Acute onset and rapid progression are characteristic of anaphylaxis. Hypotension and airway obstruction are ominous signs
Anaphylaxis is an acute, life-threatening, usually IgE-mediated allergic reaction that occurs in previously sensitised people, when they are reexposed to the sensitising antigen.
Diagnosis is clinical
Acute onset and rapid progression are characteristic of anaphylaxis
Recurrent episodes are common
There is often (but not always) a history of previous sensitivity to an allergen, or recent history of exposure to a new drug (eg vaccination)
Initially patients usually develop skin symptoms include generalised itching, urticaria and erythema, rhinitis, conjunctivitis and angio-oedema
Anaphylactic reactions can vary in severity and rate of progression - they may progress rapidly (over a few minutes)
Occasionally in a biphasic manner, with symptoms recurring 12-24h later
Rarely manifestations may be delayed by a few hours (adding to diagnostic difficulty), or persist for more than 24 hours
Definition of Anaphylaxis:
Severe, life-threatening, generalised or systemic hypersensitivity reaction
Anaphylaxis can occur at any age
In one study, the mean age was 29.3 years (range, 0.8 to 78.2 years). In another, there was an age range of 1-79 years, with a mean of 37 years
1-3 episodes per 10,000 population pa
Lifetime prevalence: 1-2%
Rare cause of hospital admission (0.02%)
Prevalence appears to be rising
Anaphylaxis is probably underdiagnosed
Pathophysiology of Anaphylaxis
When allergen binds to IgE-sensitised mast cells and basophils, histamine is released from their intracellular granules. Mast cells are widely distributed but are most concentrated in skin, lungs, and GI mucosa; histamine facilitates inflammation and is the primary mediator of clinical atopy. Histamine causes the following:
Local vasodilation (causing erythema)
Increased capillary permeability and edema (producing a wheal)
Surrounding arteriolar vasodilation mediated by neuronal reflex mechanisms (causing flare)
Stimulation of sensory nerves (causing itching)
Smooth muscle contraction in the airways (bronchoconstriction) and in the GI tract (increasing GI motility)
Increased salivary and bronchial gland secretions
When released systemically, histamine is a potent arteriolar dilator and can cause extensive peripheral pooling of blood and hypotension; cerebral vasodilation may be a factor in vascular headache
IgE dependent mechanisms. Common allergens include foods (especially nuts eg peanuts, tree nuts; shellfish); venom (bee, wasp stings); drugs: beta-lactam antibiotics (penicillins and cephalosporins), vaccines, NSAIDs, muscle relaxants, radiocontrast media, heparin, iron injections; blood products, immunoglobulins; other: latex
IgE independent immunologic mechanisms: eg IgG mediated, T cell activation. Causes include dextran and infliximab
Direct mast cell activation: May be due to physical factors (exercise, cold, heat, sunlight/UV radiation), alcohol, drugs (acetylcysteine)
Idiopathic: unknown trigger? mastocytosis/clonal mast cell disorder?
Anaphylaxis Risk factors
Comorbidities: asthma (particularly if poorly controlled), atopy, COPD, psychiatric disorders (due to under recognition), cardiovascular disease, mastocytosis
Concurrent medications:, alcohol/antidepressants/sedatives etc impair recognition of symptoms, beta-Blockers and ACE inhibitors worsen them
Recent anaphylactic reaction
Age: children (under recognised), adolescents (risk-taking behaviour), elderly (increased mortality due to multiple medications)
Symptoms are acute in onset, variable and may affect:
Skin/mucosal tissue: pruritus, generalised hives, flushing, swelling of lips, tongue, uvula/palate, larynx, nose, eyes + other areas (angio-oedema)
Respiratory tract: dyspnoea, wheeze, nasal congestion, rhinorrhoea, sneezing, hoarseness, cough
GI: nausea, vomiting, abdominal pain, diarrhoea, incontinence
Cardiovascular: chest pain, palpitations, syncope, altered mental status, shock, cardiac arrest
CNS: sense of impending doom, throbbing headache, dizziness, confusion, tunnel vision, loss of consciousness
Other: metallic taste in mouth, dysphagia, dysphonia, uterine contractions
“Have you been exposure to a known allergy/trigger?"
“When did symptoms start, and what are you current medications?"
“Has this happened before?”
“Are you asthmatic?”
Pale, clammy skin, urticaria
Hypotension, tachycardia, bradycardia (a late sign), other dysrhythmia
Increased respiratory rate, wheezing/bronchospasm, stridor (laryngeal obstruction), cyanosis
Decreased level of consciousness
Mast cell tryptase can rule out anaphylaxis; intradermal testing can rule it in. Do not delay resuscitation to take blood samples
FBC, ESR, CRP,
U+E, LFT, Bone, Glucose, Tryptase (within 6h)
Mast cell tryptase
Tryptase; timing important. Optimally measured 15mins-3 hrs after onset; within 6h; may be high
Histamine: optimally measure 15-60mins after onset. Special handling required
Intradermal challenge testing (especially useful for drug causes)
Differential diagnoses of Anaphylaxis
All causes of collapse
All causes of hypotension
Acute generalized hives, vasovagal reaction, panic attack, aspiration of a foreign body (infants), neurologic event (seizure, stroke)
More rarely: postprandial syndromes (pollenfood syndrome, scombroidosis), excess endogenous histamine syndromes (mastocytosis), flush syndromes (perimenopausal flushing, carcinoid, autonomic epilepsy), capillary leak syndrome, vocal cord dysfunction syndrome
Remove bee stings. If patient is shocked, or has significant airway obstruction, treat immediately
Treatment (first line)
IM ADRENALINE (1:1000) 0.5 ml (500mcg); repeat at 5 minute intervals if no improvement. This route is not recommended after cardiac arrest
Or, IV (1:10,000) 0.5 ml (50mcg) if severely ill, peri-arrest or pulseless; ie the dose is different
NEB SALBUTAMOL 5mg (if wheezy)
IV HYDROCORTISONE 200mg
IV CHLORPHENIRAMINE 10mg
High flow oxygen: >10 l/min
IVI + IV fluid challenge: 500 – 1000 mL. Repeat if necessary
Lie patient flat, elevate legs
Monitor cardiac and respiratory function
Any drug thought to be cause
Inform GP if drug cause possible
Treatment (second line)
Further bronchodilator therapy: salbutamol (nebulised or IV), ipratropium bromide (nebulised), aminophylline (IV)
Glucagon may be useful if patient on beta-blocker
(Longterm) consider prophylactic steroids for severe idiopathic cases
Medical Admission or Observation Ward, when stable
Death is uncommon for patients who are treated appropriately
Side effects of adrenaline (hypertension, tachycardia, arrhythmias, MI – these may also occur due to exposure of subclinical coronary artery disease)
Hypotension and airway obstruction are poor prognostic signs. Bradycardia is late sign
Clinical immunology. Refer to regional centre
+ Health promotion
Educate patient about symptoms and signs of a recurrent attack, and known common triggers
For patients with recurrent or severe attacks, arrange
- Skin prick or IgE testing
- Medical alert bracelet/card/letter
- Adrenaline autoinjecter (0.3g Epipen) for patients to carry at all times
1 in 15 patients have a biphasic response with symptoms recurring 12-24 hours later - warn patients about this issue
IM and IV drug doses are different
Inform GP if drug cause possible
Timing important when testing for markers of degranulation
Histamine requires special handling
Decreased conscious level
Synonyms: severe allergic reaction, anaphylactic shock, allergy, hypersensitivity, acute anaphylaxis guidelines, acute anaphylaxis treatment
First of all, ascertain whether the confusion is really acute; ie does the patient have chronic confusion (dementia)?; or is this acute on chronic confusion? Not doing this (and recording it) is one of the most medicolegally dangerous things a junior doctor can do
Acute Confusional State:Introduction
An acute confusion state is a neuropsychiatric syndrome which is difficult to define but involves abnormalities of perception, thought and awareness levels
Patients may appear confused or 'not with it' when talking to them. It may be their family or carer who notice the confusion, alternatively
Typically confusion is fluctuating, and worse at night. It can occur acutely, or subactutely
It is very common, especially in the elderly, and not a benign syndrome. Many of these patients subsequently do not return to their baseline function and some even require long-term institutionalisation
20% medical and surgical acute admissions have some confusion
10% of elderly admissions are primarily due to confusion (often due to drugs)
Sepsis, drugs/alcohol (excess/withdrawal) and metabolic disturbance are the 'big 3', ie three commonest causes of an acute confusional state
TIA/CVA rarely presents as confusion. Think about alternative diagnoses. But hyponatraemia is a common cause in the frail elderly
Removal from home can cause acute confusion. The skills are not to admit the frail elderly unless its necessary (or make their stay as short as possible), and accident prevention
Pain and opiates can both cause confusion (think about post-op, especially post #NOF). Think about nursing issues and it's important to sedate only if essential
There is a 5% in-hospital mortality, 10% mortality (+25% functional decline) at 3 months
50% of patients are diagnosed with dementia in following 2 years
Acute Confusional State Medicolegal Aspects
Patients are vulnerable
It is a common scenario for errors, eg missing the diagnosis and poor management. This is why this area has the potential to become serious
So, do a full examination, and a full set of bloods, BC, CXR, and CT head, if necessary
Do not assume confusion is due to long-term dementia or learning difficulties, even in the elderly and those with either. The diagnosis may be not true, or mild, or barely affecting their QoL. Their family may love them just like that. In other words, check previous level of function from relative/carer/home circumstance
If this is not possible treat as acute confusion until proven otherwise; not doing this is medicolegally dangerous. Do not go there. You need to make great efforts to find out their baseline mental state; ring family, GP, anyone; 2am, 2pm, anytime
Why is this so important? It is because as soon as a patient acquires the diagnosis 'Dementia' or 'Learning Difficulties', some doctors (followed by the nurses, and PAMs) then assume that they have a proven, chronic and worsening condition, and try less hard; even being more likely to fill out a DNA-CPR form. So, if this goes wrong, and it ends in legal action, it can look very bad; ie like you did not care. Doctors may be forgiven for making mistakes, but not caring is unacceptable
Anyway. Who says that patients with such longterm conditions should have any better/worse care than patients without these diagnoses
Acute Confusional State Definitions
Neuropsychiatric syndrome characterised by disorientation in time and place, impaired short-term memory, and impaired consciousness; occuring over hours/days, with a tendency to fluctuate over the course of the day
Delirium = in addition, there are disorders of perception (hallucination, illusion, delusion)
Importantly, confusion and delerium are reversible
DSM-IV Diagnostic Criteria for Delirium Due to a General Medical Condition (2000)
Disturbance of consciousness (ie, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention
A change in cognition (such as memory deficit, disorientation, language disturbance, or all 3), or development of a perceptual disturbance that is not better accounted for by a pre-existing, established, or evolving dementia
The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day
There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition
Acute Confusional State : Epidemiology
20% medical and surgical acute admissions have some degree of confusion
10% of elderly admissions are primarily due to confusion often due to drugs
Ie its very common. Just ask all patients some simple questions Note: only 10% of admissions with confusion have a primary neurological problem (vs sepsis, drugs and metabolic; which are the most important groups of causes)
Acute Confusional State Mnemonic Causes
HIDEMAP (from GP notebook):
H+H = hypoxia (CCF, respiratory failure, AKI) + head trouble (head injury; SOL (SDH? brain abscess?); meningitis; rarely .. encephalitis, cerebral malaria)
I = infection (UTI, chest, wound, line, post-op, neutropenic sepsis, especially if immunosuppressed)
D = DRUGS DRUGS DRUGS = recreational or prescribed, excess or withdrawal, eg: benzodiazepines, analgesics (especially opiates), anti-cholinergics, anti-convulsants, anti-parkinsonism medication, steroids
E = endocrine (hyper/hypoglycaemia, hypothyroidism (especially elderly))
M = metabolic (AKI, ALF, hypercalcaemia, hyponatraemia)
A + A = alcohol (excess or withdrawal) + anaemia (B12/folate deficiency)
3Ps = psychosis + postictal + postop (especially post #NOF; often multifactorial, eg septic, dry and drugs) Notes: TIA/CVA does not usually present as confusion; and steroids can cause 'steroid psychosis' presenting as confusion, as well as a psychiatric state
Dementia (ie worsening confusion)
Alcohol + recreational drugs
Recent surgery (especially neurosurgery)
Acute Confusional State Symptoms
History has limited value
But in mild confusion, patients may be able to recognise it, and may have an idea of cause (ask them)
Vital to get history from witnesses (relative, carer, ambulanceman)
Do you have depression (ever taken an overdose?) or other mental health problems, or epilepsy?
How much alcohol do you drink? Ever taken a recreational drug? (you may have to explain)
What tablets are you on? Any changes recently?
Any recent operations (eg head and neck infection (brain abscess); cerebral shunt)? Note: pick up the phone if necessary. Remember, the 'poor historian' is you
Acute Confusional State Signs
Record mental test score (partly as baseline) Note: if you are in a hurry, do at least the first three, ie is the patient orientated in time, place and person?. If they know the date, they are not confused
Look for needle tracks, and signs of head injury and alcohol
Check for bladder (retention can cause confusion in elderly) Note: patient may be a danger to you (aggression or HIV/Hep B/C positive, ie wear gloves)
Investigation for Acute Confusional State
First of all, check the blood glucose. Don't forget the '3 Treatable Ts' = Thyroid(hypo), TPHA + BTwelve deficiency
U+E, LFTs, GGT, Bone (?calcium), Glucose
B12/folate,TFTs, TPHA/VDRL Note: don't forget the '3 Ts' (Thyroid(hypo), TPHA + BTwelve deficiency. Even though these are rare causes of acute confusion, they (and subdural haemorrhage) are 4 of the important reversible causes of chronic confusion ie dementia. In fact, many dementia clinics will not take a referral from a GP, unless those 4 things have been excluded
O2 saturation (± ABG, if low), BC
± CK, if has been on floor for long
± Thick/thin films (malaria)
± SLE serology
Urinalysis: leucocytes? nitrites? (catheterise slowly if cannot get sample)
Urinary toxin screen (overdose?)?
CXR (pneumonia, ?carcinoma if patient hyponatraemic)
AXR: ?constipation (can cause confusion in elderly)
CT head ± LP , if no obvious diagnosis, or not improving at 48 hrs Note: look on back of drug card. The diagnosis may be there
CT head ± LP
Learning difficulties, dementia (chronic confusion) - all easy to confuse
Other psychoses eg schizophrenia
Treatment of Acute Confusional State
Patients with ACS may be a danger to themselves, and others; ie the most important 'treatment' may be making them safe - so think about nursing issues. If necessary, you may have to make decisions, against their will, under the Mental Capacity Act (2005)
Treatment (first line)
IV GLUCOSE 20 mls 50%, if BG < 4 mmol/L Note: GLUCOSE increases risk of Wernicke's encephalopathy, so give IV PABRINEX first, if suspect patient is alcohol dependent and hypoglycaemic
IV PABRINEX 2 vials tds, if ?Wernicke's or alcohol withdrawal possible
PO CHLORDIAZEPOXIDE 20-40 mg qds, reducing over 5d; if alcohol withdrawal; but benzodiazepines can make confusion worse; so, only Rx with benzodiazepine if sure Note: larger doses are used in severe withdrawal, eg 40 mg qds, reducing over 10 days
IV NALOXONE 400 mcg, if small pupils (?opiate OD)
IV FLUMAZENIL 200 mcg, over 15 secs, if ?benzodiazepine OD; then 100 mcg every 60 secs; max 1mg (2mg ITU) Note: flumazenil is contraindicated in patients with epilepsy on longterm benzodiazepines; you may need to give further doses of naloxone and flumazenil (see BNF)
Procedures: (see supportive measures below)
IV (+IV fluids, if dry)
OXYGEN, in hypoxic patient (this can quickly calm patient, and reduce confusion); if pulling mask off, try nasal cannulae
Warm up/cool down, as necessary
Room: don't move about unecessarily; moderately lit side room preferable. Avoid excess noise, avoid over- or under-stimulation
Communication: clear. Avoid speciality jargon. Staff consistency (both doctors and nurses). Use health advocates (eg interpreters) where needed
Orientatation: reminders of the day, time, location and identification of surrounding persons; have a clock visible
Relaxation: eg watch television. Involve family and carers.
Familiarity: have familiar objects from home around patients especially glasses, walking aids and hearing aids. Maintain competence eg maintain walking in ambulant patient
Accident prevention: nurse on floor if necessary (to prevent falls and fractures). Only use restraints if essential (patient may pull out central line and exsanguinate)
Drug cause (especially hyponatraemia secondary to diuretics and/or SSRIs)
Any sedative drug (if in doubt, stop almost everything)
Treatment (second line)
Have low threshold for broad spectrum IV antibiotics (± antivirals ± antimalarials):
IV BENZYLPENICILLIN 1.2 g qds + GENTAMICIN 5 mg/kg od; before CT ± LP, if meningitis possible
± IV ACICLOVIR 10 mg/kg tds (infused over 60 mins) for 10-14 days, if encephalitis possibility (reduced dose in renal insufficiency)
± IV QUININE DIHYDROCHLORIDE: loading dose 20 mg/kg (maximum 1.4 g) over 4 hrs; then 8 hrs after loading dose, 10 mg/kg tds (also infused over 4 hrs); doses diluted in 250 mls N Saline, if cerebral malaria possible; watch for toxicity (QT prolongation)
Avoid sedation, unless absolutely necessary. But if extremely agitated/aggressive (ie danger to themselves or others) consider O/IM HALOPERIDOL 2-10 mg (start as low as possible, even 0.5 mg); maximum 18 mg/d; or PO QUETIAPINE 12.5-200 mg od. Start with 12.5mg od especially in elderly; and if more needed than 25 mg bd, please consult psychiatrist-on-call
If unwell, urinary catheter, CVP, arterial line Note: but may pull out any of these; so can make situation worse
Mental Capacity Act (2005)
The Mental Capacity Act (MCA) is designed to protect and empower individuals who may lack the mental capacity to make their own decisions about their care and treatment. It is a law that applies to individuals aged 16 and over. You need a working knowledge of this act and the Mental Health Act (1983, amended in 2007). The MHA is more used to treat patients who lack capacity because of mental illness (eg depression, schizophrenia)
So, for a patient with an 'organic' cause of the mental disorder (like ACS), the MCA will normally be used, rather than the MHA
For a mentally ill patient, carrying out a '5/2' section on the MHA is usually more appropriate
For either, the basic issue, is whether you think the patient's mental state makes them them a danger to themselves or other people. If it is, you may need to act
Specifically, if a patient has an ACS (or dementia, or acute-on-chronic confusion) (or other reasons for lacking capacity, eg learning difficulties), you may need to use the act (ie fill out a form and sign it) to give patients short-term treatment against their will; eg calling security or using haloperidol or midazolam to control an aggressive, agitated and confused patient
If you are thinking of doing this, you should involve a senior
The MCA says:
- Everyone has the right to make his or her own decisions. Health and care professionals should always assume an individual has the capacity to make a decision themselves, unless it is proved otherwise through a capacity assessment
- Individuals must be given help to make a decision themselves. This might include, for example, providing the person with information in a format that is easier for them to understand
- Just because someone makes what those caring for them consider to be an 'unwise' decision, they should not be treated as lacking the capacity to make that decision. Everyone has the right to make their own life choices, where they have the capacity to do so
- Where someone is judged not to have the capacity to make a specific decision, that decision can be taken for them, but it must be in their best interests
- Treatment and care provided to someone who lacks capacity should be the least restrictive of their basic rights and freedoms possible, while still providing the required treatment and care
If drugs might be the cause (and no other diagnosis made), consider stopping all but essential ones - and inform GP when they go home. Polypharmacy is a problem in the elderly
Usually Note: but if frail elderly, consider alternative management plan, in community; ring GP, if you are doing this plan
Medical admission ward
Depends on cause
SALT team etc, if CVA (pneumonia, 2o to aspiration?); does patient need NG feed? PEG?
"Sedating a confused patient may make them worse"
Hospital acquired infections, eg Clostridium difficile and MRSA
Accidents: eg fractures (femoral or hip fractures from falls)
Residual psychiatric and cognitive impairment
Some progress to stupor, coma and eventual death Note: patient may be a danger to you (aggression or HIV/Hep B/C positive, ie wear gloves)
Depends on cause. Nil if cause is benign and confusion better
But consider HCE follow-up, if thought to be first presentation of dementia
Confusion may last longer than the underlying condition, sometimes for up to a year. This means that some patients will be discharged with persisting abnormalities. It is good idea to warn the family (and GP) about this issue
Good, if confusion is mild
5% in-hospital mortaliy, 10% mortality (25% functional decline) at 3 months
50% diagnosed dementia in 2 years
Quicker inpatient recovery is associated with a better outcome
2° Prevention + Health Promotion
If alcohol or recreational drugs all/part of problem, refer to appropriate community services
Encephalitis; DO NOT MISS THIS DIAGNOSIS; it's treatable
SDH; so is this
DRUGS DRUGS DRUGS (and look on back of card). If in doubt, stop almost everything. Ring GP, if necessary
Find out whether this is acute, chronic (dementia), or acute-on-chronic confusion
Look at vital signs (including oximetry) and glucose
Record mental test score (important baseline; like GCS in coma; note if fluctuating)
CT head/LP if no obvious diagnosis, or no better at 48h
Check for retention and constipation, in the elderly
'3 treatable Ts' = Thyroid(hypo), TPHA + BTwelve deficiency
Know the bascis of the Mental Capacity and Mental Health Acts
Pulling at lines, catheter etc
Falling out of bed .. ie, may be danger to him/herself (protect them)
Epilepsy, or recurrent afebrile seizures, is a pediatric disorder occurring in 5.2 to 7.3 per 1,000 school age children. Fortunately, most children who have a single seizure will not go on to develop epilepsy. Even when they do, the majority will have a relatively benign disorder that can be effectively controlled with a single antiepileptic drug and over time the disorder often resolves itself, allowing the discontinuation of treatment. Proper selection of medication is critical, since all antiepileptic drugs have a potential for significant side effects that may become more severe with higher doses and with polydrug therapy (taking more than one anti-epileptic medication.
Despite proper selection of medication and satisfactory compliance, some patients continue to suffer from epileptic seizures. In these children, drug dosages are gradually increased and polydrug therapy is instituted in pursuit of seizure control. Side effects like lethargy, dulled mentation, hyperactivity, aggressivity, double vision, nausea, tremor, and others are to be expected; they must be carefully balanced against the emotional, psychological, and physical consequences of recurring seizures.
These sequelae are extremely traumatic for epileptic children. Unsure of when the next attack may occur, they are unable to relax, play, and just be kids. In addition, other children often taunt them. The convulsive movements, loss of urinary continence, impairment of consciousness, postictal confusion, and lethargy all create a social stigma that is particularly severe in childhood. Neurosurgery is increasingly being used to treat medically refractory epilepsy, and several centers already offer this treatment.
Following a detailed documentation of your medical history, our epilepsy team arranges a series of neurological tests to definitively diagnose your condition. We often begin with an electroencephalogram (EEG), which records brain waves through electrodes placed on the scalp. In conjunction with video monitoring, the EEG detects abnormalities in the brain’s “wiring,” or electrical activity.
Also available is the complete spectrum of brain scans, including:
Computed Tomography (CT)
Magnetic Resonance Imaging (MRI)
Functional Magnetic Resonance Imaging (FMRI)
Positron Emission Tomography (PET)
Single Photon Emission Computed Tomography (SPECT)
Brain mapping, including grids and depth electrodes
Additionally, we offer the WADA test to patients preparing for surgery. This presurgical evaluation maps areas of a patient’s brain that are responsible for such functions as language and memory, for protection during surgery.
Once a diagnosis has been made, a treatment plan is developed based on your personal needs. The first step is, however, to confirm the seizure diagnosis, as a number of patients may have episodes that are not due to epilepsy. If the diagnosis of epilepsy is confirmed, we frequently start by prescribing antiepileptic drugs, either alone or in combination, as most patients respond to medication. The most common antiepileptic drugs include carbamazepine, valproate or phenytoin, and we also utilize the very latest medications. We also participate in clinical research trials of new medications for seizures. When medications prove ineffective, we can offer a range of other therapies, such as:
Vagus nerve stimulation, in which a battery-powered device, implanted in the chest and attached to the vagus nerve in the lower neck, delivers short jolts of electrical energy to the brain, thereby decreasing the frequency of seizures.
Ketogenic diet, a medically supervised diet high in fats and low in carbohydrates that has been shown to reduce epileptic episodes in children.
Surgery, performed when a lesion, tumor or seizure focus of the brain has been identified as the cause of a patient’s seizures and can be removed.
Today most people with epilepsy lead productive, normal lives, with the vast majority controlling seizures and other symptoms with medications alone. Many also are benefiting from special diets and surgical interventions. As researchers continue to introduce advanced diagnostics and new drugs and therapies, those living with epilepsy will be able to further minimize the detrimental effects of their illness and will experience an enhanced quality of life. Our epilepsy services strive to help realize these goals.
One area of controversy in the field of epilepsy is how to describe the seizures experienced by patients with epilepsy and how to catagorize them in order to sensibly discuss and treat epilepsy. Several congresses have been convined to work on this problem and out of them have come the International Classification of Epilepsies and Epileptic Syndromes. This classificaton has broadly defined seizures as either generalized ("seizures in which the first clinical changes indicate initial involvement of both hemispheres..." or sides of the brain) or partial (location related or focal/local/partial) seizures.
Idiopathic Generalized Epilepsies
These are forms of generalized epilepsies which have a generalized onset involving both sides of the brain. EEG (electroencephalography) recordings of the seizures show bilateral abnormal seizure patterns which are synchronized and symmetrical. Recordings done when no seizures are occurring are normal.
Benign Neonatal Familial Convulsions
These are rare seizures which occur just after birth (typically on the 3rd or 4th day of life) and manifest as rhythmic shaking of the body with or without breath holding. This condition is heritable and 14% of these babies will go on to develop epilepsy.
Benign Neonatal Convulsions
These seizures usually occur on the fifth day of life for no known reason and are not associated with either a risk for epilepsy or alteration in developmental potential. The convulsion caused shaking of the body and possible brief cessation in breathing.
Benign Myoclonic Epilepsy in Infancy
These occur in otherwise normal children during their first or second year of life. The seizures consist of brief jerks of the body or part of it similar to those experienced by most people as they are falling asleep. EEG recordings show brief burst of seizure activity, especially during the early stages of sleep. Later in life a few children who experience this will develop generalized tonic (body stiffening) - clonic (body rhythmically shaking) seizures and children with benign myoclonic epilepsy in infancy can have mild delay in development and minor personality disorders.
Childhood and Juvenile Absence Epilepsy
These seizures are associated with a momentary loss of consciousness (frequently not realized by others) with or without abnormal movements or loss of body tone and collapse. The childhood form occurs during early school years, may occur several times a day and are associated with the child later (during teens) developing generalized tonic-clonic seizures (GTCS). The juvenile form usually has an onset around puberty and the events are not uncommonly preceded by GTCSs. The EEG shows bilateral, symmetrical spike-waves which are synchronized and occur at a frequency of 3 per second.
Juvenile Myoclonic Epilepsy
Also termed Impulsive Petit Mal Epilepsy, these seizures occur around puberty and consist of single or repetitive jerking which is irregular, arrhythmic and occur bilaterally, predominately in the arms. GTCSs and, infrequently, absences may also occur. The most common time to see the seizures is shortly after awakening or when a person is sleep deprived.
Epilepsy with GTCS on Awakening
These seizures occur during the teen years and may be associated with absence or myoclonic seizures. The most common time for the seizures to occur is shortly after awakening from sleep (>90%) but they can also occur in the evening during periods of relaxation. Juveniles with this type of epilepsy will demonstrate a susceptibility to light induced seizures.
Generalized Cryptogenic or Symptomatic Epilepsies
Also called Infantile Spasms, this syndrome is manifest by seizures which start in the first year of life and consist of spasms with the body flexing, extending or the head may nod. There is arrest in the baby's development and the EEG has a characteristic pattern (hypsarrhythmia) which is diagnostic. The prognosis for the baby is a function of how well the baby responds to treatment with ACTH or steroids. There are two subgroups of this syndrome
Symptomatic Group - The baby has signs of an injured brain (delay in development, signs of abnormal function of parts of the nervous system or MRI/CT scans showing areas of injury in the brain) which predate the onset of the seizures.
Cryptogenic Group - There is no known reason for the seizures and examination of the baby is normal.
Children with this syndrome have intractable seizures of multiple types (absence, tonic axial, atonic, myoclonic, GTCS or partial). The frequency of the seizures is high and episodes of status are not unusual. The children exhibit psychomotor retardation and the EEG recordings are characteristic (generalized slow (<2 ½ per second) spike and wave pattern during clinical seizures). This condition can occur in children who had West Syndrome during their infancy.
Symptomatic Group - The child has signs of an injured brain (delay in development, signs of abnormal function of parts of the nervous system or MRI/CT scans showing areas of injury in the brain) which predate the onset of the seizures.
Cryptogenic Group - There is no known reason for the seizures and examination of the child is normal.
Epilepsy with Myoclonic-astatic Seizures
These seizures are mixed and include myoclonic, astatic and myoclonic-astatic seizures in association with absences, GTCS, and tonic seizures as well as non convulsive status. When the status occurs it is usually on awakening and is characterized by apathy or stupor in association with infrequent myoclonus. The onset of this condition is during early childhood and is frequently preceded by a febrile seizure. The EEG has a characteristic evolution over time and the outcome of children with this condition is variable.
Epilepsy with Myoclonic Absences
Children with this type of disorder experience absences usually accompanied by severe clonic jerking of both sides of the body. There can also be tonic stiffening of the body during these episodes. These can occur several times during the day. The age of onset is about 7 years and the EEG shows characteristic changes during these episodes which is similar to that seen that seen with childhood absences.
Symptomatic Generalized Epilepsies and Syndromes
These occur most commonly in infancy and childhood and the seizures are characterized by generalized seizures and EEG recordings which differ from those described in the idiopathic generalized epilepsies. Not uncommonly the child will exhibit more than one type of seizure and the EEG is characterized by bilateral asymmetrical activity which is less rhythmic than that seen with the idiopathic generalized epilepsies. The child has clinical signs of a diffuse encephalopathy.
Symptomatic Generalized Epilepsies of Specific Etiologies
These are seizures which are a prominent feature of a disease or disorder. Malformations of portions of the brain which cause such seizures as infantile spasms. Some malformations can cause characteristic seizures such as hypothalamic hamartomas causing gelastic seizures and infants with tuberous sclerosis commonly exhibiting West Syndrome which evolves into generalized and partial seizures with aging.
Proven or Suspected Inborn Errors of Metabolism
These are seizures, generalized or partial, which result when breakdown products of chemical reactions in the body accumulate triggering the seizure or a particular substances important to the normal function of the nervous system cannot be made and the resultant deficit leads to seizures. The seizures may be stereotypic for the condition or may be mixed and the age for onset of the seizures varies with the condition, some starting at birth, some in infancy, some in childhood and some in the teens. There are even a few which do not present until adulthood. A feature of these disorders is they are heritable.
Generalized Symptomatic Epilepsies of Nonspecific Etiology
Early Myoclonic Encephalopathy
The onset of this condition is usually by 3 months of age and starts with myoclonic seizures and evolves to more severe seizures. The EEG recordings show bursts of abnormal activity interspersed with suppression of the brain's normal activity and this pattern evolves into a hysarrhythmia. Babies with this condition arrest in their development as the seizures worsen.
Early Infantile Epileptic Encephalopathy with Suppression Burst
This starts during the first few months of life and is characterized by frequent tonic spasms of the body and an EEG recording similar to that seen with Early Myoclonic Encephalopathy. This frequently is associated with developmental arrest or delay and can evolve into West Syndrome by 4-6 months of age.
Epilepsies and Syndromes Undetermined as to Whether They are Focal or Generalized
Neonatal Seizures - These can be difficult to appreciate because of the immaturity of the nervous system. Manifestations of these type of seizures may include such subtle behavior as deviation of the eyes to one side with or without jerking, repetitive movements of the mouth mimicking lip smacking, swallowing, sucking, etc., pedaling or swimming movements in the arms/legs and apneic episodes. Premature infants may exhibit tonic extension in the arms or legs. Infrequently, there can be clonic or myoclonic seizures. These last types have greater significance with regards the baby's prognosis.Severe Myoclonic Epilepsy in Infancy
This form of epilepsy evolves out of febrile convulsions, usually in babies with a family history of febrile seizures or epilepsy. The seizures evolve during the first year of life and consist of generalized or unilateral clonic febrile seizures and evolve into myoclonic seizures and partial seizures later. There can be associated psychomotor retardation which becomes more obvious during the second year.Epilepsy with Continuous Spike-wave During Slow-wave Sleep
This is an EEG diagnosis with the children exhibiting seizures of varying types during deep sleep (partial or generalized seizures) and also absences while awake. There can be associated neuropsycholgical disorders.
Febrile Convulsions - This is a relatively benign condition seen during early childhood. The seizures are generalized and occur in association with fevers. Usually they are brief but when prolonged there is a chance of injury to the central nervous system which then results in a permanent dysfunction. As only 4% of children having these type of seizures go on to develop epilepsy, routine use of medications to prevent these is unusual unless they become a repetitive problem.
Focal or Partial Epilepsy
These are localization-related epilepsies and syndromes which are referred to as partial, focal or local epilepsies and syndromes. Either the feature or pattern of the seizures or the clinical investigation demonstrate a focal involvement of the brain in these conditions. Patients with these conditions can have a focal area of brain which functions abnormally, has a lesion or tumor or has developed abnormally. The abnormal area is responsible for the abnormal electrical discharges which result in the seizure. Some may have several areas capable of generating abnormal seizures and some may experience a secondary generalization of the seizure activity with the seizure coming to resemble a generalized seizure in very short (within seconds) order after onset of electographic onset of the focal activity. Not uncommonly, the onset may resemble a generalized seizure to a casual observer. In certain types of focal epilepsies (idiopathic age-related focal epilepsies) mirror areas of the two half's of the brain may be capable of generating seizures.
Focal seizures are commonly described as a function of their point of onset in the brain. To do this a careful history is obtained and extensive EEG recordings coupled with video taping of the patient's behavior are done to better appreciate what the first signs and symptoms of the typical seizure are and how these symptoms and signs progress as the seizure progresses. As a result descriptions of syndromes related to anatomic localization are becoming available.
Temporal Lobe Epilepsies
These include simple partial, complex partial and secondarily generalized seizures. The simple partial seizures typically have autonomic (pupillary dilation, flushing in the face, arrest of breathing) and/or psychic symptoms (fear, panic, rage) as well as auditory and olfactory sensations including illusions. The complex partial seizures usually begin with an arrest in motor activity followed by oroailmentary automatism's such as belching, rumbling in the abdomen and then other automatism's follow which typically encompass repetitive, complex movement such as opening and closing a door. The actual seizure usually lasts less than a minute and is followed by confusion and amnesia for a variable period with recovery gradually occurring.
Temporal lobe seizures can arise from the medial side of the lobe (mesial temporal lobe seizures, limbic seizures, rhinencephalic seizures) or the lateral side (lateral temporal lobe seizures).
Mesial temporal lobe seizures start deep within the brain so EEGs done between seizures are typically normal. The chances of recording abnormal activity is greatly enhance by using sphenoidal electrodes (thin wire electrodes inserted to lay at the base of the skull below the central part of the brain using thin needles temporarily inserted through the cheek). These seizures usually start with a rising sensation in the abdomen, nausea with autonomic signs and psychic symptoms following.
Lateral temporal lobe seizures are characterized by auditory hallucinations/illusions, dream like state, disorders in language reception and output and visual symptoms. The seizure can then move to involve the medial temporal lobe, occipital lobe or parietal lobe with onset of corresponding symptoms referable to these areas of the brain.
Because the memory circuits originate in the temporal lobe, repeated seizure activity which involves these structures can cause difficulties with memory and intellectual function. These seizures typically start in childhood or young adulthood, tend to cluster and are frequently associated with a history of febrile convulsions and/or a family history of seizures.
Frontal Lobe Epilepsies
These are generally short, complex partial seizures with minimal or no post ictal confusion. Secondary generalization is common and rapid. Simple partial seizures can also occur. The seizures contain a prominent motor component which is either postural or tonic. At the onset of these seizures complex gestures are common and if the activity spreads to the other half of the brain falling is common.. Given the complex nature of these seizures, they are not uncommonly mistaken for psychogenic seizures. The constellation of signs and symptoms which occur as the seizure starts and progresses offer clues to the site of origin of the seizure. The seizures take their name for the area of the frontal lobe from which they arise.
Supplementary Motor seizures
The patient assumes a fencing position with the arms or assumes another posture or exhibits focal, tonic activity. There is speech arrest or vocalizations.
Cingulate Seizures - These are complex partial seizures with complex, automatismal gesturing occurring at the onset. Commonly, there are changes in mood and affect and autonomic signs.
Anterior Frontopolar Seizures - With these seizures one sees forced thinking, loss of contact with the environment and aversive (movement toward the side of the body opposite side of brain generating seizure) head and eye movement. As these seizures evolve the head and eyes may move back to the side of seizure onset and there may be jerking of the trunk as well as autonomic signs and the patient may fall.
Dorso refers to the upper half of the frontal lobe. So these seizures arise in the upper, lateral part of the lobe and typically cause tonic and, occasionally, clonic motor activity with associated versive head and eye movement and speech arrest.
These are complex partial seizures where automatism's (motor and gestural) predominate with olfactory hallucinations/illusions and autonomic signs also occurring.
A primary feature of these seizures are signs and symptoms of alimentary tract involvement including chewing, swallowing, salivation, epigastric sensation, speech arrest, and sound generation. There can be speech arrest, fear and autonomic signs. If the activity spreads secondary sensory changes may occur such as numbness.
These are usually simple partial seizures and are localized based on what part of the body has movement at the onset of the seizure. If the face's motor region is involved there will commonly be speech arrest, difficulty in swallowing or vocalizations of sounds in association with the tonic or clonic movements of the face's muscles on the side opposite to the area of the brain generating the seizure. These seizures frequently spread (referred to as "marching"; i.e., seizure activity spreads up a arm or leg, marching to involve more and more adjacent muscles). After the seizure there is frequently a weakness for a variable length of time of muscles which were active in the seizure.
Parietal Lobe Epilepsies
These are typically simple partial seizures which can secondarily generalize. Rarely, they can evolve into complex partial seizures. Seizures from this area of the brain typically manifest sensations such as tingling, numbness, loss of the extremity, crawling, coldness or electric sensations in regions of the body but more complex sensations such as feeling that an extremity is moving, or complex alimentary sensations may occur. Rarely, there may be a painful sensation. The involvement may march as with motor seizures of the frontal lobe. There can be complex visual symptoms such as metamorphosis with distortions, foreshortening and elongation may also occur. Severe vertigo or disorientation is a sign of involvement of the lower part of the lobe. If the dominant (usually the left) lobe is involved there can be dysfunction in processing language input and output. These seizures commonly generalize secondarily.
Parietal Lobe EpilepsiesThese are typically simple partial seizures which can secondarily generalize. Rarely, they can evolve into complex partial seizures. Seizures from this area of the brain typically manifest sensations such as tingling, numbness, loss of the extremity, crawling, coldness or electric sensations in regions of the body but more complex sensations such as feeling that an extremity is moving, or complex alimentary sensations may occur. Rarely, there may be a painful sensation. The involvement may march as with motor seizures of the frontal lobe. There can be complex visual symptoms such as metamorphosis with distortions, foreshortening and elongation may also occur. Severe vertigo or disorientation is a sign of involvement of the lower part of the lobe. If the dominant (usually the left) lobe is involved there can be dysfunction in processing language input and output. These seizures commonly generalize secondarily.
Occipital Lobe Epilepsies
There are two categories of Localization-Related Epilepsies or Syndromes with regards their etiology. Each have several subtypes of seizures.
These are simple partial seizures which commonly undergo secondary generalization. With spread, the seizure can evolve into a complex partial seizure. The initial visual symptoms are usually sparks, flashes or phosphenes but may be scotoma, hemianopsia or amaurosis with the symptoms occurring toward the side opposite the involved part of the brain. There can also be distortion of vision with objects appearing altered in size (too large or small), shape or tilted. Distances may also appear altered.
Idiopathic Localization-Related Epilepsies
These are age-related epilepsies in children whose clinical examinations and testing fail to demonstrate anything other than a focal area of abnormal electrical discharge as recorded by EEG. There is no known causative factor for these children's epilepsies except for a number being hereditarily acquired. These seizures are brief, not associated with neurologic or intellectual abnormalities. The pattern of seizure is generally constant for any given child.
Benign Childhood Epilepsy with Centrotemporal Spikes
These are focal seizures commonly occurring around sleep which involve the face, can have a sensory component and can generalize into a GTCS. They are most common in males and can start as early as age 3 and typically burn out between ages 15 and 16.
Landau-Kleffner Syndrome is a atypical form of Benign Partial Epilepsy occuring in the speech region of the left frontal lobe.
Childhood Epilepsy with Occipital Paroxysms
These seizures start with visual symptoms such as amaurosis, phosphenes, illusions or hallucinations and 25% of patients with this condition will have migraine headache prior to onset of their seizures. The seizure can then spread to involve the posterior temporal lobe and central areas of the brain with onset of behavior which can include clonic activity in one side of the body or complex patterns of body movement. Otherwise, these seizures are very similar to Benign Childhood Epilepsy with Centrotemporal Spikes.
Symptomatic Focal Epilepsies
These are epilepsies which are focal in origin and are due to known or suspected disorders of the brain as demonstrated by clinical investigations such as CAT or MRI scans, laboratory testing, etc.
Chronic Progressive Epilepsia Partialis Continua of Childhood (Kojewnikow Syndrome)
This is one of the two forms of Kojewnikow Syndrome (the other being Rasmussen's Syndrome) which is a partial motor seizure which can progress to a myoclonic seizure involving the same muscle groups as are involved by the motor seizure. These type of seizures can begin at any age and are usually associated with a demonstrable lesion such as a tumor or vascular abnormality. The seizure disorder will not progress unless the causal lesion does.
Syndromes Characterized by Seizures with Specific Modes of Precipitation
These are seizures which reliably result from an environmental or internal factor. A memory or recognition of a specific pattern triggering a complex partial seizure would be an example. Less common would be partial seizures triggered by a simple sensation (a smell, etc.) as such stimulus specific induced seizures are usually generalized. Partial seizures can also be caused by sudden, unexpected arousal, but, again, generalized seizures are more common in this setting.
What type of testing is used during surgery?
This localizes precisely the region of seizure focus within the brain. Electrodes either on the surface of the brain or in its depths are used to pick up and record EEG. After resection of the focus is completed, a second recording is done to assure adequacy. These tests can be done on either an awake or anesthetized child.
Intraoperative Somatosensory Evoked Potentials
These localize the primary areas of the brain responsible for sensing touch (the postcentral gyrus) and thereby the adjacent region responsible for movement of the body (the precentral gyrus). This test may also be done on an awake or anesthetized child. It is useful not only in identifying motor cortex, but also in establishing landmarks to be used for avoiding injury to cortex important in language processing.
Intraoperative Cortical Stimulation for Brain Mapping
This is the type of monitoring typically associated with epilepsy surgery. It may be either gross stimulation of motor cortex to confirm its identity after intraoperative somatosensory recording, or stimulation of cortex to delineate regions important in higher cortical function (e.g., speech centers). While stimulation of motor cortex for purposes of its identification can be done on an anesthetized child, more sophisticated mapping requires an awake, cooperative patient who can communicate with the operative team. For that reason, mapping of the functionally important regions of the brain in children is frequently done outside of the operating room using implanted sheets of electrodes laying on the surface of the brain.
Implantation of electrodes for localization of seizure focus and brain mapping
Children frequently require electrode implantation to both precisely localize the focus triggering the seizures and to map regions of the brain important to movement of the body and to speech. Information gained from previous, non-invasive video-eeg monitoring is used to determine what surfaces of the brain must be covered with the electrode sheets. Rarely, a preliminary surgery is required to better define which regions of the brain are responsible for the seizures. In these cases, strips of electrodes are fed through small holes in the skull to accomplish broad coverage over the brain's surfaces. Coverage to define the focus of the seizure is broad so that all borders of the focus can be delineated (typical electrode coverage). Once the site of origin of the seizures has been determined, the electrode sheet is used to map brain function. A surgical plan is then devised using both the map of brain function and the map of site of origin of seizure activity.
What will be done during surgery?
The anterior temporal lobe is the most common seizure focus site in patients with partial seizures. Thus temporal lobectomy is the most widely used surgical procedure for epilepsy, and has the greatest rate of success. Approximately 60% of patients become seizure-free, and 85% enjoy a marked reduction of seizures. Behavioral disorders like aggressivity and hyperactivity are often improved.
Seizure foci may be located in the frontal, parietal, or occipital lobes of the brain. Surgical therapy can also be effective for these patients, but the extent of resection is often limited because of important adjacent functional areas. The success rate with extratemporal resections is consequently lower than with temporal ones.
Multiple Subpial Transections
This refers to vertical cuts being made through a region of the brain with a seizure focus. Approximately 3/8" of brain must simultaneously discharge to generate a seizure. Nerve fibers which run horizontally through the brain's surface connect this critical mass of brain tissue responsible for initiating the seizure. Nerve fibers which connect the brain with the body run in a vertical direction. Thus, vertical cuts through the brain will transect the fibers important for generating a seizure without disrupting many of the nerve fibers important to the brain's function since these fibers run parallel to the direction of the cut. Cuts are made every 1/4" so that not enough brain tissue is interconnected to generate a seizure.
This involves the dividing the two major fiber bundles (the corpus callosum and hippocampal commissure) which connect the right and left sides of the brain. The corpus callosum is usually sectioned in two stages: first the anterior two-thirds, and, if seizures persist, the remaining posterior one-third. Candidates for callosotomy are often those who were evaluated for focal resection but have an extensive area, or multifocal areas, of the brain causing the child's seizures. In general, corpus callosotomy is palliative and not curative. It reduces the number of severe seizures and prevents secondary generalization (spread of the seizure activity to involve both sides of the brain with a resultant loss of consciousness) of seizure activity. Thus it reduces the number of injurious falls that occur with the loss of consciousness.
Subtotal hemispherectomy (either the formal removal of one of the brain's hemispheres or the functional equivalent) is now used to treat medically refractory seizures in patients with pre-existing diffuse hemispheric injury and dysfunction (e.g., infantile spasms and Sturge-Weber). Most of these children have frequent, severe seizures arising from a hemisphere with little or no function, so that the operation does not increase preoperative deficits.
Seizures must be refractory to medical therapy. Patients should have monotherapy trials with major drugs (i.e., carbamazine, phenytoin, phenobarbital or mysoline, and valporic acid). If these are ineffective or cause intolerable side effects, combination therapy should be tried. Blood testing should be done to insure an adequate amount of the drug is getting into the body. The drug should be escalated until seizures are controlled or unacceptable side effects are encountered. An adequate period of medical therapy is impossible to define precisely. It depends on seizure frequency (more seizures allow the physician to assess efficacy in a shorter period), severity, and whether there are side effects. In most cases where medical therapy is considered to have failed, seizures have been refractory for at least two years.
Seizures must have a significant adverse effect on the child's life. There is no absolute number of seizures or clinical features that defines intractability. Impairment of consciousness during the waking state is often the critical factor. However, frequent nocturnal convulsions that leave the child lethargic and cognitively impaired the next day are also not acceptable, and would mandate a more aggressive treatment plan. Frequent simple partial seizures that do not cause unconsciousness but disrupt memory function or cause prominent hallucinations and adverse symptoms should be considered for surgical treatment. On the other hand, daytime complex partial seizures in a retarded, institutionalized child may not have a significant adverse effect on the patient's life.
There are no absolute age limits for this surgery.
Patients with chronic psychosis and mental retardation are usually not considered.
Chronic psychosis is not significantly improved by epilepsy surgery. Although the seizures may cease, the patient will remain incapacitated by mental disabilities. Mental retardation (Full Scale IQ of less than 70) indicates diffuse cerebral dysfunction; these children may (1) suffer additional cognitive impairment from surgery, (2) have difficulty cooperating with the extensive presurgical evaluation, and (3) have persistent seizures after the procedure. Surgery for mentally retarded children should be considered only for those who suffer frequent, severe falls in association with seizures.
The seizure disorder must be partial.
Careful history from the patient and from witnesses, in combination with neurologic examination and routine electroencephalography (EEG) will almost always distinguish between partial and primary generalized seizures. In a few cases uncertainty may remain; here video-EEG monitoring is usually diagnostic. Patients with unilateral temporal lobe seizure foci have the best surgical outcome, while those with extratemporal foci do less well.
In summary, children with partial seizures that cannot be controlled medically and that disrupt their lives should be considered for surgical treatment.
Patients must undergo an extensive presurgical evaluation to localize definitely the focus from which the seizures arise. In addition, localization of cerebral function must be performed to identify areas that are critical to cognitive, motor, and sensory functions.
Surgery should be viewed as another available tool for the management of epilepsy. It is best utilized when partial seizures or medical treatment for them are disrupting a child's development and interpersonal relationships. After surgery, medical management will be greatly simplified, and the seizures will be completely eliminated in a significant number of cases.
Enterotube II is a rapid, multi test kit system used to identify unknown oxidase-negative, gram- negative, rod shaped bacteria from the family Enterobacteriaceae Enterotube II has a tube with a flat side and which contains 12 compartments color coded for different biochemical tests. Enterotube followed by Enterotube II, though improved it’s accuracy, the enterotube II system still may yield false positive or negative results. The Following bacterias can be identified with enterotube test
Choose a well-Isolated colonies from Perti dish, and select one colony for identification.
Obtain one Enterotube II and remove the cap from the Enterolube II.
Not the bent, but the straight wire to be used to pick up the bacteria, while the bent end Is the handle.
Without flaming the wire, touch the end to a well-Isolated colony or bocterla from a plate. Avoid touching agar, but try to touch the bacteria only.
While gently twisting the wire, pull it through all 12 compartment of the Enterotube II. Now reinsert the wire into the first four compartments (glucose, Lysine, Ornithine and H2S lndole), thereby creating an anaerobic environment.
Break the needle by bending It at the notch, and discard the handle in the breaker of disinfectant. Replace the caps loosely on both ends of the tube.
Strip off the blue tape to expose the holes ln the Enterotube II and provide aerobic conditions. Slide the clear plastic band over the glucose compartment any wax that may otherwise escape due to excessive gas production. Incubate incubated at 37 degrees Celsius for 18-24 hours and then refrigerate it until it is to be observed.
Enterotube II interpretation Guide is as under:
Examine the Enterotube II and interpret all the results except Indole and Vages Proskauer Tests.Results.
Once the 24 hours of incubation is complete, all change in color to be recorded in the manufacturer ID card provided along with the enterotube II interpretation guide.
Then reagents are added to the indole and Voges-Proskauer compartments as per the instructions and their results are recorded in the same ID card. The numerical values of the positive tests are added in their appropriate sections to yield a 5-digit ID for the organism being tested.
Once the 24 hours of incubation is complete, all change in color to be recorded in the manufacturer ID card provided along with the enterotube II interpretation guide. Bacterium are attempted to identify with the help of computer generated coding system available on report sheet from the instructor.The instructor will provide directions for the system to determine the ID value to identify the genus and the species of the organism.
The Chiari Malformation (also called the Arnold Chiari Malformation) is a developmental anomaly at the base of the brain which results in the downward displacement of some of the brain's structures into the spinal canal. These malformations have been subdivided to reflect the degree of displacement as well as the varying etiology of the malformations. Type I malformations consist of a downward displacement of the cerebellar tonsils (two pegs of tissue which hang off the inferior surface of the cerebellum at the base of the brain) out the inferior opening of the skull into the spinal canal. No other structures of the brain are displaced. There is frequently (30-75%) an associated accumulation of fluid within the interior of the spinal cord. Type ll malformations have greater displacement of brain structures into the spinal canal. In addition to the cerebellum's tonsils there is also displacement of the inferior vermis (bundle of tissue connecting the two halves of the cerebellum), fourth ventricle, choroid plexus and medulla. The displacement is variable but quite frequently can extend down to the mid portion of the neck. Type II malformations are typically part of a larger developmental syndrome associated with myelodysplasia (spina bifida). Type lll malformation is a special type of myelodysplasia where there is a spina bifida (division or defect in the posterior portion of the bony spine) in the neck with an associated herniation of a fluid sac into the overlying defect in tissue closure. Lower structures of the brain herniate into this fluid sac. Occasionally one hears of a Type IV malformation. This refers to a hypoplasia (incomplete development) or aplasia (lack of development) of a portion of the cerebellum and, in fact, is not a hind brain herniation at all in contrast to Types 1-III.
It is not unusual for the Chiari Malformations to have an associated accumulation of fluid within the interior of the spinal cord. This condition is termed syringomyelia or hydromyelia. The condition ultimately results in progressive formation intramedullary (referring to the interior of the spinal cord or brainstem) cyst associated with progressive neurological deficits. While there are other reasons for cysts to occur within the spinal cord (trauma, tumor), the bulk of cysts which occur in the spinal cord are due to anomalies in the anatomy at the skull base.
The availability of MR scanning has lead to a increasingly earlier diagnosis of the Chiari Malformation. The noninvasive nature of this test along with its superior imaging of the base of the brain has lead to its increase use in children with such relatively nonspecific complaints of headache and curvature of the spine. Now the condition is frequently diagnosed before the onset of frank neurologic dysfunction. The onset of symptoms referable to a Chiari Malformation is typically subtle and evolve slowly. Consequently, it is not unusual for the condition to be diagnosed after months or years of problems which in retrospect are due to the malformation. The symptoms attributable to the malformation will vary according to the patient's age, the degree of displacement of structures downward, the presence of associated bony anomalies of the spine and the presence of hydromyelia. The most frequent symptom groupings include:
headache, pain at base of skull/upper neck
progressive scoliosis (curvature of the spine)
cerebellar dysfunction (difficulty with balance, coordination, dysequilbrium, low muscle tone)
Compression of the lower brainstem to cause
alteration of voice
frequent respiratory tract infections
coughing when swallowing foods and fluids
Compression of the spinal cord or distention due to accumulating fluid (hydromyelia) suspended alteration of sensation (e.g., arms are effected but legs not) central cord disturbance (injury to central part of spinal cord with resultant weakness greater in arms than legs) spasticity (abnormally high muscle tone or tightness, especially with movement of the muscle) Combinations of these syndromes occur commonly.
Anomalies of the base of the skull and spine are seen in 30-50% of patients with the Chiari Malformation, Type 1. These anomalies include:
basilar impression (compression of the upper part of the spine into the base of the skull with resultant compression of the brainstem)
atlanto-occipital fusion (bony union of the first level of the spine to the base of the skull)
atlanto-axial assimilation (partial bony union of the first and second levels of the spine)
Klippel-Feil deformity (congenital union or fusion of levels of the spine within the neck with possible associated maldevelopment of levels of the neck's spine)
cervical spina bifida occulta (bony defect in a the posterior part of the spine)
scoliosis - commonly seen when hydromyelia exists (16-80% of patients), especially in children with immature spines.
There may be signs of brain stem dysfunction in some who have a Chiari Malformation (10-47%). This occurs when the displaced tissue of the malformation compresses the lower part of the brain stem. The following problems may develop as a result:
drop attacks (sudden loss of body muscle tone with collapse to floor)
postural and cough headaches (majority of cases) dull, chronic headache involving back of head or neck paroxysmal, severe headache associated with a valsalva maneuver (cough headache)
visual disturbances from nystagmus (jerking of eyes when looking to right or left), oscillopsia (vertical bobbing of eyes) or diplopia (double vision)
spasticity (muscle stiffness)
sensorimotor deficits (abnormal body sensation and/or muscle strength)
ataxia (difficulty with balance and coordination)
dysarthria (difficulty talking)
dysphagia (difficulty swallowing)
There have been reported cases of children with previously undiagnosed Chiari Malformations sustaining injuries to the spinal cord with no obvious abnormality in the x-rays of their spine. The evaluation of children who have sustained a spinal cord injury should include a MR scan of their spinal cord which includes imaging of the base of the brain to rule out a Chiari Malformation.
Chiari ll Malformation
As stated previously, this malformation is part of a larger syndrome seen in children with myelodysplasia(spina bifida). This is frequently misunderstood and I receive frequent emails from individuals thinking they have a Type II malformation in spite of the fact that they do not have a myelodysplasia It is exceedingly unusual to have a Type II Malformation without having myelodysplasia. While all children with myelodysplasia will have the Chiari malformation, only 9-21% will exhibit symptoms which warrant treatment. Those destine to exhibit symptoms will do so either early in infancy or later in childhood with the presentation and outlook differing for the two groups.
Those infants destine to develop difficulties due to their Chiari Malformation will do so after several weeks or months of relative normalcy. Their families will notice increasingly stridorsis breathing, a higher pitched crying. There may be apneic episodes. Left to deteriorate, these infants will develop dysphagia with associated nasal regurgitation, and aspiration. They will appear very uncomfortable and prefer to assume a position with their head and back arched posteriorly with the head tilted to one side. Deterioration will rapidly progress from this point. Treatment of infants with this condition is controversial. The first question to be answered is the shunt malfunctioning for if it is, these symptoms can rapidly be reversed with correction of the shunt's functioning. On the other hand, if the symptoms are due to the Chiari Malformation, treatment becomes more difficult and controversial. This is because it is particularly difficult in infants to differentiate symptoms due to mechanical compression of the lower brain stem from symptoms due to a untreatable malformation of the lower brain stem. Additionally, there can be a combination of the two processes when an abnormally formed brainstem which is marginally functional sustains an additional injury due to compression rendering the situation unretrivable. Invariably a judgment is made based on the condition of the baby before onset of symptom progression and the degree of disability at the time of decision making.
Older children and adolescents have a more insidious presentation with headache and lower cranial nerve dysfunction (weakness in gag, tongue, voice and swallowing) predominating early with fainting episodes and abnormal eye movement following. If hydromyelia develops there will be increasing spasticity in the arms and legs as well as progressive weakness and changes in sensation. Once again the first question to be answered is "is there a shunt malfunction?" If there is not then attention is directed towards whether the severity of symptoms mandate a surgical decompression of the malformation.
Traditionally, when symptoms as discussed in the previous chapter have lead your physician to suspect a Chiari Malformation, plain x-rays of the head and spine were performed followed by a myelogram (a contrast agent is injected via a spinal tap into the spinal fluid and then a series of x-rays are taken which image the spinal fluid space and its contents including the spinal cord and nerve roots). Due to its invasive nature, there was always a reluctance to perform this test until the severity of the symptoms warranted it. The introduction of modern imaging techniques, specifically the MR scanner, has radically changed the evaluation of symptoms referable to the spinal cord. This test is non-invasive and as a consequence is performed much earlier in the evolution of the condition, frequently before permanent injury has occurred within the nervous system. MR imaging is now the procedure of choice for imaging the spinal cord and the fluid surrounding it. There are several different types of studies and these are used to delineate normal from abnormal anatomy. The resolution of these studies approaches that of the actual anatomy so the treating physician can gain a good understanding of the anatomical substrate which is giving rise to the symptoms. If there is concern about the surrounding bony spine, the CT scan is usually used since it can better show the bony anatomy.
The treatment of Chiari Malformation and associated anomalies is controversial, largely owing to a lack of complete understanding of the entity. All would agree that abnormal accumulation of fluid within the brain, when present, must be dealt with prior to considering any other type of procedure to treat a Chiari Malformation. There are numerous treatment strategies for Chiari Malformations. Most of these procedures report a 70% success rate in dealing with the symptoms referable to the Chiari Malformation and its associated anomalies. These procedures can be grouped into four categories:
Decompression of the hindbrain malformation by the removal of overlying bone (suboccipital (base of skull in the back) craniectomy (opening of the skull) and upper cervical (neck) laminectomy (removal of the posterior portion of the spine to gain access to the underlying spinal cord and nerves).) Opening of the soft tissue coverings over the base of the brain and upper spinal cord with placement of an patch to enlarge the coverings might be included.
Drainage of the syrinx or syringomyelia/hydromyelia; i.e., removal of bone overlying syrinx, then opening spinal cord to drain fluid cavity (myelotomy) and possible placement of catheter (syringotomy) from cavity to other space to establish pathway for continued drainage.
Establishment of outflow pathway for fluid cavity by cutting off lower tip of spinal cord (Terminal Ventriculostomy)
Percutaneous aspiration of the syrinx
As stated above, there is an expected failure rate of up to 30% with these various techniques. Consequently, there has been a recent trend toward simultaneous treatment of the Chiari Malformation and its associated anomalies such as hydromyelia. Some advocate plugging of the congenital inlet (the obex) to the spinal cord's central fluid canal to prevent the ingress of fluid. This is based on a feeling that the fluid found within the syrinx arises within the brain and is sucked or pushed through the obex and central fluid canal of the spinal cord to reach the syrinx. Some advocate simple drainage of the cavity feeling that the accumulation process is either static or that the mechanism driving the accumulation has been dealt with in dealing with the Chiari Malformation. Others would argue that re-accumulation of the syrinx can occur and therefore a more permanent egress path should be establish by placing a small tube into the cavity with the other end either resting in the fluid space outside the spinal cord or in some other body cavity to which the fluid can drain. Our bias has been to decompress the hind brain malformation by removing both the overlying bone and opening the soft tissue coverings (the dura). For Chiari Malformations, Type I we remove the tissue which is hanging down and compressing the spinal cord (the cerebellar tonsils). We use an intra-operative ultrasound to image the interior of the cord. If the syrinx ascends to the level of the brain stem, the outlet of the fourth ventricle is inspected to ensure that it is open. If not, it is opened and we sometimes lay a small tube through the outlet to prevent it from re-closing. A graft is then used to enlarge the dural sleeve investing the spinal cord. If the pre-operative MR scans show the syrinx to be distended, consideration is given to treating the syrinx surgically.
Surgery for the treatment of Chiari Type I Malformations and Chiari Type II Malformations in older children and adults is safe with recent reports showing near zero surgical deaths. Morbidity or side effects from the surgery are not infrequent. Many are left with continued discomfort at the base of the skull and in the neck. This can be due to an unrecognized hydrocephalus, aseptic meningitis (an inflammatory reaction at the surgical site due to the dural graft, blood breakdown products or other materials), bradycardia (slow heart beat), and breathing dysfunction with apnea (failure to breath). When a myelotomy is performed, there can be alteration in sensation (loss of touch or position sensation, or pins and needles sensation). Whether or not morbidity is increased with more extensive procedures remains unclear.
Great care must be taken in accessing the results of any given treatment for symptoms referable to a Chiari Malformation. Since many will show evidence of symptom recurrence within two years of surgery, follow-up must be for at least this duration.
Symptoms directly referable to the hind brain malformation seem to be more amenable to treatment. Cough headache and symptoms due to cerebellar dysfunction (dizziness, difficulty with coordination, unsteadiness in gait) resolves over 80% of the time by report. Symptoms due to an associated syrinx are somewhat more problematic. Scoliosis will stabilize or improve in 50 to 100% of children. Younger age, the absence of extreme angulation, and MRI confirmed resolution of hydromyelia are associated with a better chance for improvement. Central cord syndrome (a characteristic pattern of weakness effecting the arms more than the legs due to a injury to the central portion of the spinal cord) in association with a syrinx has generally been associated with a poor response to treatment with only one third experiencing a sustained improvement.
A review of all the reported cases of hydromyelia and the Chiari I malformation operated on prior to the advent of MRI found that 46% improved, 32% remained stable and 20% progressed postoperatively. Thus 78% of those operated on, regardless of the surgical technique used, experienced an outcome better than that seen if no treatment is offered. The authors of the paper concluded that surgery was preferred to conservative management. However, while patients reported improvement of their complaints and functional capabilities, not infrequently there were persisting neurologic deficits and symptomatic complaints.
Infants with myelomeningocele (spina bifida) and symptomatic Chiari Type ll malformations continue to have significant morbidity and mortality. Most report up to a 50% long term mortality, regardless of the treatment strategy. Tracheotomy (creation of a new airway outlet through the neck) and gastrostomy (creation of a new food inlet through the abdominal wall) or nasogastric (a tube through the nose, down the throat to the stomach) feedings are often required for months after surgically dealing with the malformation. Intervention prior to the onset of bilateral vocal cord paralysis is associated with a better outcome.
The increasing utilization of MRI for screening children and adults with minimal neurological disease has resulted in an increased appreciation of the true incidence of Chiari Malformation. It has also allowed for the opportunity to intervene at a much early stage in the condition's evolution. It is my feeling that this certainly lessens the risks associated with any surgery and will result in less long term morbidity for those with this condition.
Guillain-Barré syndrome is a medical emergency, with predominantly motor features; requiring constant monitoring and support of vital functions, often in ITU
A heterogeneous group of immune-mediated processes characterised by motor (and some sensory, and autonomic) dysfunction. In its classic form, GBS is a rapidly progressive acute inflammatory demyelinating polyneuropathy characterised by a progressive symmetrical ascending LMN muscle weakness, paralysis, and hyporeflexia; with or without sensory or autonomic symptoms
Typically, it starts in the lower limb (with reduced tendon reflexes); and progresses into the arms; with mild distal sensory loss. 50% have cranial nerve involvement
Most common acquired inflammatory neuropathy. Although the cause is not fully understood, it is thought to be autoimmune; and in most patients, is associated with antecedent infection
Several variants. In some, there is an inflammatory demyelinating polyradiculoneuropathy; others affect the axon
Diagnosis is clinical; as the classical LP findings (v high protein) may not appear for a week
Treatment includes immunoglobulin OR plasma exchange; and, for severe cases, mechanical ventilation
Prognosis: 2% mortality; 5-10% require ventilation; 10% cannot walk independently at 1 yr; 30% have some deficit at 3 yrs; 2-5% recur
Complete paralysis is compatible with a full recovery
1-2/100,000 pa. Increased incidence in males. Peak ages: 15-35 and 50-75 yrs
Lymphomas - especially Hodgkin's disease
Pregnancy - incidence decreases during pregnancy but increases in the months after delivery
Acute inflammatory demyelinating polyneuropathy (AIDP) - is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an auto-immune response directed against Schwann cell membrane
Miller-Fisher Syndrome (MFS) - is a rare variant of GBS and manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS. It usually affects the ocular muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia. There is little significant limb weakness
Acute motor axonal neuropathy (AMAN) (or Chinese Paralytic Syndrome)
Acute motor sensory axonal neuropathy (AMSAN)
Bickerstaff’s brainstem encephalitis (BBE)
Acute panautonomic neuropathy
Did you know?
The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and Andre Strohl diagnosed two soldiers with the illness; and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count
GBS is also known as: Guillain-Barré-Strohl syndrome; and, Landry’s paralysis, Landry's ascending paralysis, Kussmaul-Landry syndrome, Landry's syndrome, Landry-Guillain-Barré syndrome, Landry-Kussmaul syndrome, acute inflammatory demyelinating polyneuropathy (AIDP), acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis and French Polio
Various famous people have had GBS: Joseph Heller, Franklin D. Roosevelt (paralysis long attributed to poliomyelitis), Markus Babbel, William “The Refrigerator” Perry, Tony Benn
In about 2/3rds of patients, the syndrome begins 5 days to 3 wk after a banal infectious disorder, surgery, or vaccination. Infection is the trigger in > 50% of patients
Common pathogens include Campylobacter jejuni (especially Penner serogroup 19), enteric viruses, herpesviruses, HIV, cytomegalovirus, Epstein-Barr virus, and Mycoplasma sp
A cluster of cases followed the swine flu vaccination program in 1975
Antibodies to ganglioside GM1 are found in 20-30% of cases. There is a strong association with ganglioside GQ1b and the Miller-Fisher syndrome
Can start with paraesthesis in toes; rapidly (hours) followed by LMN symmetrical weakness, usually beginning in the legs; ascends to arms; 90% maximal weakness at 3 wks
More marked proximally than distally
May involve intercostal or bulbar muscles, or muscles of mastication; causing respiratory failure, dysphasia or dysphagia (can be life-threatening)
Muscle wasting develops if axonal degeneration has occurred
Sensory complaints; also frequent (less so than motor though)
A few patients (possibly with a variant form) have significant, life-threatening autonomic dysfunction causing labile BP, inappropriate ADH secretion, tachycardia, cardiac arrhythmias, disturbed sweating, GI stasis (paralytic ileus), sphincter problems (eg urinary retention), and pupillary changes
Muscle/back pain (so differential diagnosis wide); it is important to not make light of the pain a patient with GBS experiences; gabapentin (or a similar neuropathic analgesic) is often required +/- a referral to the ‘pain team’ Notes: (less commonly): disease affects upper limbs only; or cranial nerves alone; 50% facial and eyelid weakness; sphincter problems rare; can start in head or arms, then progress down; or, sensory symptoms minimal or absent; or asymmetrical; acute onset of bilateral facial palsy is usually due to GBS
"When did the weakness start?"
"Have you had an infection recently?"
Fever normally absent
Sensory symptoms but limited signs
Flaccid paralysis of lower limbs, then upper limbs (usually)
Deep tendon reflexes are typically absent; plantars normal
Facial palsy (VII), ptosis
Tender muscles Note: if spinal level, assume spinal cord compresion, until otherwise proven
Very high LP protein may not appear for 1 week
FBC, ESR, CRP
U+E, LFTs, Bone, Glucose ± ABG, if hypoxic (on sats)
LP (usually very high protein, 3-10 g/L; no/few WC; but it may not appear for up to 1 wk and does not develop in 10% of patients)
MRI (brain/spine; to exclude other diagnoses)
ECG (many different abnormalities may be seen, eg 2nd and 3rd degree AV block, T-wave abnormalities, ST depression, QRS widening, and a variety of arrhythmias)
Nerve conduction studies:
- Initial testing detects slow nerve conduction velocities and evidence of segmental demyelination in 2/3 of patients
- However, normal results do not exclude the diagnosis and should not delay treatment
- Electrophysiologic studies may reveal marked slowing of motor and sensory conduction velocity, or evidence of denervation and axonal loss
- The time course of the electrophysiologic changes does not necessarily parallel any clinical developments
Differential Diagnoses (including all causes of rapid paralysis)
Neuromuscular (causes of paralysis)
Brain: brainstem CVA (rapid onset), encephalitis
Spinal cord: spinal cord compression (usually UMN); transverse myelitis (sphincter disturbance and sensory level); poliomyelitis (LMN; usually occurs in epidemics); tick paralysis (causes ascending paralysis but spares sensation); West Nile virus (causes headache, fever, and asymmetric flaccid paralysis but spares sensation)
Peripheral nerve: autoimmune, toxic and metabolic neuropathies (vasculitis, toxins, porphyria)
Neuromuscular junction: myasthenia gravis (intermittent and worsened by exertion); botulism (LMN; may cause fixed dilated pupils (in 50%) and prominent cranial nerve dysfunction with normal sensation)
Muscle: hypokalaemia, hyperkalaemia, myositis
Causes generalised muscle/joint pain (myalgia predominates; eg viral illness)
Ventilate sooner rather than later
Treatment (first line)
IV NORMAL IMMUNOGLOBULIN 400 mg/kg od, for 5 days; it has some benefit up to 1 month from disease onset (OR plasma exchange) - senior specialist decision
SC ENOXAPARIN 40 mg od (prophylaxis)
IV line (+ fluids, if dry, or dysphagic)
OXYGEN, if hypoxic Note: therapy is otherwise symptomatic, the aim being to prevent such complications as respiratory failure or vascular collapse; eg volume replacement or teratment with pressor agents is sometimes required to counter hypotension
Compression stockings (DVT/PE prevention). Careful nursing, with physio, to prevent pressure sores, chest infection, contractures - and maintain morale
Treatment (second line)
NG feeding, if dysphagic
Ventilation (if suspect paralysis ascending to respiratory muscles)
Early tracheostomy (muscle activity can take weeks-months to recover)
Temporary cardiac pacing (if bradycardic)
Steroids of no value
Key management decisions
Medical admission, then neurology ward ± ITU
Neurology ± ITU
Don't ignore people when they say they 'cannot walk'. There are several treatable causes (GBS, sc compression, hyperkalaemia etc)
Urinary retention and extreme constipation can occur; so, catheterise, and pay attention to bowels
Respiratory failure (respiratory muscle weakess; 25% patients); 5-10% require ventilation
Respiratory involvement is very serious
Mortality < 2%. About 25% of deaths occur during the first week and about 50% during the first month. 10% cannot walk independently at 1 yr
Most patients improve considerably over a period of months, but about 30% of adults and even more children have some residual weakness at 3 yr. Patients with residual defects may require retraining, orthopedic appliances, or surgery
2-5% recur; some have further acute episodes; other develop chronic inflammatory demyelinating polyneuropathy
2° Prevention + Health promotion
Warn about recurrence, and progression to chronic form
Give immunogloblins ASAP
Respiratory involvement is serious
VENTILATE SOONER > LATER; assess respiratory function 2xday
Manage on ITU if any concern
Examine regularly (progression)
If worried, get MRI to exclude sc compression
Complete paralysis compatible with full recovery
The usual incidence of myelomeningocele, or Spina Bifida, is about one in every thousand live births. While there is no definitive etiology, it seems clear that the pathological process begins before the 4th week of gestation. Neurulation (the normal closing process of the fetus's brain and spinal cord) is normally complete by that time, but it is uncertain whether this disorder represents a failure of neurulation in the base of the spinal cord, or a rupture there after neurulation has become complete. Whatever the cause, there is a defect in the spinal cord's base, with protrusion of the spinal cord and its coverings through a defect in the skin. The condition is often associated with disruption of the cerebrospinal fluid pathways with a resulting hydrocephalus.
The degree of neurological deficit is directly relates to the level of the spinal cord defect and its extent. If only the bottom of the spinal cord is involved (conus), there may be only bowel and bladder dysfunction, while the most extensive lesions can result in total paralysis of the legs with accompanying bowel and bladder dysfunction. It is because of the varying neurological manifestations of meningomyelocele that there has been so much controversy regarding appropriate treatment.
The overall incidence of meningomyelocele appears to have decreased in recent years, at least in part, because of prenatal testing. Serum alpha-fetoprotein examination (a blood test given to the mother during pregnancy) and ultrasonography can identify a large number of these afflicted fetuses between 16 and 20 weeks. Many parents have then made the decision to interrupt the pregnancy, which is probably why there has been a significant decrease in the number of those born with this anomaly.
One of the serious questions faced by pediatric neurologists, pediatric neurosurgeons, and obstetricians is how to advise parents of such afflicted babies who seek advice. There is no easy recommendation, it is necessary to weigh a number of issues in an overall assessment of the problem. This is an awesome responsibility for any physician, and there are really no guidelines. If a child has a large lesion, advanced hydrocephalus, and little mobility of the lower extremities, it is easy to predict that neurological function will be severely limited. However, smaller lesions without significant hydrocephalus are a much more difficult problem, even after lengthy discussion, there is often no obvious right or wrong decision. It is a very personal one, and must be made by parents after all the appropriate information is made available to them.
There have been some differences of opinion as to whether a fetus with known meningomyelocele should be delivered normally or by cesarean section. Advocates of the latter maintain that pressures on the spinal cord during passage down the birth canal may result in irreversible injury and loss of neurological function. Other physicians can find no evidence that this has any bearing on future neurological function, and feel that normal delivery is preferable.
It is our perspective that there has been no clear-cut, proven benefit of cesarean section, and that both the baby and the parents are better off if delivery is carried out normally.
The first question always asked is whether there is permanent brain damage, and if the child will have useful leg function. Unfortunately, the neurologist or neurosurgeon can always predict the minimal expected deficits, but not the maximal ones. If a child is paraplegic (has no movement in the legs from the hips down), one may say with certainty that this patient will always remain in a wheelchair. On the other hand, if the child is born with movement of the thigh muscles and feeling down to below the knees, the chances are good for walking with some sort of brace support. When there are no anomalies of the brain (maldevelopment), it is always possible that intelligence will be normal or above, even if there is advanced hydrocephalus at birth. Thus it is possible to predict for a family how well the child will do, but not how poorly.
The clinical manifestation of meningomyelocele is directly related to the amount of spinal cord involved. As noted earlier, children may have a very wide spectrum of sequelae, ranging from no detectable neurological impairment (other than bowel and bladder), to total paraplegia. In addition, some may be born with a spinal curvature anomaly (either scoliosis or kyphosis), as well as advanced hydrocephalus.
Much has been written about whether to treat severely afflicted children. Some years ago, John Lorber, M.D., of Sheffield, England, who had enormous early experience in treating children, enumerated what have become known as the "Lorber criteria." According to them, a child born with one of these problems should be excluded from medical or surgical treatment. 1) advanced hydrocephalus, 2) total paraplegia, 3) scoliosis or kyphosis, or 4) an associated anomaly. Dr. Lorber contended that a child with any of these disabilities had a very poor prognosis, and that to prolong that infant's life was, in fact, a disservice. These criteria were employed for some years by North American pediatricians, pediatric neurologists, and neurosurgeons.
However, it eventually became evident that Dr. Lorber was wrong. He believed that none of these children would survive without treatment, whereas it was the North American experience that about two-thirds of them did. It ultimately turned out that under the British health system at that time, it was common to sedate these children, feed them only on demand, and essentially practice a form of "passive euthanasia." This philosophy was never accepted in North America, with the result that the most afflicted infants not only survived, but were even more disabled through lack of treatment.
There might conceivably be fewer ethical problems with practicing this sort of selection if to treat equaled life, and not to treat equaled death. But it became obvious that most children survive with or without treatment, so that it was clearly necessary to reassess the overall approach to these unfortunate infants.
At present time, all children whose parents consent are treated, irrespective of the severity or neurological dysfunction. If parents feel very strongly about withholding treatment, of course, it is generally the position to defer to them. But this rarely happens because from a practical point of view it is impossible to place a child either at home or in custodial care with an open back and a growing head. There is simply no way to arrange any sort of future life without first giving appropriate surgical treatment.
The basic treatment for meningomyelocele has been well established for many years. The surgeon must replace the neural tissues within the spinal canal and then close the muscle and the skin. A plastic surgeon is occasionally needed if there is a large area that may be difficult to close.
If there is also significant hydrocephalus, most pediatric neurosurgeons now place a ventriculo-peritoneal shunt at that same procedure. This does not appear to increase the hazard of infection, and it decreases the chance of wound disruption in the lumbosacral region as a result of transmitted spinal fluid pressure.
Meningomyelocele used to be considered an emergency, and surgery was carried out within a few hours of birth. Nowadays the situation is viewed as urgent but not emergent, in most centers it is considered entirely sufficient to close the back within 2 days of birth. Until then, the tissues are simply kept moist with a saline dressing.
It is very complicated and difficult to explain all the potential problems associated with meningomyelocele in a single session with a parent. The first question always asked is whether there is permanent brain damage, and if the child will have useful lower limb function. Unfortunately, the neurologist or neurosurgeon can always predict the minimal expected deficits, but not the maximal ones. If a child is paraplegic, one may say with certainty that this patient will always remain in a wheelchair. On the other hand, if the child is born with a L3 or L4 level, the chances are good for walking with some sort of brace support. When there are no anomalies of the brain (maldevelopment), it is always possible that intelligence will be normal or above, even if there is advanced hydrocephalus at birth. Thus it is possible to predict for a family how well the child will do, but not how poorly.
The basic treatment for meningomyelocele has been well established for many years. The surgeon must replace the neural tissues within the spinal canal and then close the muscle and the skin. A plastic surgeon is occasionally needed if there is a large area that may be difficult to close.
If there is also significant hydrocephalus, most pediatric neurosurgeons now place a ventriculo-peritoneal shunt (see Hydrocephalus and its Treatment (Shunts)) at that same procedure. This does not appear to increase the hazard of infection, and decreases the chance of wound disruption in the lumbosacral region as a result of transmitted spinal fluid pressure.
Meningomyelocele used to be considered an emergency, and surgery was carried out within a few hours of birth. Nowadays the situation is viewed as urgent but not emergent, in most centers it is considered entirely sufficient to close the back within 2 days of birth. Until then, the tissues are simply kept moist with a saline dressing.
Complications of Spina Bifida
Virtually all babies with meningomyelocele have an associated Arnold-Chiari II malformation, meaning that a portion of the base of the brain (a part of the cerebellum) is displaced down into the spinal canal within the neck. This sometimes causes pressure on the underlying brain stem, which is also elongated and partially within the neck's spinal canal. The most common early symptom of this condition is respiratory stridor, often occurring within 1 or 2 weeks of birth. This usually disappears spontaneously within a few days, or at most three months. It may, occasionally, be associated with impaired function of the lower parts of the brain (difficulty in swallowing, intermittent apnea or cessation of breathing, etc.). In these cases, serious consideration must be given to surgical decompression, a procedure involving removal of the posterior arch of the upper spine over lying the malformation. While this may lead to significant improvement, the results are not uniformly favorable, for it is often the most seriously afflicted infants who suffer from this complication.
Arnold-Chiari malformation (MRI Scans of AC Malformations) can also cause later neurological deterioration, most often in the adolescent years. It may be associated with intermittent apnea and loss of consciousness (sometimes confused with a seizure). In infants, these cases require a decompressive procedure which must be done on an emergent basis as children with these symptoms are in danger of sudden infant death from apnea. In older children, other symptoms such as suboccipital pain and lower cranial nerve dysfunction may mandate decompression. The results of decompression in this age group are much more favorable than they are in infancy, and the symptoms are completely relieved in most cases.
In the past few years it has been recognized that a tethered spinal cord may cause progressive loss of function in the lower extremities any time after a child is 3 or 4 years old. Until recently it was assumed that those born with a L3 or L4 level often used a wheelchair as they got older simply as a matter of convenience. It is now understood that every child who has undergone closure of meningomyelocele has a tethered spinal cord, for the neural plate invariably becomes adherent to the surrounding dura. Most patients will probably not develop symptoms, but a significant number of ambulators will gradually deteriorate as a result of this phenomenon. However, if the cord is untethered as soon as symptoms develop, the likelihood of returning to the previous baseline is excellent.
It has been recognized for several years that rapidly evolving scoliosis may also be associated with a tethered spinal cord, even in the absence of lower extremity function. Therefore, any child with fast-moving scoliosis should have an untethering operation prior to a definitive orthopedicprocedure. If this is done before the scoliosis exceeds 30 degree, there is an excellent possibility of reversal.
A few of these children will develop hydromyelia (water within the interior of the spinal cord), which is usually manifest clinically by rapidly evolving scoliosis (similar to tethered spinal cord). The hydromyelia may be drained by various techniques (all satisfactory), and the scoliosis will often be arrested.
There are few conditions that require so many specialists to assure the best attainable result. The pediatric urologist, physiatrist, neurologist, orthopedist, and surgeon must all be involved in assessing these children and be involved on a regular basis. It was because of this necessity of multi-disciplinary care that spina bifida clinics evolved in which setting all the specialists are available at a specific time. Thus the child receives optimal care and the parents are spared the necessity of making many different appointments at many different times.
It is now recognized that at least 70% of children with meningomyelocele have normal intelligence. We now realize, however, that many children who are retarded sustained brain injury simply as a result of a intracranial infection and malfunctioning shunts, in an era in which technology and diagnostic scanning were less sophisticated than they now are.
Other children died between the ages of 3 and 5 from kidney failure. This danger too is being handled with more advanced methods, particularly intermittent catheterization. In addition, the development of artificial sphincters is progressing well and is expected to be very important in handling urinary incontinency which according to the children themselves, is the most distressing of all the sequelae of meningomyelocele.
Some 70% of those with this disorder are ambulatory, with or without support. This represents a large number of children who are being integrated into society, mainstreamed in schools, and who are very satisfied with the quality of life they have achieved.
Achieving Bladder Control in Spina Bifida
Management of the neurogenic (referring to an abnormally functioning bladder due to compromised nerve supply) bladder secondary to myelomeningocele should be started when a child normally obtains bladder control; however, a baseline urological evaluation should be attained within the first month of life and at regular six month to yearly intervals thereafter.
A regular bladder routine initially preformed by the patient parents (at about 3 years of age) consists of intermittent clean catheterization performed 3-4 times per day based on the patient's residual urine volume (that amount of urine left in the bladder after the patient voids without the assistance of a catheter) and the bladder's capacity to hold urine. As soon as the patient is cognitively and physically able to perform self-catheterization, instruction should be started with the goal; of independent catheterization. Yearly urological follow-up examinations is imperative in patients with spina bifida to monitor bladder pressure (an indicator of whether the bladder is being stretched by over filling due to excessive intervals between catheterization) as well as bladder capacity, sphincter function (how well the muscle controlling the outlet of the bladder is functioning), and monitoring for bladder or renal stones. Pharmacological agents are prescribed as indicated for high pressure bladder and bladder or sphincter spasticity. Urinary incontinence in a patient on a regular bladder routine is most often due to a urinary tract infection but may also be due to bladder/sphincter dysynergia.
Control of bowel function in a patient with myelomeningocele is individualized and must be done on a consistent basis. As in starting a bladder routine, a regular bowel routine should be started at about the age of normal bowel continence (~ age three). Prior to the age of beginning a routine, parents should be instructed to modify the child's diet, assure adequate fluid intake and use a laxative as required to prevent constipation over and over distention of the bowels. Bowel management in the child over 3 years of age should be attempted on a daily or every other day schedule. It is best to take advantage of the rectocolic reflex which occurs after eating in the morning or evening as the time of rectal evacuation. An initial combination of a stool softener, irritant cathartic (e.g., ducolax) or peristaltic agent (e.g., Senecot) and suppositories may be tried to establish a regular routine. Modification of the diet as well as the addition of metamucil may be indicated. The end goal is to attain a regular routine without the use of a laxative. Typically, digital stimulation of the rectal outlet is the mechanism used to stimulate evacuation once the routine is established. It must be kept in mind that there cannot be a rigidly prescribed bowel routine which is applicable to all patients - each patient must be tried on a series of medications until a successful bowel routine can be attained.
Prenatal detection will undoubtedly become more refined, and may well continue to reduce the incidence of meningomyelocele. Another possible advancement that is often discussed concerns intrauterine surgery (surgery on the fetus while still in the womb) to close a meningomyelocele prior to birth. Experimental work has clearly demonstrated that the exposed neural elements are vulnerable to damage from contact with amniotic fluid. There may in fact be progressive loss of lower extremity function during the latter part of gestation. Since this is the case, it would seem reasonable to close the back as early as possible.
This is certainly attractive from a theoretical point of view. However, in light of the present state of the surgical art, there is, unfortunately, little likelihood that this sort of procedure will be feasible in the foreseeable future.
The incidence of meningomyelocele has declined as a result of prenatal testing. At the present time virtually all children born with this affliction are treated, irrespective of the magnitude of neurological deficit. This is done because there is simply no way to arrange for future care if the back is open and the head growing.
It is essential that there be a continuing interchange between parents and physicians to avoid misunderstandings about the complexity of the problem and the necessity of future treatment. But with the assistance of a multitude of specialists, social workers and psychologists, many of these children will have the potential for enjoying an excellent quality of life.
You read over your notes. Then you read them over again. Then you read them over a third time. Then you take the test and are surprised at just how much you missed. Despite reading everything three times!
A lot of study time is wasted because of one problem: you fail to learn things the first time around.
Repeatedly going over the same information like putting a band-aid over a sieve. It may reduce the water that slips through, but it doesn’t solve the fundamental problem: that you have too many holes.
The key to reducing the amount of time you study is simple: learn things the first time you see them, instead of after dozens of repetitions.
This is all easier said than done. I’m sure if your mind was without holes you could easily capture any information that slipped into it. The real question is how can you do this? I don’t believe it is just a matter of being a genius or chance, but based on how you study.
Step One: Find the Holes
If you want to repair a leaky brain, you need to figure out where the holes are. Identify what type of information you have trouble remembering. Recognize when you’ve just gone over information you don’t quite understand.
Here’s a few questions to ask yourself after every chunk of ideas to find your holes:
What from this section am I most likely to forget?
What concepts are completely new to me? (Rather than ones that feel familiar)
Which ideas am I having the most difficulty grasping?
When you identify weak points, you can invest more time in fixing those instead of wasting time with a blanket studying technique of all information.
Step Two: Repair Weak Points
Once you’ve identified potential weak-points, you should immediately seek to fix them. Drop everything your doing and seek out a fix for the problem. Programmers understand that a bug left in the system can create several hundred times the cost to fix it later. As a learner, you need to understand that the same principle of fixing problems quickly also applies.
There are hundreds of books written on various strategies to fix weak points, which is a bit outside the scope of this quick article. But here are a few starting points:
Memorizing? If you need to store arbitrary information, try using the link method. This is where you visualize an exaggerated image that combines the two things you want to associate. You can memorize formula’s this way by linking vivid pictures to the different symbols. A formula such as F = C/A, could become a scale with hundreds of (F)eathers on side and a giant (C)aterpillar sitting over millions of (A)nts.
Conceptualizing? If you need to understand information try drawing a picture or diagram to combine the ideas.
Retaining? If you need to retain a complicated mass of information try using metaphors and vivid examples to connect the abstract information into something you can easily relate to.
Repairing weak points in your understanding isn’t that difficult – if you first know where they are. Simply focusing on a piece of information can help you understand it. But if you don’t know which parts you’re missing, it is easy to skim over everything and not realize what you’ve missed.
Step Three: Check Your Understanding
Do you “get” it. Does the information make sense to you at a deeper level, or does it seem arbitrary, meaningless or difficult to derive? Most school tests and virtually all real-life tests are designed to answer a single question: do you understand what you’re studying?
If you aren’t sure, that’s when you need to start working deeper. Keep asking yourself “why” until you reach a point where the subject makes sense. Here are some tips for improving your understanding:
Look for sensory descriptions.Your brain isn’t a computer. It’s designed to retain emotional, vivid and sensory information better than abstract or dry details. Link a sensation, picture or story to the abstract details. When learning how to do determinants (a form of math using matrices) I imagined my hands moving through the diagonals, one adding and one taking away.
Get the background. A lot of information that seems meaningless makes more sense when given a context. If your stuck on trying to wrap your head around a particular point, do some research into it’s origins. This may take more time up-front, but can save hours as future concepts are built upon it.
Step Four: Test Yourself
Whenever you’re experimenting with new learning methods, you need to measure the results. Check to see whether your new system is actually helping you remember more. Once you get familiar with a system, you can more accurately judge the extent of your knowledge. But until then, test regularly so you can tweak the system to fix errors.
The best tests are objective ones. If you’re in school, look for past exams, tests or textbook questions to check your understanding. If you’re teaching yourself, come up with short exercises that can prove to you conclusively you know what you’re doing.
The most important piece of advice I can give is this: treat study time as being sacred. Go in with the expectation that you will either learn everything through the first go, or you will identify areas that need further clarification. Focus and become aware of any potential holes so you can learn things once.
Handheld ultrasound device is the future of all USG scanners. No wires, no more clutters. These devices are so user friendly, cozy and portable that any radiologist can hardly resist from getting one. We compare the best of them available in today.
1 Clarius Wireless Handheld Ultrasound Device
Clarius manufactures one of the most advanced handheld ultrasound device, which wirelessly streams data to most iOS and Android devices. You can see view live view on your iPad or Android screen with the help of a simple app. There is a cloud storage option also, and a digital library is just a touch away.
It has passed recently CE Mark approval for the commercial sale of the C3 and L7 Clarius Wireless Ultrasound Scanners for use by medical professionals. C3 Scanner is capable of multipurpose scanning of all parts of the patient’s torso, including the heart. The devices exhibit outstanding resolution with its convex array for abdominal and lung images. L7 is Linear Array Ultrasound Scanner and ideal for guiding procedures. Easy to sterilize and keep clean. One can easily get fine detail from 1 to 7 cms from L7. Both the devices come with full body metal jacket which gives a premium look. These devices have 45 minutes of active battery life and 7 plus hrs standby time.
$6,900.00 for BW / $9,900.00 with Color Doppler
Ultimate Portability, User friendliness, Premium Look and feel, Cloud Storage, FDA CE Approved, Included Warranty
2 Philips Lumify App Based Handheld Ultrasound Device
Phillips Lumify handheld ultrasound probes are time tested device and connects to your tab or smartphone with a micro USB port. Its got a simple interface to manipulate and requires just an installation of the Lumify App. Lumify goes where you go, so you can start scanning without searching for equipment in the emergency department. It looks more or less like a standard ultrasound probe with a micro USB on the far end. Lumify doesn't need to be charged. Once connected, It is powered by your Android device. The Lumify app enables users to store scans, images and has the ability to share via email. It also has cloud based storage ability. The app only recognizes Lumify probes, and during first set up device registration is required. Unfortunately Lumify doesn't support iOS.
Lumify has three types of probes, S4-1, L12-4 and C5-2. Lumify S4-1 is suitable for Lung, Echo, Abdomen, Ob Gynae and FAST. Lumify L12-4 is meant for soft tissue, superficial, MSK and Vascular in addition to Lungs.
Flexible pricing options starting at $199/month, with 12 & 24 month subscriptions
Portable Design, Flexible Pricing
Wired Connectivity, No support for iOS, Only available for distribution in the USA
3 Healcerion SONON 300L Handheld Ultrasound Machine
Healcerion’s SONON 300L, 300C and 300MC are both CE and FDA approved product line in mobile ultrasound device compatible with iOS and Android technology. Quite a small to fit in your pocket and light enough to operate with two fingers. With a weight of 369g and 78(W) x 229(L) x 38(H)mm dimension, it's one of the best devices to carry around.
Just like Clarius it has Wifi (2.4GHz) connectivity and can be paired with an existing smartphone or tablet to conduct scans. The device has a 2600 mAh Li ion Rechargeable battery, which delivers amazing scan time of 3 hrs. The SONON mobile application supports both iOS and Android device and providers can scan patients and transmit images and recordings securely to any hospital via Wi-Fi, 3G, or LTE networks. SONON 300L is for MSK(Muscular-skeletal), Orthopedics, Vascular, Pediatrics, Sports medicine, Point of care, Ultrasound-guided procedures and color doppler. 300MC is basically designed for Veterinary, Pediatrics, Neonatal, Point of care, while 300C is only suitable for general and Ob Gyne.
SONON 300L: 8,000USD, SONON 300C: 6,000USD
High Resolution, Color Doppler, Wireless Connectivity, Portable and Sleek Design, Compatible with any Smartphone or Tab, CE and FDA approved
4 Fujifilms Sonosite iViz Handheld Ultrasound Device
Unlike Claurius and Lumify, Fujifilm Sonosite is not compatible to Tab or Smartphones via apps. It comes with a 7 inch display system. The high-resolution touch screen and innovative thumb operated user interface helps the doctor quickly go through various modes and enables quick diagnosis. iViz supports a range of clinical applications, interchangeable transducers, and optimization controls allowing accurate assessment. The display unit can be easily held on left hand enabling the user operate with his thumb, while his right hand scans through the transducer.
Integrated Wi-Fi and Bluetooth connectivity allows iViz to connect to Hospital Medical IT Systems, Cloud Solutions or Patient Vital Sensors. There is a remotely diagnosing capability via secure cloud-based telemedicine solutions where patient information can be accessed iViz and send reports to the EMR, Other connectivity like Micro USB, HDMI ports, and audio ports allow iViz fully compatible to any other medical Info systems.
Cloud Strage,Connectivity, Flexible Pricing, Telemedicine Functionality
Comes with a display unit, cannot go really mobile
5 Mobisante MobiUS SP1 System Handheld Ultrasound Mobile
Mobisante's MobiUS is an irresistible deal when it comes to appearance and feel. MobiUS SP1 System comes with a 800×480 WVGA touchscreen that easily slips in pockets. Along with the probe it weighs 11.6 oz. only. It has 8GB internal storage and connects to PC or other devices via WiFi or PC sync. There is another option for 3G connectivity. The in built battery allows continuous scan time over 60 min. It supports two types of transducers 3.5 and 5.0 MHz which is for Abdominal, OB/Gyn and guidance procedures. The Second type is 7.5 and 12 MHz and suitable for vascular, guidance procedures, small organs. The product is FDA approved.
Wireless Connectivity, Size, FDA approved
Low resolution display, No Cloud, Non compatible with other Smartphone or Tab,
LASIK is a surgical methodology that uses a laser to correct partial blindness, farsightedness and astigmatism. The LASIK surgery is done by an ophthalmologist who utilizes a laser to reshape the eye's cornea, keeping in mind the end goal to enhance visual acuity. For most patients, LASIK gives a lasting alternative to contact lenses or eyeglasses.
LASIK can likewise adjust astigmatism by smoothing an irregular cornea into a more usual shape. If you are thinking about LASIK eye surgery, your initial step is to pick a decent LASIK specialist who can assess whether LASIK is appropriate for you. Your LASIK specialist will analyze your eyes to decide their health, what sort of vision revision you need, and how much laser ablation is required.
LASIK is most like any other surgical remedial methodology, photo-refractive keratectomy (PRK). As per the year 2011, more than 11 million LASIK methods had been performed in the United States in 2009 more than 28 million have been performed around the world.
ELIGIBILITY FOR A LASIK EYE SURGERY:
LASIK surgery is a kind of refractive eye surgery. Amid the strategy, an eye specialist makes a flap in the cornea and later on uses a laser to reshape the cornea and correct the refractive issues in the eye. LASIK surgery is suitable for the individuals, who have a direct level of refractive error, causing:
Astigmatism, in which you see nearby objects, yet far off objects are hazy.
Farsightedness (hyperopia), in which you can see far things easily but nearby things is blurry.
A decent surgical result relies upon cautious assessment of your eyes before the surgery. To be qualified for LASIK surgery, potential applicants must meet the accompanying criteria:
AGE - Candidates must be no less than 18 years of age.
GENERAL HEALTH - LASIK applicants must be in good health and should not have certain medical issues, including uncontrolled diabetes, collagen vascular illness, or take any pharmaceutical.
EYE HEALTH - Candidates ought to be free of eye ailments including keratoconus, glaucoma and certain retinal and optic nerve diseases.
EYE INJURY - Patients should not have any eye diseases.
DRY EYE CONDITION - Patients should not persistently experience the ill effects of dry eyes.
STABLE VISION - The vision of the candidates must be steady for no less than one year prior to the procedure date.
CONTACTS - Prior to your LASIK surgery consultation and LASIK strategy, you should not wear contact lenses for a specific time. The exact length will be controlled by your specialist on an individual basis. This guarantees corneal soundness and precise evaluation of your prescription prior to the LASIK surgery methodology.
NURSING/PREGNANCY - Candidates should not be pregnant or nursing while experiencing the LASIK procedure. Hormones may influence the strength of your prescription, so pregnant or nursing ladies are not qualified to seek LASIK surgery until three menstrual cycles in the wake of nursing has been ceased.
These are some of the points which show if you can go for a LASIK eye surgery or not.
Via Lasik Eyes Surgery
Many operational considerations for MR imaging are similar to those for CT. Differences occur because of fringe magnetic fields, radio frequency shielding, geometry of the magnet bore, and lack of known biological hazard with MR imaging. The magnet is always on, especially in an MRI that is high-filled 1.5 Tesla or higher. This is so that the cooling of the superconducting magnet can take place and maintain an effective electromagnetic field for image acquisition. If there is some sort of incident or injury that requires a "quench" or purge of the coolant in order to turn off the magnet, the liquid helium must be vented quickly and safely directly into the atmosphere. This is why MRI machines are often on upper floors of hospitals, especially older hospitals. Liquid helium is super expensive and to quench and replenish takes time and lots of money. This is why you can also find videos on YouTube and such of people trying to pry office chairs out of an MRI with two by fours and other non ferrous items.
Ignoring Standard recommendations to setup an MRI machine not only caused malfunctioning or low quality imaging, its a life hazard. There were several instances in the recent past, when people and equipment were stuck inside MRI.
Nevertheless, a patient’s condition can deteriorate during MR imaging, requiring emergency intervention. MR imaging systems can interfere with both patient monitoring and cardiopulmonary resuscitation. Appropriate architectural and administrative measures can lessen these difficulties. The long, narrow magnet bore makes it difficult to observe the patient. Locating the operating console near the axis of the magnet provides a better, although still limited, view of the patient being scanned. Fringe magnetic fields may require location of the console relatively distant from the magnet. Magnetic shielding of the video display unit in the console can allow placement closer to the magnet. The window between the magnet room and control or console room usually requires RF shielding, which is often two layers of copper screen or perforated sheet. This shielding reduces patient visibility by light attenuation and by the distracting effect of Moire patterns and reflections. These problems can be reduced by appropriate window selection and attention to lighting details. Charge-coupled device (CCD) television cameras can be operated in relatively high magnetic fields and can be quite helpful in patient monitoring. Medical personnel and/or family members can remain near the patient to monitor or reassure the patient. The magnetic field within the scanner can affect or limit the performance of patient monitoring and communication equipment. For example, the magneto-hydrodynamic effect from flowing blood distorts electrocardiograph signals. Various solutions are being developed for these problems, such as using the main magnetic field as the field for a speaker or piping in sound via airline style head phones or providing a pneumatic squeeze bulb as a call button for the patient. Interfacing these devices with external systems is sometimes difficult. The operation of patient support equipment such as respirators, and infusion pumps can be affected near some types of magnets and other equipment such as stretchers, oxygen tanks and intravenous (IV) poles may be subjected to strong attractive forces near the magnet bore. These problems and difficulties with monitoring will make some patients inappropriate candidates for MR imaging until better solutions are found. MR lmager Site Planning Page 17 Cardiopulmonary resuscitation (CPR) is severely limited adjacent to some magnets because of the possible malfunction of CPR equipment in high fringe fields and the danger of ferromagnetic objects brought by the resuscitation team being attracted toward the magnet. The screening of arriving personnel for ferromagnetic objects is, of course, impossible. The usual solution is to remove the patient, by means of a non-ferromagnetic stretcher stationed in the scan room, to an area where CPR can be carried out. This area might be equipped with an emergency cart, monitors, oxygen and suction. Coordination of this phase of the design with the hospital’s CPR committee may be helpful. Means of preventing other personnel, who have responded to the emergency, from wandering into the magnet room during the activity surrounding CPR, should be considered. Useful means include distance, doors, warning signs and administrative procedures, such as training of the CPR team or assigning a member of the MR Imaging staff to close the magnet room door. Such situations necessitate a means of emergency shut down of the magnet. Claustrophobia and other forms of anxiety may interfere with imaging as well as patient comfort. Helpful solutions include good patient preparation, communication during scanning, someone remaining with the patient during scanning, disguising the intimidating appearance of the magnet, hiding the computer room from patient view, use of warm architectural finishes, keeping the magnet room size undramatic, disguising the vault-like appearance of the RF-shielded door, and making safety procedures and warning signs as nonthreatening as possible, consistent with adequate protection. The warm appearance of carpet must be weighed against the durability and maintenance advantages of traditional floors. Controlled access to the MR lmager suite is necessary because of possible harm to people with ferromagnetic medical implants and harm to people and equipment from unrestrained ferromagnetic objects in the vicinity of the magnet. A single entrance to the suite is helpful in this regard. Provision must be made for housekeeping personnel with floor polishers, for security personnel with keys, radios and guns, and for firemen with air tanks and axes. Non-ferromagnetic mops and buckets in a special closet or a built-in vacuum cleaner with plastic implements can be supplemented by direct supervision and/or training. If a special lock on the magnet door, which is not part of the hospital master key system, is used, emergency access to the key will be required.
Although it can be difficult to accept, physicians are at risk for the same challenges and illnesses as other people, including drug addiction. Anesthesiologists, in particular, have consistently been shown to have an unusually high rate of drug abuse compared to other physicians. A survey of 260 anesthesiologists from the Medical College of Wisconsin graduating between 1958 and 1988 reported that 32 percent used drugs to “get high” and 15.8 percent had been drug dependent.
Physician health programs (PHPs), which are responsible for managing and monitoring addicted physicians, report that anesthesiologists show up in their programs with substance abuse at approximately 2.5 times the rate of other specialties. Anesthesiologists have also been reported to be similarly over-represented in substance abuse treatment centers that specialize in treating physicians. As a result of the high rates of substance abuse among anesthesiologists, some disability insurance companies have even decided to discontinue coverage for anesthesiologists.
Why are anesthesiologists particularly vulnerable to drug abuse? Studies point to the following factors:
• The proximity to large quantities of addictive drugs
• The relative ease of diverting drugs for personal use
• A high-stress work environment
• Control-oriented personality
• Workplace exposure that sensitizes the brain to substance abuse
Drug Abuse Trends Among Anesthesiologists
Dr. Gregory Skipper, the former medical director of the Alabama Physician Health Program and current Director of Professional Health Services at Promises Treatment Centers, and colleagues completed a longitudinal cohort study involving 904 physicians consecutively admitted to one of 16 state physician health programs between 1995 and 2001. They analyzed a subset of the data involving 102 anesthesiologists and compared them with other physicians. The main outcome measures included relapse (defined as any unauthorized addictive substance use, including alcohol), return to anesthesiology practice, disciplinary actions, physician death and patient harm.
The researchers uncovered a number of drug use trends among anesthesiologists:
• The primary drug of choice among anesthesiologists is opioids, such as fentanyl, sufentanil, meperidine and morphine (whereas alcohol is the primary substance of abuse among other physicians).
• Anesthesiologists had a higher rate of IV drug use compared to other physicians (41 percent vs. 10 percent).
Treatment & Monitoring Help Addicted Anesthesiologists Successfully Return to Work
Although anesthesiologists are at increased risk of drug addiction, research suggests that they respond exceedingly well to drug rehabilitation treatment and long-term monitoring. PHPs have achieved remarkable outcomes with physicians and are equally effective for anesthesiologists. Most physicians managed and monitored by PHPs have reported 75 to 90 percent success rates five or more years after completing substance abuse treatment.
Despite these statistics, controversy remains surrounding anesthesiologists’ prognoses and ability to return to the operating room. Even with strict monitoring in place, some argue that anesthesiologists should not be permitted to return to anesthesiology practice after receiving substance abuse treatment. These conclusions stem from two poorly designed surveys of training program directors regarding substance-abusing residents, which reported very poor outcomes among addicted anesthesiologists.
In contrast, according to Dr. Skipper’s research, which is the first long-term outcome study based on actual data from records of anesthesiologists, most anesthesiologists can safely return to practice if certain safeguards are in place. In his study, anesthesiologists who were treated and monitored for substance use disorders under the supervision of PHPs had excellent outcomes similar to other physicians. At the end of the five-year follow-up period, 71 percent of anesthesiologists and 64 percent of nonanesthesiologists had completed their contracts and were no longer required to be monitored.
Although they face greater stigma, the research shows that anesthesiologists:
• Were less likely to fail a drug test during monitoring
• Were as likely to complete treatment and return to practice
• Experienced suicide risks, relapse rates and disciplinary rates that were no higher than other physicians
• Did not put their patients at risk of significant harm from relapse
Addiction Treatment for Addicted Anesthesiologists
Treatment for addicted anesthesiologists typically involves specialized drug rehabilitation programs that provide comprehensive assessments, intensive individual and group therapy for professionals, 12-Step support, and extensive aftercare and relapse prevention planning. Certain long-term monitoring measures have proven particularly effective in deterring substance abuse among anesthesiologists:
Long-acting natlrexone administration
Regular periodic hair testing (which is more accurate, particularly in detecting opioid abuse, than urine testing)
Enhanced security measures in and around the operating room (e.g., using witnesses for drug access and disposal, automated distribution devices, monitoring cameras, and spectrometric scanning of waste)
There is a growing body of evidence that the stigma against anesthesiologists returning to work is unwarranted. Although any incidence of overdose, suicide or patient harm is unacceptable, and re-entry must be handled on a case-by-case basis, studies show that addicted anesthesiologists who receive substance abuse treatment and are managed by PHPs have good long-term outcomes, on par with other physicians.
Image Source NurseTogether.com
Medical Miracles in Indian movies a common appearance. One in every 10 Indian movies patients are cured by super power, miracle medicines and God's blessings. But this one surpassed all the limits. Doctors, please brace yourself, many doctors have already 'committed suicide' and several left medicine forever after watching this. So, watch it at your own risk.
Hrudaya Kaleyam is a 2014 Telugu spoof action comedy film directed by Steven Shankar. It stars debutant Sampoornesh Babu in the lead role. The film revolves around Sampoornesh Babu, a petty thief who robs parts in electronic shops and why he robs electronic shops and departmental stores.The movie was considered a hit at Box Office.
Learn How to Make an Artificial heart:
Yes, you heard me.. An artificial heart is not tough to design. First you have to assess patients vitals by putting the stetho on forehead. Keep your tools ready before proceeding further
Human Anatomy Book
Physiology Book on Circulatory System
An true size heart image for measuring the dimensions
Other equipment like hex blade, knives, paints, welder, colors and chemicals
Once you are ready with these please follow the procedure as shown on this video:
Heart Implantation is Easy:
Transpiration or more correctly implantation part is rather easy. In the movie, the leading character couldn't perform it himself. However he assisted the doctors by throwing the heart accurately on to patients chest. Doctors did only the suturing and closure of the thorax. Don't miss the suturing procedure.
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