Croup !

This is an Excellent video by Dr. Jim Sears on how to identify Croup , even I'm as a pediatrician was really impressed by the amount of high yield information he mentions, just a quick highlights to what he is mentioning ...

1- Croup is a narrowing of the upper airways caused by Para influenza virus infection , it would simply start by manifestations similar to common cold ( low grade fever , runny nose) then narrowing of the airways occur, so imagine when air passes through a narrowed pipe it would look like a barking sound , and would result in a mild Inspiratory stridor.

2- Once you hear this sound the best initial step to do is to expose the child to humidified/moist air to help relax the air ways 

3- Nebulized epinephrine or steroids are preserved only for severe cases

4- Never use Antihistaminics in croup because they would dry your airways which in fact would worsen the sound

5- Condition usually worsens at night

6- Best preventive method washing your hands and general hygiene before dealing or handling the child 

7- I guess the only interesting piece of information to add, is that croup occurs in children between 3 months and 5 years of age , it doesn't involve older age groups because the size of the airway tracts (glottis and sub-glottis) enlarge with growth, making its narrowing upon inflammation very unlikely.

Developmental Milestones !

for me developmental milestones are very difficult to remember and easy to make mistakes on, I usually used to study by remembering the age and expected development of social and motor skills associated , but this method wasn't by any means good enough So in a trial to memorize them I would try another pattern Q&A ,and to reverse pattern of memorization , if you have a mnemonic or a certain way to help in memorizing this topic please provide your feedback ! : )

So here we go ! 
 
WHEN Do you Expect the child to ?

know his name ? 9 Months

draw lines or scribble? 15 Months

jumps with 2 feet ? 2 years

tells stories ? 4 years

play with the ball ? 1year

feeds himself ? 15 months

hold a pincer ? 9 months
 
walks down the stairs ? 18 months

rides a tricycle ? 3 years

runs ? 2 years

Crawls ? 9 months

say 1 word ? 1 year 

say 2 sentences ? 2 years

say 10 words ? 18 months 

builds 3 cubes ? 15 months

          4 cubes ? 18 months

          7 cubes ? 2 years

hops on 1 foot ? 4 years

descend the stairs with alternating legs ? 3 years

stand in line ? 3 years

play in a group ? 4 years 

know age and sex ? 3 years

threads shoelace ? 2 years 

for me this is one of the challenges to remember a pediatrician : )



                                           I'm a So Cute baby ! HAHAHAHAHAAAA  !
                                                      

Beckwith-Wiedemann syndrome

I  don't know the named of the disease whether it was related to the first scientists who described this syndrome or how it's related to the syndrome in one way or another !

however, I believe the alternative name would typically describe it; "Exomphalos-macroglossia-gigantism triad" , it's a typically described as "Overgrowth syndrome" enlargement of organs and body parts , may be symmetrical or even Asymmetrical ! expect also hypoglycemia and polycythemia secondary to hyperinsulinemia



                                          note the Macroglossia and plethora  !

                                           
it's caused by different genes mutations all have the same location at 11p15 (short arm of chromosome 11), one of them IGF-2 gene encoding somatomedins
 
and also monitoring for the development of abdominal tumors , particularly hepatoblastomas and Wilm's tumour through serial ultrasounds and AFP levels up to the age of 6 years is important.

Most Common Cause of Mental Retardation in Boys ?!

Do you Know what is the most common cause of Mental Retardation in boys ?

Fragile -X- Syndrome ..

don't get confused with the concept Fragile ! in fact it results from the gross appearance of the X chromosome and is believed to be as a result of methylation / Silencing of the FMR1 gene (fragile mental Retardation gene) that would result in X-chromosome constriction at a certain point , so it would seem to be fragile at this point ! AMAZING !

what happens is that there's a trinucleotide repeat sequence of CGG codon that will expand with more than 200 repeats ! and eventually would result in silencing the gene that encodes familial mental retardation gene protein.

       methylation /silencing/constriction site of X- chromosome so that it would appear as if it's fragile !
 
                          http://thebioside.ning.com/forum/topics/pre-class-ch-15-the-chromosomal-basis-for-inheritance


Mode of inheritance is X-linked DOMINANT .

characteristic appearance of this boy would be enlarged forehead "Macrosomia", elongated face, protruded jaw "prognathism", enlarged ears and testicles "Macrotia" and "Macrorchidism"

Mental retardation with liability to develop glioblastoms , ADHD is due to associated neurodegeneration of this disease.

this an Excellent link for better demonstration of this condition

http://www.gfmer.ch/genetic_diseases_v2/gendis_detail_list.php?offset=15&cat3=131

Satellite Stories - Lights Go Low

Holoprosencephaly !

 whenever I studied chromosomal aberrations and associated syndromes , I always got confused between Patau and Eduard's syndromes and that wasn't solved even during my Residency, since those heartbreaking syndromes- luckily- are extremely rare, because I felt that they are a combination of developmental anomalies that carries no link in between , so I couldn't link up all the symptoms together and usually mistaken to replace a symptom for another in describing one of them , luckily Down syndrome is much simpler and more famous as it's more presentable and the common associations would be found in many areas in medicine , but those syndromes and Patau  (trisomy 13) in particular, are rare to find difficult to remeber, Holoprosencephaly allowed me to understand Patau and never be confused with other syndromes.

Holoprosencephaly is a characteristic feature in Patau syndrome, though it may be associated with other genetic and non-genetic conditions, it carries broad spectrum of variation , in fact a Patau face is very unique when you see , Holoprosencephaly means that the prosencephalon failed to divide into the charateristic 2 cerebral hemispheres , so it ends up with one , it has a broad spectrum of presentations and variations , but this made sense to know and connect it with the associated forearm and eye (Micropthalmia) abnormalities and Mental Retardation, also there would be cleft lip and palate.

                                                   MRI demonstrating Holoprosencephaly

                http://www.gfmer.ch/genetic_diseases_v2/gendis_detail_list.php?cat3=1248

Neonantal Seizures

 this is an EXCELLENT video to demonstrate this form of seizures and this Youtube channel is very beneficial particularly for the ER situations,

 Neonates and Infants don't present with the typical Tonic-Clonic or Myoclonic patterns when they develop a seizure, they are atypical in their presentation.

A Seizing Neonate may show Jitters or Repetitive pattern of movements in the form of staring ,blinking , fixed deviation of the eye to one side without being corrected by a spontaneous motor movement, tongue protrusion, chewing movement, apnea (may be noticed through a drop of O2 saturation detected using pulse Oximeter)


Management of neonatal seizures:

 A- Stoppage of seizures:

 Phenobarbital is the first line, if fails Phenytoin can be administered
and always keep in mind that the beat way to control seizures is to detect the cause and correct it,

 B- Work-up is simple but you have to know that EEG in neonates may be normal, infantile seizures will show hypsarryhthmia , full labs CBC with differential , blood chemistry, electrolytes, glucose , blood culture, coagulation profile, amino acids profile and TMS, cranial ultrasound and lumbar puncture for CSF analysis and culture.

Work-up of Neonatal Jaundice

                                               Phototherapy,     Cool ! Isn't it ?!

   http://used-medicalequipmentblog.blogspot.com/2012/02/how-neonatal-phototherapy-for-babies.html

Neonatal Jaundice is a very common condition that you would see if you are a pediatrics resident , my approach to this topic would be on how you would think in a case with neonatal jaundice , but first you should have a good platform of knowledge regarding each cause by its own and understand its pathophysiology, so a quick reminder of its causes would be

  A- Physiological

  B- Pathological causes which may be :

    i- Conjugated hyperbilirubinemia:

       1- Sepsis (Neonatal/Infections-UTI)
       2- TORCH
       3- Total Parenteral Nutrition (TPN)
       4- Choledochal cyst 
       5- Galactossemia
       6- Tyrosinemia
       7- Hypothyroidism

   ii- Unconjugated Hyperbilirubinemia

 +ve  Coomb's test:

    1- ABO blood Incompatibility
    2- Thalassemia Minor

 -ve  Coomb's test:

   High Hb value :
    Polycythemia and its related conditions like Infant of a diabetic mother, twin-twin transfusion. Materanl fetal transfusion- intrauterine hypoxia/Intrauterine growth retardation
    also consider delayed separation of the umbilical cord

    Low Hb value :
  then consider intrinsic RBC's wall or enzyme defects like Hereditary Elliptocytosis- Spherocytosis
Glucose-6-phosphate Dehydrogenase Enzyme Deficiency and Pyruvate kinase enzyme deficiency

So suppose you are a resident and got a case with a Neonatal Jaundice , how to organize your thinking ?

1st question that should pop out into your mind would be , Is it Physiological or Pathological ?
 generally speaking, a jaundice that develops in the first day of life or  PERSISTENT hyperbilirubinemia through the second week of life, should always make you suspect a pathological cause, physiological jaundice develops later after birth but never in Day 1 and self limited

also the following signs are highly suggestive of pathological jaundice :

1- total bilirubin levels that exceeds 12mg/dl and direct bilirubin levels that exceeds 2mg/dl in a FULL TERM infant
 
2- a Rapid rise of bilirubin levels by a rate of 5mg/dl/day

Suppose you find a Neonatal jaundice in the first day of life how should you manage ?

1st you would consider Acute and life threatening causes of Neonatal Jaundice , so you would have to exclude Sepsis or intravascular hemolysis, that doesn't mean that other causes wouldn't be investigated or managed but at this stage a severe hyperbilirubinemia in day 1 could be life threatining and unconjugated hyperbilirubinemia may carry complications that you would look forwards to preventing so I believe first you would do the following :

 Liver functions
 CBC/ Blood smear - ESR- Blood Culture- Urine Analysis/Culture
 Reticulocytic count - Coomb's test- ABO blood group testing for both mother and neonate,

consider management of Jaundice with Phototherapy and Exchange transfusion, 

Unconjugated hyperbilirubinemia would result in bilirubin deposition in basal ganglia and brain stem with complications including delayed motor development,hypotonia, opsithotonous, chorio-athetosis, sensorineuronal hearing loss and consequent delayed/absent speech.

later on, after you already ensured the above, you would start screening for other causes through TORCH screening tests, screening for reducing substances in urine, congenital cataracts, Galactose-1-phosphate Uridyl transferase enzyme essay for galactossemia, succinylacetones in Urine for Tyrosinemia, Abdominal Ultrasonography and liver biopsy, assesment for Intrinsic RBC membrane/Enzymes defects.

PedBowl Questions

I Absolutely knew NOTHING of those !! 

: 000000

Psoriasis

Psoriasis simply is a Silver Scaly skin lesions over the extensors surfaces of the body (elbows for example) and can have mild or more severe forms

                                                       http://noskindiseases.com
Notice the Silvery Crusty plaques on the extensor surface of the forearms and elbow joints




Management is interesting , it can be achieved through topical steroids , however the silvery scales /crusts may block steroids to reach to the deeper layers and decrease its efficacy , therefore salicylic acid is used to remove scales

prolonged topical steroids can be harmful ! Vit A and Vit D are acceptable also in management in extensive Psoriasis

also Coal Tar  is used  in widespread Psoriasis , Vaseline or mineral oil all are acceptable.

new lines of therapy include TNF monoclonal antibodies , however you should be taking precaution with these drugs as it may predispose to T.B. infection or reactivation.

Kaposi's Sarcoma

when a patient diagnosed with HIV or suffering from opportunistic infections presents with a skin ulcer (usually a Pink lesion), you have to consider Kaposi's Sarcoma.

Needless to say (a common misconcept) that  Kaposi's Sarcoma is not caused by HIV, yes it occurs secondary to HIV Infection with severe immunosuppresion with CD 4 cell count less than 100 cells/mm3,
but the causative agent is Human Herpes Virus 8 "HHV-8" (A DNA virus not an RNA virus !)

the best management is HAART regimen to manage Immunosuppresion, also liposomal Doxorubicin or Vinblastine are used in treatment.

classic picture is a mouth with a  jaw lesion/ulcer with extensive oral candidiasis

            http://www.thecancerblog.org/images/blogs/7-2007/kaposi-sarcoma-5481.jpg

                   http://hardinmd.lib.uiowa.edu/pictures22/cdc/6058_072_lores.jpg

Simple Concepts about Skin Cancers

Skin Cancers include Melanomas (most common form) Squamous cell carcinomas (SCC) and Basal cell Carcinomas (BCC) .

(Kaposi's Sarcomas are also included, however it would be associated with an HIV patient ).

what I want to highlight  is when to consider Metastasis , Melanomas usually carry poor prognosis because they are highly metastasizing carcinomas, unlike SCC or BCC which rarely metastasize.

and when you consider distant metastasis, the single most important prognostic factor would be the DEPTH of Invasion of the lesion, though the size of the tumor could give you a rough estimate about the depth of the lesion, with 1 cm size melanomas are generally less than 1 mm in depth , a 5 cm melanomas are generally considered to carry no further need for intervention and an extremely poor prognosis !

Melanomas are irregularly size mole in sun exposed areas  that I believe require a high index of suspicion and a good history taking for diagnosis.

Squamous cell carcinomas are usually solitary and Ulcerative lesions , may occur secondary to Actinic Keratosis and would commonly present as a Non-healing ulcer

Basal cell Carcinomas are highly characteristic with their shiny or pearly appearance .
both of them rarely metastasize

Management would be simple Excision and Biopsy.

                               http://www.dermis.net/dermisroot/en/19032/image.htm
                                     A PIC. of an Ulcerative Basal Cell carcinoma


I really like this Picture because it may trick you with its ulcerative central part to say it would be a SCC , however if you noticed the "shiny/pearly" look of the margins it would make you realize the possibility it would be a BCC condition, and this would also be a great example to highlight the importance of Excisional/Punch Biopsy in ACCURATE diagnosis of these conditions

Actinic vs Seborrheic Keratosis

I'm sorry , I'm the LAST person who may help you how to clinically differentiate between both, I believe it requires an expert Dermatologist and thanks GOD I'm a Pediatrics Resident who wouldn't have to face this Dilemma, however let us think about it in a Sincere trial to get this sense !

Both occur in the elderly, in Fact, Actinic type is called "Senile Keratosis" and Seborrheic keratosis is called "Senile warts"

these are some Important facts :

Seborrheic keratosis are wart like , hyper pigmented lesions nearly found in all the elderly above 50 years of age , in fact if you approached your Father/Mother right now you may find some of them in clusters upon his/her body, good news is they aren't Premalignant !

Actinic type is also a hyper pigmented lesion that may be crusty or scaly, occurs in sun exposed areas like face, neck, chest and back, the bad news is that they may be premalignant (1:1000) and develop into squamous cell carcinoma, and to make things worse it's usually late diagnosed after atypical changes or cancer already has developed due to its similarity with seborrheic keratosis , however a solitary mole in a sun exposed area in a fair skinned individual should raise your suspicion on the diagnosis .

if there are  Definite Criteria/Guidelines for diagnosis and investigations for skin moles generally , please enrich this topic with your kind replies !

 also check this exciting blog:  http://dermoscopic.blogspot.com/2010_07_01_archive.html
by Dr. Eric EHRSAM

Management of Dermatophytes !

when I think about Dermatohytes I don't worry about their SILLY names Capitis , Corporis ! (So cute : 0 !)

and I used to always think about topical antifungals (Ketoconazole or clotrimazole)

but in fact it's pretty Inaccurate or Incomplete !

particularly for Tinea Capitis (ring worm of the scalp -Cap=Hat=scalp : ) and Onychomycosis (very irritating dermatophytes infection of the nails ) , you would need to initiate treatment with systemic Antifungals , particulary Terbinafine or Itraconazole

and since Terbinafine is generally a Hepatotoxic drug , Don't think to administer it to a patient with a liver condition and always regularly check for liver function when you administer drug as it totally worth to know that you are going to use the drug for at least 6 weeks (nearly 2 months ).

practically speaking, I have seen a dermatologist who used oral anti-fungals in treatment of ring worms of the groin, so I believe it's not a basic rule.

                                                    it's easy to diagnose Tinea Versicolor
                     (Excellent blog for Dermatology) :   http://blog.drseymourweaver.com/

Malassezia Furfur, that causes Tinea versicolor is treated with topical Selenium sulfide besides systemic Itraconazole (because usually this infection is expansive through the body to the limit the topical creams alone wouldn't cover all affected areas !)

Erythema Nodosum

It's simple and high yield !

                                                           http://www.perinatology.com

Red Nodules , or Erythematous areas ,

Tender

ALWAYS on the Anterior surface of lower extremities, 

Generally , they don't Ulcerate (ulcerative form is related to chron's disease)

and Always think about secondary association to ;

 1- Recent Streptococcal Infection (it's IMPORTANT check for ASO Levels and a history of a recent infection, it could diagnose an associated Rheumatic fever ! )

 2- Granulomatous Conditions whether infective or Autoimmune , so Expect it with T.B., Histoplasmosis, coccidiodomycosis or Sarcoidosis

 3- Inflammatory Bowel Diseases

it's a granulomatous Inflammatory condition affecting wall of blood vessels (it always intimidates me when I read the pathogenesis if it may be considered as a sort of secondary vasculitis, but this is purely from my mind , I haven't find this description in any book I've read before)


Primary Management is to treat the cause of the disease, also you can use NSAIDs as Ibuprofen.

Coldplay - Speed of Sound

How long before I get in ?!
Before it starts before I begin ?!
How long before you decide or ?
Before I know what it feels like ?
Where to, where do I go?
If you never try then you'll never know !
How long do I have to climb ?
Up on the side of this mountain of mine ?!!

Look up, I look up at night
Planets are moving at the speed of light
Climb up, up in the trees
Every chance that you get is a chance you seize
How long am I gonna stand
With my head stuck under the sand ?
I start before I can stop or
Before I see things the right way up

All that noise and all that sound
All those places I got found
And birds go flying at the speed of sound
To show you how it all began !
Birds came flying from the underground
If you could see it then you'd understand !

Ideas that you'll never find
All the inventors could never design
The buildings that you put up
Japan and China all lit up
A sign that I couldn't read
or a light, that I couldn't see
Some things you have to believe
When others are puzzles, puzzlin me

All that noise and all that sound
All those places I got found
And birds go flying at the speed of sound
To show you how it all began
Birds came flyin from the underground
If you could see it then you'd understand
Oh when you see it then you'll understand

All those signs I knew what they meant
Somethings you can't invent !
Some get made, and some get sent !
Birds came flying at the speed of sound
To show you how it all began
Birds came flying from the underground
If you could see it then you'd understand
Oh when you see it then you'll understand !

Stevens-Johnson syndrome (SJS) - Toxic Epidermal Necrolysis (TEN)

I believe both of them are of similar morphology, though oral lesions and respiratory tract involvement are more noticed at SJS with total body distribution less than 30%

TEN is more severe as it may involve  more than 30 to even 100% of the total body surface !

both of them are very devastating conditions with high mortality rates and bad prognosis,

during my residency, I've seen a case of SJS and trust me even when this case is presentable it may raise confusion upon the differential with other similar conditions and with Staphylococcal scalded skin syndrome (I'd be glad if there are any special or more diagnostic criteria to know or if you may add).

both are managed by admission to a Burn Unit , as they both carry the same Mortality Risk factors, Sepsis and Dehydration

in SJS treatment of choice besides prophylactic antibiotics would be Intravenous Immunoglobulins IVIg , also cyclophosphamides and other Immunosuppressives may be considered .

however in TEN , Immunosuppressives may exacerbate the condition ! and antibiotics aren't indicated for this as a primary condition ! and this just to add to our trouble at these conditions

Morbilliform OR Urticaria !

This is a VERY confusing topic form me !

How can you differentiate between Urticarial Rash or Morbilliform Rash as both are caused  by nearly same agents , have the same distribution and in fact they both in many books carry the same description , in fact I believe in a clinical situation in a clinic or during practice unless you are an experienced dermatologist you'd be confused !

both are caused by Penicillins, Phenytoin, Quinolones , Sulfa drugs

the good thing that Antihistaminics are effective for both of them !

you may notice that Erythema Multiforme also may be caused by the same agents/ drugs , though this drug induced hypersenstivity skin manifestation in particular you should be highly aware of because it's more commonly caused by infective agents like Herpes , Hepatitis or Mycoplasma (trust me you will forget it !).

if it may help this website better describes Hives or Wheals to be an elevated papular lesions with well circumscribed edges, an Erythematous borders and Pale centers , which isn't the case for just diffusely Red simple maculopapular rash of Morbilliform rash

                                                                   Morbilliform Rash !

this link is useful 

  http://missinglink.ucsf.edu/lm/dermatologyglossary/drugeruption.html


 

Porphyria Cutanea Tarda !

This topic by itself typically describes me !

If you asked me what's the cause of Porphyria Cutanea tarda ?

I'd answer without thinking : Uro-porphyrin-ogen Decarboxylase enzyme deficiency !

what it should be manifested by ?

photo sensitivity and skin ulcers !

yet if I got a question on an Examination on this topic , I'd -usually get it wrong or may be even never think about it in the differential , because usually it would be just a simple picture of Multiple skin ulcers !

So how you may get it Right ?!

when you mention photo sensitivity always think of Sun-exposed areas , particularly in our case Back of the hands and forearms (if you google for pictures of Pophyria Cutanea Tarda you'd almost find all pictures are of ulcers on the back of the hands !)

remeber ! they are NON-healing ulcers!

                                                  http://www.dartmouth.edu

and when you have a history of photo-sensitivity with a history of Alcoholism , OCPs, liver diseases (HCV- haemochromatosis), then Porphria Cutanea tarda have to jump in your mind !

How to Manage :

Stop Alcohol or any sort of estrogen intake 
sunscreens
Phlebotomy (as you may notice there should be an associated Iron Overload )
Chloroquine, YES ! the antimalarial agent !

Pseudotumour cerebri

Etiology of Pseudotumour Cerebri is one of the things that makes me hate medicine , because I can't find any connection or pathogenesis that may help me understand the relation , just Gross memorization !

Vit A ,Tetracyclines and oral contraceptives
Obesity, Chronic lung diseases and Addison Disease

medicine is lovely ! isn't it ?! (with a Dr. Conrad Fischer smiley face )

Management of Seizures

Management of seizures is a very Important topic, extremely High yield in Examinations and also a very common condition in the ER or wards :

suppose a patient presenting to the emergency room with a seizure or a history of seizure, your workup should include:

1- ABCDE , secure airway, breathing ,circulation,check for disabilities and adequate exposure for any signs of trauma or injuries
2- History taking
3- assess the type of seizure whether it's a status epilepticus or Generalized or a partial seizure
4- In status epilepticus you are targeting 2 things, first to stop the seizures, which you can achieve through the following and regular organized scheme of medications:
   a- Diazepam or Lorazepam (Benzodiazepines)
   b- Phenytoin or fosfophenytoin
   c- try again Phenytoin!
   d- Phenobarbital
   e- if all above measures failed you would need an anesthesia consultation, usually Midazolam or Propofol would be used

the second thing is to detect the etiology of the seizures while all these events are taking place , blood samples should be collected to check for CBC, full chemistry and electrolytes profile, bleeding and clotting factors profile , glucose levels, CT scan and lumbar puncture, should be performed

although, EEG is the most important test in diagnosing seizures , though it's usually established after you exclude all other causes that cause the seizures , in other words after controlling the status epilepticus , make your priority to RAPIDLY detect the cause of the epilepsy and manage it as soon as possible and when applicable


5-in other types of seizures medications would differ though management would be essentially the same, with highlighting again the importance to identify possible cause of seizure and manage it when applicable before starting antiepileptic treatment
 
   a- Generalized seizures: 

        Tonic-Conic : Valproic acid is the first line, Lamotrigine is the second line
        Abscence: Ethosuximide is the first line, Valproic acid is the second line
        Myclonic and Atonic: Valproic acid is the first line
        Pregnancy : Carbamazepine is the drug of choice

   b- Partial seizures:

       Carbamazepine and Phenytoin are first line drugs

When to stop anti epileptic treatment ?  
if seizures stopped developing for 2-3 years, + a Negative sleep deprivation EEG test.

due to the prolonged and chronic course of administration of the anti epileptic drugs, you should be aware of their expected side effects :

Phenytoin : rash , ataxia, diplopia, hirsutism,gum hyperplasia and lymphadenopathy

Phenobarbital : Rash and ataxia

Valproic Acid : Rash , GIT Irritation (vomiting and diarrhea), hepatotoxicity, 
thrombocytopenia and hyponatremia

Ethosuximide : Stevens-johnson syndrome

in the Emergency Room

when you receive a case in the Emergency Room, for example a case suffering of a Disturbed Conscious level , don't get confused ! and let the differential of the cause disrupt you from what's more essential at this stage, the famous scheme ABCDE ,In other words think of the differential of what may be the cause of the Disturbed conscious level while you are actively working on the following and making it your first priority : 

A : Securing Airway , check for airway patency and Intubate when indicated, note that any patient with GCS less than 8 should be intubated, even if he was breathing spontaneously !

B : Breathing , check whether the patient can breathe spontaneously, the pattern and rate of breathing

C : Circulation, check whether the patient pulses are palpable , rhythm , rate assessment,check if there any signs of dehydration or there's a need for urgent I.V fluid support

D : Disability

E : Exposure, for any signs of traumatic or burn injuries, or any other clinical signs that may give a hint or a clue to the diagnosis

Dementia and Delirium !

there are more than 100 causes of Dementia and Delirium, this is not my case as review books are stuffed with them.

but the only thing that I wanted to stress on is their Definition and how to differentiate between them.

Dementia : is IRREVERSIBLE loss of memory usually associated with other cognitive functions such as concentration, language, Praxia, Visual and spatial recognition, social, interpersonal relationships, Agnosias , Aphasias,....etc.

Delirium : is cloudy consciousness and diminished intellectual and executive functions that tend to be ACUTE in ONSET and COMPLETELY REVERSIBLE.

always remember that some features , manifestations and etiologies of Dementia and delirium are interconnected and common to each other , so the only way to determine the difference between them is through determine whether these symptoms are REVERSIBLE or PROGRESSIVE !

Multiple Sclerosis

Points to highlight in Multiple sclerosis :

• Multiple Sclerosis (MS) : is an Autoimmune demyelinating disorder with characteristic remission and relapsing-progressive-course.
• it's multifactorial, with significant genetics susceptibility i.e. always look for positive family history, commoner in young females, with North European Anscent, exacerbated by infections, trauma or psychological stress
• it presents with multiple focal neurological disorders, involving peripheral numbness , tingling or parasthesias , it may be associated with limb instability or ataxia
• blurry vision or Diplopia
• Urinary URGENCY or even RETENTION also may be associated with sudden onset erectile dysfunction in males
• a sentence I like to describe MS is to always consider if a young female presented with multiple focal neurological signs with no connections of anatomy or time.
•  MS can have the following course of progression

1. Remission and relapsing course , though you may consider that once a deficit has developed it wouldn't recover i.e it will always be progressive yet in a Relapsing and remitting pattern
2. Secondary progressive: secondary attacks after the first primary attack is progressive but with no spontaneous remission to the acute exacerbation this time.
3. Primary Progressive , which has the worst prognosis and with no single acceptable management to induce remission 

• MRI is the most Sensitive test for diagnosis with characteristic hyper intense T2 signal and decreased T1 signal intensity
• Evoked Response potential to various visual, auditory or somatosensory stimuli would show decrease potential, though it's a nonspecific finding.
• Lumbar puncture and CSF analysis would show pleocytosis and increased oligoclonal bands IgG via electrophoresis , increased protein content above 100mg/dl is a highly suggestive sign of MS.
• Management of MS:

1. Induction of remission: during acute exacerbation management is started with prednisone IV. for three days then a 4 weeks gradually tapered course of oral corticosteroids , you may also need plasmapharesis
2. maintenance therapy: in remission and relapsing form consider interferon-alpha1B and glatiramir, in secondary progressive type : interferon-alpha1B and mitoxantrone though it is important to know that mitoxantrone is absolutely contraindicated in a patient with underlying cardiac condition with diminished ejection fraction, because it's a highly cardiotoxic drug, there's no acceptable treatment for primary progressive type.
3. complications are treated symptomatically, spasticity is managed with baclofen , urinary retention is treated with Bethanechol (exclude obstructive uropathies) and urgency is treated with oxybutynin, erectile dysfunction is treated with sildenafil.

Understanding Infantile Spasms

 This is to demonstrate the character of Infantile spasms, a form of seizures which are characterized to have an Extensors muscles Spasms or Rigidity involving Neck ,Trunk and extremities, you may notice that the child seems to be fine , with no constitutional manifestations with no signs of delayed developmental motor or social milestones, (consider at this age a recent inability to sit unassisted ) most likely to be cryptogenic Infantile spasms.which have an excellent prognosis.
though you may consider associated developmental regression signs in West syndrome or secondary to Tuberous Sclerosis.

typically infantile spasms presents between 4-8 Months of age.

these features and this characteristic video is important to understand because it excludes the need to perform a lumbar puncture to exclude meningitis, and as you could listen from the video the best next step to confirm is to do an EEG which would show Bizzare spike and waves AKA "hypsarrhythmia" 
 

I delayed to mention that the suggested pathogenesis of infantile spasms is increased CRH release from the hypothalamus which increases neurological excitability (however still couldn't understand why it always involves extensors muscles or why it occurs preferentially in head and trunk ?) , this is only to clear any confusion that the suggested treatment would be ACTH administration,or sometimes Predinisone administration.

 though I would recommend further readings in this topic if you are interested in pediatrics Neurology.

Management of Disk Herniation

 I had a misconcept regarding management of disk (nucleus Pulposus) Herniation , when you consider a case for a disk herniation , the best next step in Management isn't always or better to say- basically - Radiological investigation through X-rays , CT scans or even better MR Imaging.

in fact radiological investigations are only preserved for those patients suscpected or at high risk of development cancers (elderly- positive family history) or the Pain is associated with fever and constitutional symptoms associated with infections.

the Ideal management would always to promote Bed rest for 1-2 days followed by NSAIDs for 6 weeks duration, if conservative measures didn't show relieving signs, you may consider physiotherapy or even surgery !

Coldplay - Things I Don't Understand (Instrumental) Excellent Audio (+pl...

How tides control the sea and what becomes of me
How little things can slip out of your hands
How often people change, no two remain the same
Why things don't always turn out as you plan

These are things that I don't understand
Yeah, these are things that I don't understand

I can't and I can't decide
Wrong, all my wrong from right
Day, all my day for night
Dark, all my dark for light
I live, but I love this life

How infinite is space, and who decides your fate
Why everything will dissolve into sand
How to avoid defeat, when truth and fiction meet
Why nothing ever turns out how you planned

These are things that I don't understand
Yeah, these are things that I don't understand

I can't and I can't decide
Wrong, all my wrong from right
Day, all my day for night
Or dark, all my dark for light
I live, but I love this life

Induced Hypocapnia , in a case of an Intacerebral Hemorrhage !

 This has always been a very confusing concept even during my work in the PICU , why always in a case suffering from intra-cranial hemorrhage, it's always recommended that after intubation and mechanically ventilate the patient , you have to keep the patient in a hypocapneic state where pCO2 tension should be between 30 and 35 mmHg ?


when there's a hemorrhage , there's - obviously - an Increase in the intra-cranial pressure (simple physics, "inelastic" "tough"'non-compliant" meninges, so any intracranial mass would compress the soft brain tissue)
so when there is an increase in the intra-cranial pressure there would be a consequent Increase in the interstitial hydrostatic pressure that opposes the normal capillary hydrostatic pressure responsible to maintain the perfusion of the brain tissue ! leading to more brain hypoxia!


So , to override this issue decreasing pCO2 tension would induce cerebral vaso-constriction , though it -sounds terrifying to say- but yet this would help to maintain the capillary hydrostatic pressure high enough to overcome the mass effect hydrostatic pressure and maintain enough cerebral perfusion.

A tricky Concept !

Yes! COPDs are IRREVERSIBLE unlike bronchial asthmas which are reversible

BUT! EVEN COPDs would improve up to 15% with B agonists or even better with Ipratrpoium bromide,

Think of it in other way (which why I’m below average, because I didn’t think of that until I got the question wrong , why we would be on earth administering those agents as first line drugs unless we would have been expecting a relatively significant improvement ?!, you Stupid me : 0  ?!!