or inadequate management of medications
o If muscle weakness affects swallowing and breathing: aspiration, respiratory insufficiency, and infection may result.

Myasthenia Gravis: Symptoms
* Weakness of skeletal muscle
o Muscles are strongest in morning
o Evening: muscle weakness is prominent
* Impaired facial mobility and expression
* Prolonged speech resulting in fading voice
* Possible difficulty in chewing, swallowing
* Proximal muscles of neck, shoulder and hip may be affected
* Course of the disease is variable It most commonly affects young adult women (under 40) and older men (over 60), but it can occur at any age.
* CRISIS: myasthenic crisis is weakness affecting the muscles that control breathing, creating a medical emergency and requiring a respirator for assisted ventilation
Diagnosis
* Diagnosis may be made by H&P.
* Blood tests:
o antibodies to ACh in 90%
* EMG:
o show decreasing response to repeated stimulation of hand muscles
* Tensilon test: shows improved contractility with IV injection of medication.
* NEURO ASSESSMENT: MG expected findings: impairment of eye movements or muscle weakness without any changes in the individual's ability to feel things

Treatment
* Drug therapy – anticholinesterase agents, corticosteroids, immunosuppressants
* Surgical therapy - Thymectomy
* Plasmapheresis
* Intravenous IgG
* Rest!

Huntington’s Disease
* Autosomal dominant genetic disorder
* Deficiency in the acetylcholine and GABA results in excess dopamine.
* Symptoms:
o Clinically opposite of Parkinson’s
o Chorea, intellectual decline, emotional lability
http://www.youtube.com/watch?v=UKbC1jRjs3M
http://www.youtube.com/watch?v=gBtji6Ibbso

Huntington’s Disease: Symptoms
* Abnormal & excessive involuntary movements (chorea)
* Writhing and twisting movements of face, limbs, body.
* Facial involvement affects speech, chewing, swallowing causing aspiration, malnutrition.
* Gait deteriorates with loss of mobility.
* Mental function declines including intellect, emotional lability and psychotic behavior.

Huntington’s Disease Diagnosis
* By symptoms
* By genetic testing as an adult: IMPLICATIONS??
* By prenatal screening

Treatment
* Palliation, symptomatic
* Neuroleptics
* Antidepressants
* Chorea antagonists (Klonopin)
* Fetal tissue transplant (experimental)

Parkinson’s Disease
Definition & Pathophysiology
* Disease of the basal ganglia
* Substantia Nigra:
o Degeneration of dopamine producing neurons
o Disrupts normal balance between dopamine and acetylcholine in the basal ganglia
* Dopamine is essential for normal function of extrapyramidal motor system which controls
o posture
o support
o voluntary motion

Dopaminergic Synaptic Activity
Good to know: These neurotransmitters and functions highly related to “reward” and to psych drug actions
Symptoms
* Onset:
o gradual, insidious, and prolonged
* Classic triad:
o tremor, rigidity and bradykinesia
* Initially:
o may involve one side of the body with mild tremor, slight limp and decreased arm swing
* With progression:
o classic shuffling and propulsive gait with flexed arms and loss of postural reflexes develops
o Slowed reflexes include decrease blinking, drooling, and masked facies

Parkinson’s Presentation

Parkinson’s Disease

A firm diagnosis of Parkinson’s is made only if at least two of the classic triad symptoms are present.

Diagnosis Confirmed: improvement of symptoms once anti-parkinsonian drugs initiated

Parkinson’s Disease: Treatment

Drug
* Dopaminergic (levodopa, sinemet, parlodel, etc.)
* Anticholinergic (artane, cogentin, symmetrel, etc.)
* Antihistamine * MAO inhibitor
* COMT inhibitor’s (comtan, tasmar)

Symptom relieved
* Bradykinesia, tremor, rigidity
* Tremor
* Tremor, rigidity
* Bradykinesia, tremor, rigidity
* Slows breakdown of levodopa

Parkinson’s Disease: Treatment Surgical
* Ablation
* Deep brain stimulation
* Fetal tissue transplant

Nutritional
* Hi fiber
* Mechanical soft
* Frequent small meals
* Lo-protein in HS

Nursing Care Planning
* Impaired physical mobility
o Teaching necessary
* Dressing/grooming self-care deficit
* Impaired skin integrity-risk/actual
* Impaired urinary elimination
* Sexual dysfunction
* Interrupted family process

Seizure Disorders & Epilepsy
Definitions
Seizure:
o paroxysmal, uncontrolled electrical discharge of neurons in the brain that interrupts normal function
Epilepsy:
o spontaneously recurring seizures caused by a chronic underlying condition

Question:
* The population with the highest prevalence of new-onset epilepsy is:

A: over the age of 60
B: children under 5
C: adolescents between 12-18 yrs
D: middle-aged men

Seizure Classification
http://www.youtube.com/watch?v=CDccChHrgRA

Seizure Disorders & Epilepsy: Classifying Seizures
Two major classes:
* Generalized
* Partial

Depending on type, phases may include:
* Prodromal phase- signs & activity preceeding seizure
* Aural phase- sensory warning
* Ictal phase- full seizure
* Postictal phase- recovery

Seizure Disorders & Epilepsy: Generalized
* Absence
* Myoclonic
* Clonic
* Tonic
* Tonic-Clonic
* Atonic

Seizure Disorders & Epilepsy: Partial Seizures
* Simple: no impairment of consciousness
o Symptoms: motor, somatosensory, autonomic, psychic
* Complex: impairment of consciousness
o Simple with progression to LOC/impairment
+ Symptoms: no other features, simple partial seizure features, automatisms
o Impairment of consciousness at onset
+ Symptoms: no other features, simple partial seizure features, automatisms

Seizure Disorders & Epilepsy: Status Epilepticus
* Medical emergency
* Seizure repeated continuously
o Tonic clonic: hypoxia could develop if muscle contraction is lengthened. Also: hypoglycemia, acidosis, hypothermia, brain damage, death
+ IV administration of antiepileptics
+ Maintain airway patency

Seizure Disorders & Epilepsy: Diagnostic Studies
* Most useful tool:
o a reliable and accurate description of the event, and the patient’s health history
* PE
* Electroencephalography (EEG):
o only useful when it shows abnormalities
* Labs:
o CBC, U/A, BMP
* PET scan, CT, MRI, MRA, MRS

Drug Therapy
* Can be helpful in preventing ongoing seizures following a head injury and should be first priority to decrease likelihood of second seizure

Seizure Disorders & Epilepsy Drug Therapy for Tonic-Clonic and Partial Seizures
* Carbamezepine/ Tegretol
* Divalproex/ Depakote
* Gabapentin/ Neurontin
* Lamotrigine/ Lamictal
* Levetiracetam/ Keppra
* Phenytoin/ Dilantin
* Tiagabine/ Gabitril
* Topiramate/ Topamax
* Valproic Acid/ Depakene
* Felbamate/ Felbatol *
* Phenobarbitol**

*Felbatol has been associated with aplastic anemia
**Phenobarbitol is a barbituate
Seizure Disorders & Epilepsy
Drug Therapy for:
Absence, Akinetic, & Myoclonic Seizure
* Clonazepam/ Klonopin
* Divalproex/ Depakote
* Valproic Acid/ Depakene
* Ethosuximide/ Zarontin
* Phenobarbitol

Seizure Disorders & Epilepsy Toxic Side Effects
* Diplopia
* Drowsiness
* Ataxia
* Mental slowing
assess for dose related toxicity including nystagmus, hand and gait coordination, cognitive function, general alertness
Seizure Disorders & Epilepsy
Idiopathic Side Effects
* Skin rash
* Gingival hyperplasia (dilantin)
* Bone marrow & blood dyscrasia
* Abnormal liver function
* Abnormal kidney function

Seizure Disorders & Epilepsy: Nursing Care

* Assure oxygen and suction equipment at bedside
o http://www.youtube.com/watch?v=H2vH1igOoh0
* Safety precautions in active stage
o Support/ protect head
o Turn to side
o Lossen constricted clothing
o Ease to floor
* Time seizure, record details of seizure and post-ictal phase
* Patient teaching:
o importance of good seizure control using medication as ordered
o Medical alert bracelet
o Avoid decreased sleep, increased EtOH, fatigue
o Regular meals/ snacks

A Potpourri of Neurological Disorders.ppt

Read more...

Myasthenia Gravis

Myasthenia Gravis

Chronic autoimmune disease of the neuromotor junction presents as muscle weakness and fatigue

Clinical manifestations
* Weakness
* Fatigue
* Ptosis
* Diplopia
* Facial muscles weakness
* Dysphagia
* Nasal quality to speech
* Respiratory distress
* Muscles involved – eyes, eyelids, chewing, swallowing
* Speech affected
* Muscles of the trunk and limbs less affected
* Proximal muscles of the neck, shoulder and hips are affected
* No sensory loss
* Reflexes normal
* Muscle atrophy rare
* Pt may have exacerbation and remission

Exacerbation of MG
* Emotional stress
* Pregnancy
* Menses
* Secondary illness
* Trauma
* Temperature extremes
* Hypokalemia
* Drugs – aminoglycosides antibiotics, beta blockers, procainamide, quinidine, phentoin, and some psychotropic drugs

Diagnostic
* History and physical
* Antibodies to ACH receptors
* Upward gaze
* EMG
* Tensilon test

Management
* Anticholinesterase drugs – mestinon, prostigmin
* Corticosteriods
* Immunosuppressant drugs – imuran, cytoxan
* Must check for other drug interactions antibiotic, antiarrhythmics, diuretics etc.
* Surgery – removal of thymus gland
* plasmapheresis

Nursing care
* Admin. anticholinesterase drugs
* Respiratory assessment – suction
* Elevate HOB when eating
* Check swallow reflex – oral motor strength
* Plan activities – muscles strongest in morning
* Assess muscle strength before and after activity

Myasthenic crisis
* Due to exacerbation of myasthenia or failure to take drug
* S/S – improved strength with anticholinesterase drugs, inc. weakness of skeletal muscles, ptosis, difficulty on swallowing, articulating words, dyspnea

Cholinergic crisis
* Due to overdose
* S/S – weakness within 1 hour of taking anticholinesterase drug, ptosis, dyspnea, blurred vision, salivations, diarrhea, N/V, abd. cramps, inc. bronchial secretions, sweating, lacrimation
* Due to overdose
* S/S – weakness within 1 hour of taking anticholinesterase drug, ptosis, dyspnea, blurred vision, salivations, diarrhea, N/V, abd. cramps, inc. bronchial secretions, sweating, lacrimation, difficulty swallowing, dyspnea

Nursing DX
Discharge teaching
* Instruct on disease process
* Importance of drug regime – sch drugs at peak action at mealtime, other drug interactions
* Suction equipment at home
* S/S of underdose and overdose of meds
* Instruct on precipitating factors
* Diet – semisolid food
* Rest, Plan activities
* Use of adaptive devices – OT, home care
* MG support group, Community resources

Amyotrophic Lateral Sclerosis
* Known as Lou Gehrig’s disease
* Cause unknown
* Motor neurons in the brainstem and spinal cord gradually degenerate
* Electrical and chemical messages originating in the brain do not reach the muscles to activate them
* Death within 2-6 years after diagnosis

ALS
* S/S – weakness of upper extremities
* Dysarthria
* Dysphagia
* Weakness may begin in legs
* Muscle wasting, fasciculations
* Sensory intact
* Death usually results from respiratory infection

Dx
* Difficult to dx- rule out other diseases
* EMG
* MRI
ALS
* Treatment – Riluzole to slow progression
* No cure
* Cognition is intact

Management
* Supportive therapy – OT, PT, RT
* Assess client’s ability to do ADL
* Conserve energy
* Encourage small freq meals
* Suction equipment
* Soft collar to stabilize head
* Adaptive equipment
* Allow time to complete activities
* Avoid exposure to anyone with respiratory infection
* Good posture and swallowing techniques
* Diaphragmatic breathing
* Follow up pulmonary tests
* Home care
* ALS support group

Multiple Sclerosis
* A chronic progressive degenerative disease that affects the myelin sheath of neurons in the CNS
* Cause unknown – genetic, virus, autoimmune response, inherited, antigen-antibody reaction

Clinical Course
* Relapsing – remitting: relapses with full recovery and residual deficit with recovery
* Primary – progressive: dx progression from onset with occ plateaus and temp. minor improvements
* Secondary – progressive: relapsing-remitting course followed by progression with or without relapses, minor remission and plateaus
* Progressive – relapsing: Progressive dx, with acute relapses with or without full recovery, periods between relapses cont. progression

Dx
* History and Physical
* CSF analysis
* CT scan
* MRI

Clinical manifestations
* S/S may vary
* Motor- weakness or paralysis,of the limbs, trunk, or head, speech problems, spasticity of the muscles
* Sensory – numbness, tingling, paresthesia, visual changes, vertigo, tinnitus, decrease hearing, chronic neuropathic pain, radicular pain (pain in thoracic area and abdominal region), lhermitte’s phenomenon – electric shock radiating down the spine, into the limbs with the flexion of the neck

Clinical manifestations
* Cerebellar signs – nystagmus, ataxia, dysarthria, dysphagia
* B/B function can be affected
* Constipation a problem
* Spastic bladder – incont.
* Flaccid bladder – no sensation of voiding
* Mood swings, Intellect intact
* S/S may be triggered by physical, emotional trauma, fatigue and infection

Medical Management
* Corticosteriods
* Immunomodulators – B-interferon
* Immunosuppressants
* Cholinergics - flaccid bladder
* Anticholinergic – spastic bladder
* Muscle relaxants
* Surgery – control tremors

Nursing Dx
Guillain Barre
* An acute form of polyneuritis
* Etiology unknown
* A cell mediated immunologic reaction directed at the peripheral nerves
* Involves degeneration of the myelin sheath of the peripheral nerves
* In half of cases, an upper respiratory or GI infection precedes the onset of the syndrome by 1-4 weeks
* Antecedent illness-cytomegalovirus, Epstein Barr virus, mycoplasma pneumonia, salmonella typhosa, campylobacter jejuni, HIV
* A chronic form of GB paralysis evolves more slowly with no involvement of respiratory of cranial nerves
* With support, pt will recover

DX
* History and physical exam
* Electrophysiological studies
* Cerebrospinal fluid with elevated protein levels
* EMG

Characteristics of GB
* Ascending weakness usually beginning in the lower extremities and spreading to trunk, upper extremities and face
* Improvement and recovery occur with remyelination; if nerve axons are damaged
* Some residual deficit may remain
* Recovery is usually 6 months with 85%-90% of clients recovering completely
* 10% have recurrence and 20% have long term disabilities/emotional trauma

Guillian Barre
* Complication- is respiratory failure
* Impt to monitor respiratory rate, depth, vital capacity
* Client may be intubated with mechanical ventilation
* Complications can occur due to immobility

Clinical Manifestations
* Flaccid quadraplegia
* Facial weakness, dysphagia, diplopia, hypotonia
* Autonomic dysfunction found in severe muscle involvement and respiratory muscle paralysis – orthostatic hypotension, hypertension, pupillary disturbances, sweating dysfunction, bradycardia, paralytic ileus, urinary retention
* Weakness
* Paresthesia of the limbs
* Loss of deep tendon reflexes
* Deep, aching muscle pain in shoulder and thighs
* Respiratory compromise or failure-dyspnea, dec. breath sounds, dec. tidal volume (air in & out)

Medical/Nursing Management
* Supportive care
* Immunoglobulin therapy
* Pain control worse at night due to paresthesia, muscle aches and cramps
* Problems - airway, aspiration, communication problems, orthostatic hypotension, nutritional intake
* Plasmaphoresis
* ABGs
* Assist ability to perform self care
* Set communication system
* Work closely with PT, OT
* Monitor for complications of immobility
* Safety measures provided

Myasthenia Gravis.ppt

Read more...

Differential diagnosis of the flu-like illness

The sepsis syndrome: Differential diagnosis of the flu-like illness
By:Divya Ahuja, M.D.

Med Micro 2008 Clinical Correlations #5
Traditional definitions

* Bacteremia (or fungemia): presence of microorganisms in the blood
* Sepsis: Harmful consequences of microbes or their toxins in blood or tissues
* Septicemia (or bloodstream infection): bacteremia with clinical manifestations
* Septic shock: shock due to sepsis, often with bloodstream infection

Revised definitions
* Systemic inflammatory response syndrome (SIRS)
* Sepsis
* Severe sepsis
* Septic shock

Systemic Inflammatory Response Syndrome (SIRS)
* Two or more of the following
o temperature > 38 degrees C (100.4 F)
o respirations > 20/minute
o Heart rate > 90 beats per minute
o leukocyte count > 12,000/cmm or < 4000/cmm or with > 10% band forms

Sepsis and Severe Sepsis
* Sepsis: SIRS plus a documented infection (culture proven or identified by visual inspection)
* Severe sepsis: Sepsis associated with organ dysfunction, abnormalities due to hypoperfusion (such as lactic acidosis, oliguria, or acute alteration in mental status), ARDS, DIC, low platelets

Septic shock
* Definition: Sepsis-induced hypotension despite fluid resuscitation and/or inotropic support, plus hypoperfusion abnormalities
* The hallmark of septic shock is low systemic vascular resistance, which distinguishes it from hemorrhagic shock and cardiogenic shock.

Multiple Organ Failure
* Some physiologic descriptors
o Serum creatinine
o Platelet count
o pO2/FiO2 ratio
o Serum bilirubin
o Glasgow coma score

Sepsis
* Sepsis has a 20-50% mortality
* Severity has increased recently
* Hospital case-fatality has declined
* Incidence is greatest in winter
* Risk factors for sepsis
o Bacteremia
o Advanced age
o Impaired immune system
o Community acquired pneumonia

Continuum of severity
* Incidence of positive blood cultures increases along the continuum
* Increased mortality rate
* Severe organ dysfunction manifested as
o Acute respiratory distress syndrome
o Acute renal failure
o Disseminated intravascular coagulation

Disseminated intravascular coagulopathy
Case #1
* 20-year-old college student in ER
* General malaise, low-grade fever, and rapid development of purplish discoloration on his face. (from when he left his house to the time he arrived at the emergency room).
* Blood cultures were drawn and he was admitted to the intensive care unit

Presentation
* Febrile, tachycardic, systolic BP-70
* Creatinine- 3.6, poor urine output
* Platelets-46000
* INR- 2.6
* Obtunded mental status
* Needing maximum ventilatory support
* Meningococcemia with Waterhouse-Friderichsen Syndrome and DIC
* Treat with penicillin, ceftriaxone or chloramphenicol.
* Family members and hospital employees in contact with respiratory secretions should receive prophylaxis. Attack rates for household contacts is 0.3-1%, 300-1000 times the rate in the general population (rifampin x 4 doses or cipro x 1 dose)

Epidemiology of meningococcal disease

Evaluation of blood cultures
* True-positive versus false-positive (contamination; pseudobacteremia)
* Transient versus intermittent versus continuous
* Polymicrobial versus unimicrobial
* Primary versus secondary

Clues to contamination
* Microorganisms that are usually not pathogenic, unless isolated from multiple cultures (e.g., coagulase-negative staphylococci; Bacillus species)
* < 2 positive cultures and/or delayed growth and/or < 1 cfu/ml
* Doesn’t “fit” the clinical picture

Patterns of bacteremia
* Transient: caused by manipulation of a flora-containing body surface
* Intermittent: typical of most infections giving rise to positive blood cultures
* Sustained (or continuous): characteristic of intravascular infections--endocarditis, endarteritis, suppurative thrombophlebitis, infected AV fistula

Number of microorganisms
* Unimicrobial (or “monomicrobial”) bacteremia: one isolate
* Polymicrobial bacteremia: more than one microorganism; typical of complicated situations often with surgical implications

Epidemiology of sepsis
* Contributes to > 100,000 deaths in the United States each year.
* Annual incidence is probably between 300,000 and 500,000 cases.
* About 2/3rds of cases occur in patients hospitalized for another illness (nosocomial infection).

Risk factors for nosocomial sepsis
* Gram-negative bacilli: diabetes mellitus; tumors; cirrhosis; burns; invasive procedures; neutropenia
* Gram-positive cocci: vascular access lines, devices
* Fungi: immunosuppression; broad-spectrum antibiotic therapy

Host factors in sepsis
* Mortality is directly related to severity of underlying disease: rapidly-fatal> ultimately fatal (i.e., within 5 years)>nonfatal.
* Elderly have increased mortality.
* Mortality is higher in patients with subnormal temperatures than in those with fever.

Clinical findings in sepsis
* Early: apprehension, hyperventilation, altered mental status
* Complications: hypotension, bleeding, leukopenia, thrombocytopenia, organ failure
* Lungs: cyanosis, acidosis, full-blown ARDS
* Kidneys: oliguria, anuria, tubular necrosis
* Liver: jaundice and transaminitis
* Heart: heart failure, stunned myocardium
* Gastrointestinal: nausea, vomiting, diarrhea, stress ulceration
* Systemic: lactic acidosis
* Petechiae early in course: suspect especially meningococcemia, RMSF
* Ecthyma gangrenosum: Ps. aeruginosa
* Generalized erythroderma: Toxic Shock Syndrome

Petechiae
Ecthyema gangrenosum

Skin lesions in septicemias (1)
* Neisseria meningitidis: erythematous macules or petechiae and purpura
* Rocky Mountain spotted fever: petechiae, purpura
* Staphylococcus aureus: “purulent purpura”
* Pseudomonas aeruginosa: ecthyma gangrenosum
* Salmonella typhi: “Rose spots”
* Hemophilus influenzae: cellulitis
* Endocarditis: petechiae; Osler’s nodes (painful lesions of finger and toe pads); Janeway lesions (painless lesions of palms or soles)
* Anthrax: papules-->vesicles-->eschar
* Fungemias

A 50 yo man presents to emergency room with severe pain and swelling of LLE. On exam, temperature is 40.0 ºC, pulse rate is 135/min, respiration rate is 35/min, and blood pressure is 80/40

Which of the following is the most appropriate initial therapy?
* LLE elevation
* X-ray of LLE
* Surgical consultation
* Oral antibiotics

Necrotizing fasciitis
* Necrotizing fasciitis usually results from an initial break in skin (trauma or surgery)
* It is deep: may involve the fascial and/or muscle compartments
* The initial presentation is that of cellulitis

Necrotizing fasciitis: Red flags
* Severe pain (out of proportion of skin findings)
* Bullae (due to occlusion of deep blood vessels)
* Skin necrosis or ecchymosis
* Gas in soft tissue (palpation or imaging)
* Systemic toxicity
* Rapid spread during antibiotic therapy

Necrotizing fasciitis
* Monomicrobial: S. pyogenes, S. aureus, anaerobic streptococci,…. Most are community acquired and present in the limbs in patients with DM or vascular insufficiency

* Polymicrobial: aerobic and anaerobic (bowel flora), Usually associated with abdominal surgical procedures, decubitus ulcer, perianal ulcer, bartholin abscess, IV drug injection

Staphylococcal bacteremia
* Complications: endocarditis; metastatic infection; sepsis syndrome
* Staphylococci adhere avidly to endothelial cells and bind through adhesin-receptor interactions
* Fulminant onset; high fever, erythematous rash with subsequent desquamation, and multiorgan damage
* DDx: Rocky Mountain spotted fever, streptococcal scarlet fever, leptospirosis

Streptococcal toxic shock syndrome
* Early onset of shock and organ failure associated with isolation of group A streptococci
* Necrotizing fasciitis present in about 50% of cases
* Early symptoms: Myalgias, malaise, chills, fever, nausea, vomiting, diarrhea
* Pain at minor trauma site may be first symptom

Sepsis in the asplenic patient

* Frequently fulminant with massive bacteremia
* Streptococcus pneumoniae accounts for 50% to 90% of infections and 60% of deaths
* Other pathogens: Haemophilus influenzae, Neisseria meningitidis, Capnocytophaga canimorsus (after dog bites),
Babesia microti (babesiosis)

64 year old WM
* Presents with fever, hypotension, cellulitis with bullous skin lesions
* PMH: cirrhosis
* SH: recently returned from New Orleans, likes oysters

Vibrio vulnificus sepsis
* Organism found in warm seawater and in shellfish (90% of deaths due to seafood in U.S.)
* Cirrhosis a major risk factor to sepsis, with rapid onset
* Chills, fever, characteristic skin lesions (bullae with hemorrhagic fluid; necrotizing fasciitis, other)
* Also causes wound infection after exposure to salt water

41 year old WM
* Fever, “worst headache ever,” myalgias, rash
* Returned from family camping trip in Smoky Mountain National Park 1 week PTA

Rocky Mountain spotted fever
* Generalized infection of vascular endothelium
* Headache typically severe. Fever may be low-grade and rash may be absent (“spotless fever”) when patient first seen
* Suspect with flu-like illness and severe headache in endemic areas!

65 year old woman
* PMH diabetes
* During influenza epidemic, presents with fever, chills, aching all over (myalgia)
* PE: bibasilar rales; no murmur
* Admitted to hospital for treatment of heart failure

Infective endocarditis: definitions

* Septic vegetations of the endocardium usually involving the heart valves or other areas of turbulent flow
* Acute endocarditis occurs on normal heart valves, is caused by highly virulent bacteria and leads to death in < 6 weeks
* Subacute endocarditis is caused by less virulent bacteria and has a more indolent course.

Pathogenesis of endocarditis
* Sterile vegetations arise downstream of high-flow areas of the heart
* Damaged endothelium and foreign bodies increase turbulent flow
* Microorganisms implant on the sterile vegetations during transient bacteremia
* Septic vegetations become a source of infection elsewhere

Diagnosis of endocarditis
* Revised Duke Criteria : positive blood cultures plus echocardiography with or without minor criteria
* Heart murmurs (especially regurgitant)
* Splinter hemorrhages (nail beds)
* Osler nodes (finger pulps; painful)
* Petechiae; “pustular purpura” (Staph)
* Roth spots (fundi)

Etiologies of endocarditis
* Viridans streptococci most common (30-40%)
* Other streptococci include enterococci and Streptococcus bovis
* Staphylococci cause 20-30%)
* Less common: aerobic gram-negative rods; HACEK organisms; fungi; anaerobic bacteria; Brucella; Coxiella burnetti; Chlamydia psittaci
* “Culture-negative” (<5% to 24%)

Case
* 42 year male
* Previously healthy, non smoker
* 2 week history of progressive cough, dyspnea, fever
* Intubated within 48 hours of admission

Case
Hamman-Rich syndrome
* Also known as acute interstitial pneumonia, is a rare, severe lung disease which usually affects otherwise healthy individuals
* Cough, fever, dyspnea
* Hamman-Rich syndrome progresses rapidly, with hospitalization and mechanical ventilation within days to weeks after initial symptoms

Sepsis-summary
* Look at the host (age, immunedeficiency,-HIV, cancer, steroids, cirrhosis, dialysis,
* Clinical assessment for MOD (vitals, perfusion, mental status, urine output)
* Lab parameters-platelets, creatinine, coags, leukocytosis vs. leukopenia
* Hemodyanamic, ventilatory support, antibiotics
* Hit hard and hit early and then deescalate based on emerging microbiological data

The sepsis syndrome: Differential diagnosis of the flu-like illness.ppt

Read more...