[ashishMember]

thanks kkumarmd.

i completely agree with you. thanks for helping out in the forum.

[ashishMember]

You guys are absolutely correct!

U/s till 4 mo, then x-ray. No need for CT.

– ashish

 

[ashishMember]

Oh my goodness… I LOVE IT!

Yours or someone else’s?

[ashishMember]

Ahh… you’re right, and THANK YOU for bringing it to our attention.. For the first one it looks like I fell into the terminology trap, which can get confusing. For the second one, it was a copy/paste error from topic above it.

Here goes….

HypOcapnea means there is low CO2 in the blood, and this occurs due to HypERventilation. Therefore you get a RESP ALKALOSIS and a compensatory nongap metabolic ACIDOSIS.

HypERcapnea means there is high CO2 in the blood, and this occurs due to hypOventilation. Therefore you get a RESP ACIDOSIS and a compensatory metabolic ALKALOSIS.

Revised versions of both topics are below

NON-ANION GAP METABOLIC ACIDOSIS

Non-anion gap metabolic acidosis conditions include Ureterostomy, Small bowel fistula, Extra chloride, DIARRHEA (most common cause), Carbonic anhydrase inhibitors (acetazolamide), Adrenal insufficiency, Renal Tubular Acidosis, and Parenteral nutrition/Pancreatic fistula/PosthypOcapnea. Look for HYPERCHLOREMIA and a LOW BICARB. Here are a few mechanisms to keep in mind:

* Extra chloride: Too much saline causes a hyperchloremic non-gap metabolic acidosis

* Diarrhea: Acidosis occurs from bicarbonate loss.

* RTA: Mechanism varies.

* Carbonic Anhydrase Inhibitor: Promotes renal bicarbonate loss.

PEARL: -CAPNEA refers to how much CO2 is in the blood and is NOT referring to how fast someone is breathing. So, hypOcapnea means there is low CO2 in the blood, and this occurs due to HypERventilation. Therefore you get a RESPIRATORY ALKALOSIS and a compensatory nongap metabolic ACIDOSIS. HypERcapnea means there is high CO2 in the blood, and this occurs due to hypOventilation. Therefore you get a RESPIRATORY ACIDOSIS and a compensatory metabolic ALKALOSIS. Make sure you look carefully at the terminology in the question stem or vignette.

MNEMONIC: “Acid-azolamide”

MNEMONIC: NON-GAP CRAP! Several stool related issues cause a non-gap acidosis (diarrhea, small bowel fistula, ostomies).

MNEMONIC: USED CARP (Ureterostomy, Small bowel fistula, Extra chloride, DIARRHEA, Acetazolamide/Adrenal insufficiency, Renal Tubular Acidosis, and Parenteral nutrition/Pancreatic fistula/Poshypercapnea.

MNEMONIC: If you do not know your normal values for routine chemistries, a non-gap acidosis can be tricky. If you just calculate the gap and see that it’s normal, you could get in trouble. You should look closer at the chloride and bicarbonate levels. So, what I’m saying is that the chemistry looks good on the outside (i.e. gap looks good), but it’s actually falling apart on the inside (low bicarb and high chloride), LIKE A USED CARp!

MNEMONIC: Building on the one above mnemonic, a USED CARp can only travel on smooth roads WITHOUT GAPS/potholes!

===

RESPIRATORY ALKALOSIS

A respiratory alkalosis can be caused by basically anything that causes tachypnea. Sometimes this is due to hypoxia. The list includes, but is not limited to, early asthma, pneumonia, one of the aspirin phases, high altitude, fever and anxiety/hyperventilation.

PEARL: If given an ABG and you note a respiratory alkalosis, ALWAYS calculate for compensation. You do this by looking at the decrease in PCO2 from the baseline of 40, and checking to see if the compensatory decrease in bicarbonate (compensatory metabolic acidosis via bicarb excretion) is appropriate. If the bicarbonate level is even lower, then you have an additional primary metabolic acidosis. If it’s higher than expected, then there is an additional primary metabolic alkalosis. Keep in mind that the compensatory decrease in bicarbonate could be 2 per CO2 decrease of 10, or 5 per CO2 decrease of 10. That depends on whether or not you are dealing with an acute or a chronic respiratory alkalosis.

[ashishMember]

I’m guessing you mean hyperglycemia?…

Regardless, as much as I can… I “guarantee” they will not ask you about the pathophysiology of the Dawn Phenomenon in patients with diabetes. The would test you on the treatment of the Dawn Phenomenon

-> Treat by giving the nighttime insulin dose LATER than usual.

[ashishMember]

It’s the microcephaly that differentiates hypothyroidsm from Beckwith-Wiedemann Syndrome. It’s not a commonly associated finding in hypothyroid kids In fact, a AAP Pediatrics article even states that hypothyroid kids may have MACROcephaly compared to body size: http://pediatrics.aappublications.org/content/59/4/628.abstract

Hope that clarifies.

[ashishMember]

I can see how that article might be confusing, but the dosage is 4 MILLIGRAMS, though there is no good data to prove it. Basically the article is saying that when a woman becomes of reproductive age, she should start taking 0.4 mg of folic acid per day (400 mcg). If a woman is trying to conceive but has NEVER had a child with a neural tube defect, the optimal dose is unclear, but most OBs will still give 4 mg (4000 mcg) and recommend that it be started before conception. For any woman who has HAD a child with a neural tube defect, they must absolutely take 4 mg (4000 mcg) starting at least 1 mo prior to conception. So basically… for a woman not trying to get pregnant, 0.4 mg (400 mcg), and for a woman trying to get pregnant, 4 mg (4000 mcg) of folic acid is recommended.

Hope that helps!

Here’s the revised version:

FOLIC ACID

For any woman who is trying to conceive, 4 mg of folic acid per day is recommended to prevent neural tube defects. For any woman NOT trying to get pregnant, 0.4 mg (400 mcg) of folic acid per day is recommended.

MNEMONIC: FOUR mg of FOURlic acid (not 0.4 mg)

[ashishMember]

You are correct and thank you for the catch!

Here’s the updated version:

VITAMIN D & ITS EVALUATION

The liver sends 25-Vitamin D to the kidneys where it gets hydroxylated to 1,25 Vitamin D (the active form). If looking for a nutritional deficiency, obtain a 25-Vitamin D level. SUPPLEMENT with 1,25 Vitamin D (the ACTIVE form). Typically, 25-Vit D is the first one you should check (especially if they ask for a screen).

MNEMONIC: Where is the Vitamin D produced that carries 2 numbers with it (1 and 25)? TWO organs = TWO kidneys = TWO numbers (1 and 25)!

MNEMONIC: Which one is the active form? Think of it this way… if you ingest a calcium containing food in its natural form, it will first go to the gut, then the liver, then the blood, then finally the kidneys! So keeping the above mnemonic in mind, it’s the Vitamin D with TWO numbers!

PEARLS: Here are some ways Vitamin D deficiency could present

* African-American (AA) breastfed child whose mom is not on Vitamin D supplementation

* African-American (AA) breastfed child whose mom is not getting enough sunlight

* Child with symptoms consistent with malabsorption

* Child with a history of epilepsy who is on anti-seizure medications

[ashishMember]

It refers to the peak height velocity. The accelerated growth phase is interesting, but from a test standpoint, you should memorize the peak height velocity.

[ashishMember]

Hey ppat. I think you misread it. It says “the PERTUSSIS (aP) component is contraindicated in future vaccinations. Instead, give DT. “ Right? Perhaps I’m missing something. If you’re still confused, please post an update here.

[ashishMember]

Thanks! You’re right… Here’s the AAP guideline – http://pediatrics.aappublications.org/content/122/5/1142.full

Here’s the revised version:

EXCLUSIVELY BREAST FED BABIES

In exclusively breast fed babies, look for Vitamin D and Vitamin K deficiencies.

PEARL: ALL BABIES/KIDS are now supposed to get a total of 400 IU (international units) of Vitamin D per day in their diet. For formula fed babies, this is usually attainable through the formula. Breastfed babies need supplementation.

PEARL: Patients with CF (CYSTIC FIBROSIS) or RICKETS need > 1600 IU per day!

[ashishMember]

You’re correct. The number 1 association with CP is actually prematurity. Infection is #2 or #3. Great catch. Here’s the revised version:

SPASTIC CEREBRAL PALSY (CP)

Spastic cerebral palsy (CP) is a motor impairment due to brain lesions or anomalies. The condition that does NOT progress, but the motor component can change with time. The diagnosis is usually made by 1 year of age. Intelligence can be fully intact. The increased incidence is due to improved survival of preterm infants.

* SPASTIC HEMIPLEGIA: Arms are affected (good cognitive prognosis).

* SPASTIC DIPLEGIA: Legs are affected (great cognitive prognosis).

* SPASTIC QUADRIPLEGIA: All extremities are affected (horrible prognosis)

* PEARL: Though asphyxia is often thought to be the most common etiology for cerebral palsy, it’s NOT. It’s actually only responsible for a small number of cases. Prematurity, IUGR and intrauterine infections have a much higher association with cases of cerebral palsy.

[ashishMember]

You’r right. And thanks so much for the references. It really helps when I get those!

I also reviewed the AAP guidelines in a Pediatrics article. No mention of CT. Just radiographs. – http://pediatrics.aappublications.org/content/105/4/896.full.pdf+html

Here’s the revised section from the book. I’ve also modified the Q&A book.

DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)

Infants with developmental dysplasia of the hip (DDH) may be noted to have a leg-length discrepancy or extra creases at the thigh. Girls and breech deliveries pose a higher risk. Workup varies by age and family history. Treatment requires a Pavlik harness.

* CRITERIA FOR A CHILD LESS THAN 4 MONTHS:

• ASYMPTOMATIC: If there is a history of DDH in a first degree relative, get an ultrasound!
• SYMPTOMATIC: If there are signs of developmental dysplasia of the hip (DDH) on exam, get an ultrasound!

* CRITERIA FOR A CHILD GREATER THAN 4 MONTHS:

• ASYMPTOMATIC: If there is no family history, then no workup is needed. If there is a history of DDH in a first degree relative and an evaluation was never done, then since the child is now greater than 4 months of age, plain radiographs (hip x-rays) would be indicated. Plain x-rays are more reliable than an ultrasound at this age (femoral head ossification centers are more developed).
• SYMPTOMATIC: For any child greater than 4 months of age that has signs of developmental dysplasia of the hip (DDH) on examination (regardless of family history), they need to be worked up. Therefore, get plain radiographs (not an ultrasound) since they’re more reliable at this age.

* PEARLS:  The age cutoff for ultrasounds is 4 months, NOT 6. When it comes to the Barlow and Ortolani signs, EITHER of them being positive should prompt a workup!

* IMAGE: http://bit.ly/qHTScy

* IMAGE: http://bit.ly/qTQrK8

 

[ashishMember]

You’r right. And thanks so much for the references. It really helps when I get those!

I also reviewed the AAP guidelines in a Pediatrics article. No mention of CT. Just radiographs. – http://pediatrics.aappublications.org/content/105/4/896.full.pdf+html

Here’s the revised section from the book. I’ve also modified the Q&A book.

DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)

Infants with developmental dysplasia of the hip (DDH) may be noted to have a leg-length discrepancy or extra creases at the thigh. Girls and breech deliveries pose a higher risk. Workup varies by age and family history. Treatment requires a Pavlik harness.

* CRITERIA FOR A CHILD LESS THAN 4 MONTHS:

• ASYMPTOMATIC: If there is a history of DDH in a first degree relative, get an ultrasound!
• SYMPTOMATIC: If there are signs of developmental dysplasia of the hip (DDH) on exam, get an ultrasound!

* CRITERIA FOR A CHILD GREATER THAN 4 MONTHS:

• ASYMPTOMATIC: If there is no family history, then no workup is needed. If there is a history of DDH in a first degree relative and an evaluation was never done, then since the child is now greater than 4 months of age, plain radiographs (hip x-rays) would be indicated. Plain x-rays are more reliable than an ultrasound at this age (femoral head ossification centers are more developed).
• SYMPTOMATIC: For any child greater than 4 months of age that has signs of developmental dysplasia of the hip (DDH) on examination (regardless of family history), they need to be worked up. Therefore, get plain radiographs (not an ultrasound) since they’re more reliable at this age.

* PEARLS:  The age cutoff for ultrasounds is 4 months, NOT 6. When it comes to the Barlow and Ortolani signs, EITHER of them being positive should prompt a workup!

* IMAGE: http://bit.ly/qHTScy

* IMAGE: http://bit.ly/qTQrK8

 

[ashishMember]

I think I was trying to give a more detailed description of what a child might look like in a picture. Revised version below:

SUBLUXED RADIAL HEAD (aka NURSEMAIDS ELBOW)

A subluxed radial head (aka nursemaids elbow) usually occurs in young children when a child is picked up or pulled by the arm. The forearm will be pronated and the arm will be flexed and close to body. It almost looks like the patient is wearing an invisible cast, and sometimes patient’s are noted to hold the affected elbow with the unaffected hand. Treat with forced supination.

PEARLS:  Know that it involves the annular ligament (it slips over the radial head allowing radial head dislocation). Also, it’s fine to look and feel for fractures, but there is NO NEED for imaging if the story fits.

IMAGE: http://bit.ly/o3sMYW

IMAGE: http://bit.ly/p6LkXH

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