Tag Archives: endocrine

DKA & HHS – treatment myths busted

26 Jun

submitted by Amit Kumar, M.D.


*ABG >VBG: False, ABG = VBG.

Additionally, VBG is less painful and avoids complications like radial artery aneurysms, hematoma, and radial neuropathy. Lactate on VBG is equally reliable despite length of tourniquet time or temperature. pH of VBG is assumed to be 0.03 less than ABG. Only level missing in VBG are PaO2 and SpO2 (for which we have the pulse-ox). In general, ABGs are only useful in patient where knowing PaO2 is vital, and A-a gradient is desired.


*Shotgun insulin order s/p IVF: False. Correcting electrolytes is higher priority.

Serum K is low to begin with due to acidosis. Additional insulin and IVF will shift more K into cells, further depleting serum K. If K <3.5, replete K and hold insulin. If K 3.5-5.5, replete K with insulin. If K >5.5, may just give insulin.


*Insulin bolus, then drip: False.  Pediatric guidelines actually do not recommend bolus for potential risk for hypercorrection of serum glucose and cerebral edema.

Hypoglycemia is worse than hyperglycemia for mortality. So why do it? Per comparison studies, gtt at 0.14U/kg/h is better at providing a good therapeutic plateau, compared to 0.1U/kg bolus followed by 0.1U/kg/h gtt.
Replete Phos <1 mg/dL (vital for generating ATP) and Mg <2. Monitor Ca as well.


*HCO3 for pH <7.1: False. Bicarbonate exacerbates hypokalemia, and may even potentially increase risk of cerebral edema.

Bicarb also shifts O2 dissociation curve leftward, inducing hypoxia in a state of high demand. If given, just start a drip sans bolus, and mix with D5W (mixing with NS will cause precipitation and make solution hypertonic).



*Kitabchi AE, Hirsch IB, Emmett M. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. In: UpToDate (Accessed on July 27, 2016)

*Swaminathan A, Herbert M. (2013, May). DKA Myths [Audio podcast]. Retrieved from: emrap.org

*Wolfson AB, Hendey GW, Ling LJ, Rosen CL, Schaider J, Sharieff GQ. Harwood Nuss’ Clinical Practice of Emergency Medicine. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.


Understanding Insulin Pumps

14 Aug

Basic function:pump1

~200-300 units of short acting insulin is in the insulin reservoir. This connects through the tubing to be infused via the cannula to the subcutaneous tissue of the patient.

Frequent BG monitoring is still required.  In fact more these patients check more frequently than patients without pumps d/t the possibility of pump problems.

-Patients have a basal rate they get continuously and then type in their desired bolus amount with meals.

-Patients need to move the needle site every 2-3 days (otherwise increased risk of infection and decrease in glycemic control)



  1. Local reactions to adhesive or insulin preparation
  2. Lipohypertrophy or lipoatrophy
  3. Cellulitis at the needle insertion site
  4. Pump failure. Any part of the device can fail- dead batteries, kinked/cracked tubing, depleted or broken reservoir…
  5. Air in tubing causing missed insulin
  6. Insulin leakage (at insertion site or infusion set connection site causing missed insulin


* Pumps frequently will not given any indication that there is a problem

* As the patient is getting only short-acting insulin, device failure can rapidly lead to DKA. 


Submitted by Heather Groth.



Academic Life in Emergency Medicine

Pickup, John. “Insulin-Pump Therapy for Type I Diabetes Mellitus” N Engl J Med 2012; 366:1616-1624

UCSF Website: http://dtc.ucsf.edu/types-of-diabetes/type2/treatment-of-type-2-diabetes/medications-and-therapies/type-2-pump-rx/

Capnography for diagnosing DKA?

13 Jan

Interesting article from Iran:

181 adult patients, 62 had DKA

  • included: patients attendings had clinical suspicion for DKA, BG >250
  • excluded: pts likely to have metabolic disturbances (e.g. gastroenteritis, chronic renal failure, respiratory dz, ALOC, etc).

capnography > 24.5 mmHg had sensitivity & specificity of 90%

excludes a lot, but interesting

peds study from Austrailia had a similar idea:

58 kids, 15 had DKA

No patients with an ETCO(2) > 30 mmHg had DKA (sensitivity 1.0, specificity 0.86).

6 patients with an ETCO(2) < 30 mmHg did not have DKA.


some small studies with some limitations, but food for thought

in a pinch, capnography would be a quick bit of info on potential acidosis (using respiratory compensation with ETCO2 as the sideways look).  

References: adult article; peds article; picture

hyponatremia and hyperglycemia: quick hits, quick math

30 Jul


Symptoms (VAGUE, NON-SPECIFIC) include:

  • nausea, vomiting,
  • anorexia,
  • muscle cramping,
  • lethargy,
  • confusion,
  • eventually seizure/coma/death


1st step is to determine the ECF volume status.


Hypertonic hyponatremiamost commonly hyperglycemia, each 100 mg/dL reduces serum Na by 1.7mEq/L

  • quick guesstimation/rule of thumb: add 1 to the sodium level for every 50 mg/dL glucose over 100
    • e.g. glucose 200, sodium 140 -> add 2 to 140 -> corrected Na~=142
    • e.g. glucose 500, sodium 140 -> add 8 to 140 -> corrected Na~=148
  • quick internet cheat: mdcalc’s Sodium Correction for Hyperglycemia



30 seconds of the other stuff….


Isotonic hyponatremia—often referred to as factitious and does not require treatment.


Hypotonic Hyponatermia—Results from intracellular volume expansion with derangement of cellular functions (e.g. SIADH)

  • Six criteria of SIADH 
    • 1. Hypotonic hyponatremia
    • 2. Innappropriately elevated elevated urine osms (>200)
    • 3. elevated urinary Na
    • 4. Clinical Euvolemia
    • 5. Normal adrenal, renal, cardiac, hepatic, and thyroid fxn
    • 6. Correctable with water restriction


Submitted by J. Stanton.


References: uptodate.com; mdcalc.com; picture


sublingual sugar for hypoglycemia

13 May

spurred by the recent D50 shortage, I remember hearing about some EMS crews stocking a tube of cake icing for use in a pinch (since occasionally there are tough IVs, and IM glucagon only works if you still have glucose stores).   Does this really work?




children with severe malaria in sub-Saharan Africa

randomized, clinical trial comparing sublingual sugar with oral water, oral sugar, and dextrose infusion administrations.

69 children

  • oral group (OG) (n = 15): 2.5 g of sugar;
  • sublingual group (SG) (n = 27): 2.5 g of sugar under the tongue
  • intravenous group (IG) (n = 8): 8 mL of 30% dextrose in a single bolus;
  • water group (n = 11).

Blood glucose concentrations were measured every 20 minutes for 80 minutes

No treatment failures were observed in the SG and IG.

SG children exhibited glucose kinetic profiles and bioavailabilities similar to those of IG children.

Children > 7 years of age required repeated sublingual administrations to maintain normoglycemia.

CONCLUSIONS: The sublingual administration of sugar proved to be effective among moderately hypoglycemic children.



pilot randomized controlled trial among hypoglycaemic children with severe malaria in Mali.

23 children with blood glucose concentrations < 60 mg/dl (< 3.3 mmol/l) were assigned randomly

  • intravenous 10% glucose (IVG; n = 9)
  • sublingual sugar (SLS; n = 14). (a teaspoon of sugar, moistened with a few drops of water, was gently placed under the tongue every 20 minutes)

Blood glucose concentration (BGC) was measured every 5-10 minutes for the first hour. 

Treatment response occurred in 71% and 67% for SLS and IVG, respectively.

Among the responders, relapses occurred in 30% on SLS at 40 minutes and in 17% on IVG at 20 minutes.

Treatment failures in the SLS group were related to children with clenched teeth or swallowing the sugar, 

Sublingual sugar appears to be a child-friendly, well-tolerated and effective promising method…More frequent repeated doses are needed to prevent relapse.



data with smallish numbers in kids, but looks promising

sublingual sugar might be an alternative route for hypoglycemia treatment, or a bridge to other methods

re-dose frequently, if its not a bridge to something else


References: study 1; study 2; mini-review; picture




Hypothyroidism (QUICK HITS)

25 Apr


-TSH measurement is known to be the primary method of detecting thyroid disease

-After assessing TSH, Free T4 is the secondary test



-The Framingham study showed a rate of 4.4% of hypothyroidism in women over 60


Manifestations of Hypothyroidism

-Vary greatly from subclinical hypothyroidism to severe hypothyroidism

-Generally follow one of two changes

Slowing of metabolic processes:  

    • weight gain,
    • fatigue,
    • cold intolerance,
    • constipation,
    • bradycardia
    • irregular menses,
    • depression,
    • muscle weakness

Accumulation of glycosaminoglycans in tissues:  

    • Coarse hair and skin,
    • tongue enlargement,
    • hoarseness.

Myxedema (nonpitting edema) only occurs in severe hypothyroidism.

-Other important manifestations include anemia


Cardiovascular Effects

-Causes decreased cardiac contractility and decreased heart rate

-Patients often complain of dyspnea with exertion

Hypercholesterolemia secondary to decrease in cholesterol metabolism


Reproductive Effects

-Women may present with amenorrhea, hypermenorrhea, or normal cycles

-Both women and men with hypothyroidism have been shown to have decreased fertility

-Common complaints with men include decreased libido, erectile dysfunction, and delayed ejaculation. 


Metabolic Effects

-Decreased cholesterol metabolism and decreased drug clearance

Hyponatremia may occur secondary to an overall reduction in a person’s free water clearance. 


Myxedema Coma

-Severe hypothyroidism who are then exposed to new stresses including trauma, infection.

-Commonly present with hypothermic, hyponatremic, hypercapnic in a comatose patient. 



T4 Supplementation


Submitted by J. Grover.


Sources: Bensenor IM et al.  “Hypothyroidism in the Elderly:  Diagnosis and Management.  Clinical Interventions in Aging 2012:7 97-111. Tintinallis Emergency Medicine:  7th Edition. Uptodate:  Clinical Manifestations of Hypothyroidism.; picture

Thyroid Storm

11 Apr

-Usual etiology is in a patient with known hyperthyroidism with new physiologic stressor including infection, labor, surgery, uncontrolled DM, and trauma



-Can present in acute heart failure, fever, tachycardia, and occasionally with arrhythmias



  • Shortness of breath,
  • palpitations,
  • chest pain,
  • lower extremity edema,
  • fevers,
  • weight loss



 -Serum TSH is usually undetectable with extremely elevated levels of Free T4

Four Key Principles of Management

 1. Block Peripheral effects

Propranolol is drug of choice

Non-selective beta blocker

Also inhibits conversion T4 to T3 peripherally


2. Decrease new synthesis of thyroid hormone

Propylthiouracil (PTU) is drug of choice

Peripheral effects: Inhibits enzyme 5′-deiodinase which converts T4 to T3

Central effects: Inhibits the enzyme thyroperoxidase, an enzyme that is essential for T4 production



Same mechanism centrally as PTU but lacks peripheral effect



 3. Block Thyroid Hormone Release

In large doses, iodine actually inhibits the release of thyroid hormone

MUST be given greater than an hour after PTU, otherwise it can increase hormone synthesis


4. Supportive care including Oxygen, fever control, and Steroids

Steroids given because thought is that patients are relatively hypoadrenal because of high metabolism

Dexamethasone is also believed to slow conversion of T4 to T3


Submitted by J. Grover.


References: uptodate.com: thyroid storm; Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition; picture