Conference Notes 12-13-2011

Conference Notes 12-13-2011


Target HGBA1C is currently 7%.  Tighter control lower the risk of end organ disease from dm but increases the risk of hypoglycemic episodes.

Treat mucormycosis with amphotericin B.  Mucormycosis on boards is typically a black eschar on the nose.

1 amp of D50 (25g of sugar) will raise blood sugar by 100mg/dl.

ACEI’s are effective in slowing the progression of diabetic nephropathy regardless of effect on BP. Blocking angiotensin 2 is the key.

Treatment of oral hypoglycemic overdose includes IV dextrose and /SubQ/IV octreotide.

DKA treatment keys: Insulin, IV fluids,  close monitoring and treatment of Potassium/Hypokalemia.

Treatment of AKA is D5.9NS.  AKA will have an anion gap acidosis.  Cerebral edema is not a risk in AKA because pt’s are not hyperosmolar like DKA patients. 

With hyperglycemia, the serum NA should decrease 1.6 for every 100 increase in glucose.

Myxedema coma TX: IV dextrose containing fluids, water restriction for hyponatremia, passive rewarming, steroids for secondary hypothyroidism/adrenal insufficiency,  IV levothyroxine, treat precipitating factors.

Amiodarone can cause thyroid dysfunction including hypothyroidism and thyrotoxicosis.   Lithium can cause hypothyroidism.

Adrenal insufficiency can lead to hyperkalemia and peaked t waves on EKG.  Hyponatremia is also possible.   Tx  is iv fluids containing dextrose, IV hydrocortisone, vasopressors.


Most difficult thing is explaining what happened to the parents.

SUID: sudden unexpected infant death.  Occurs in infant less than 1yo who was well before.   SIDS can be said when after autopsy, no cause is identified.

Risk Factors: young mom, maternal drug use/smoking,  inadequate prenatal care,  prematurity, low birth rate, higher birth order.  Prone sleeping position, bed sharing, exposure to cigarette smoke, febrile illness, overheating,  no pacifier.

Pathophysiology: interaction of genetic and environmental factors.   Autonomic dysfunction, decreased arousal/gasping response to hypoxia or hypercarbia.   Cardiac ion channel defects.  Abnormal cytokine responses to infection.

Home electronic monitoring has not been shown to reduce the incidence of SIDS

Infant back sleeping has decreased SIDS by 50%.   Get all soft materials out of crib.

NO ROSC after 30 minutes of resuscitation has survival rate of less than 1% (0.2%).  No patient who received greater than 2 doses of epi survived.

SIDS Questions to ask: medical hx, family hx, social hx of mom, when last seen child alive,  anything unusual about infant in last 24 hours.   Who placed child down, who found child.   There is a CDC website on SIDS.

ALTE: more common in premature, mortality is about 1%.    Etiology is most commonly idiopathic.  3-5 times  higher risk for SIDS but risk is still quite low. Link is tenuous between ALTE and SIDs.   5-10% overlap of ALTE and SIDS.  The Back to Sleep Campaign had reduced SIDS but no ALTE.

LOVETT  M and M  

Rectus sheath hematoma is due to damage to superior or inferior epigastric arteries, or direct tear of rectus sheath.   Usually self limiting unless pt is anticoagulated.  Advanced age increases risk of mortality.

Retroperitoneal bleed: incidence of up to 0.6% of anticoagulated patients.   Diagnosis is frequently delayed.  Treat by reversing anticoagulation.   IR may need to be consulted if bleeding is post procedural.

Sign outs:  Leaving MD can call back in one hour to check for problems in the signed out patients. Root cause of 24% of malpractice claims is sign out problems.  Sign out is involved in 80% of medical legal liability cases.


#1 cause of death is analgesics.  #2 batteries,  #3 Hydrocarbons, #4 Plants, #5 cough/cold preps, #6 fumes like CO, #7 pesticides,  #8antidepressants.

Child Resistant:  Less than 15% of kids can open it in 5 minutes.   Then less than 20% of kids can open it even after being shown how to open the lid.   It is not “child proof”

Teen top picks: Etoh, prescription opioids, marijuana.

Munchausen by proxy: Parent gives insulin or sedative to child to make them look sick. Parent wants to go to hospital to get attention for themselves.

Serious overdoses:

 CCB’s  diltiazem, verapamil and amlodipine are worst.    Don’t discharge patients with this OD. 

Camphor is dangerous but camphor concentrations are limited by law in vapo rub and camphophenique that can’t kil a kid.  Camphor moth balls are hard to find and the other forms of moth balls are less toxic.

Clonidine and visine (clonidine in a bottle)  cause opiate-like toxidrome

TCA’s: amitryptiline and imiparmine are the worst

Opioids: worst are long acting forms=methadone, oxycodone.  Lomotil  (diphenoxylate and atropine) is very dangerous due to cns and respiratory depression.   Dextromethoraphan may cause agitation but is not a respiratory depressant.

Oil of wintergreen is very dangerous due to it’s high concentration of methylsalicylate.

Sulfonylureas: increases insulin release and suppresses glycogenolysis.  Effects are delayed and prolonged and can be severe.   Admit for observation.

Toxic alcohols: If a child swallows some you need to eval and observe.  If they only licked to substance there should be no toxicity.


Hydroflouric acid

Colchicine is a disaster.  Shuts down cellular function causing gi failure

Paraquat: Oxygen is contraindicated

Amanita phylloides

Don’t worry: brodifacum, chlorox bleach, acei’s/arb’s, diuretics, cholesterol meds, antibiotics, otc camphor products, motrin, h2 blockers, actos, avandia.

You don’t need to give charcoal to kids at any time.  High risk of aspiration.  


DKA can be initial presentation of type 1 dm 30% of the time and type 2 dm 10% of the time.

DKA produces more beta hydroxyl buterate than aceto acetate.  Urine testing measures acetacetate.   A mnemonic to remember which ketone predominates is,  pt’s with DKA get a “B” for their glucose control, not an “A”.

Cerebral edema: accounts for up to 87% of dka deaths.   Associated with low arterial CO2 and high bun, iv bicarb use, young age, and severe acidosis.  Cause could be osmotic or ischemic.  Diagnosis is a clinic one prior to CT (headache, vomiting, lethargy)  Treat with decreased IV fluids, give mannitol, consider hyperventilation. 

Hypokalemia: In DKA there is a total body depletion of potassium.   Start supplementing if K is less than 5.5.

Fluid use in Peds DKA: Unclear if volume of fluids affects incidence of cerebral edema.  No link between insulin bolus and cerebral edema.   Basically don’t bolus fluids or insulin in DKA.