Does presence of an elevated anion gap mean that there is a metabolic acidosis?

Generally yes but not always.  Aside from the organic metabolic acidoses, an elevated anion gap can also be caused by hyperalbuminemia, hyperphosphatemia or presence of an anionic paraprotein (IgA monoclonal immunoglobulin) but given that these are fairly rare occurrences, once ruled out,  metabolic acidosis is the presumed etiology of an elevated anion gap.


Source

Emmett, M.  "Serum Anion Gap in Conditions Other than Metabolic Acidosis"  Up to Date.  Nov 2012.

When should hydrocortisone be administered to treat presumed adrenal insufficiency? What is the dose of hydrocortisone?

• hypotension out of proportion to the severity of illness
• other clinical features suggestive of primary adrenal insufficiency (where hemodynamic collapse is most prominent secondary to both cortisol and aldosterone depletion) include hyperkalemia, hyponatremia, non-anion gap acidosis, hyperpigmentation and hypoglycemia. 

Hydrocortisone dose is 100 mg IV for adults and 1 - 3 mg/kg IV for children.

Source 

Burgess, B. and Roe, J.  "Adrenal Insufficiency"  Critical Decisions in Emergency Medicine.  July 2012.

50 y/o female with history of alcohol abuse presents with diarrhea for the past several days. HR 120 BP 60/30. Exam notable for cachectic appearing female with dry mucus membranes and poor skin turgor. Patient is fatigued but has a non-focal neuro exam. Na 115 BUN 60 Cr 2.0. CBC normal. No baseline labs for comparison. What is your resuscitation fluid of choice?

While normal saline is generally the favored fluid for volume expansion, use of this fluid in patients with hypvolemic hyponatremia has lead to central pontine myelinolysis.  Consider use of 1/2 NS or alternating NS with 1/2 NS.  No matter what, closely monitor Na.


Source

Oh, M. et al.  "Case Report: Danger of Central Pontine Myelinolysis in Hypotonic Dehydration and Recommendation for Treatment"  American Journal of the Medical Sciences.  July 1989.

At what glucose concentration can poorly controlled diabetics begin experiencing hypoglycemic symptoms?

Given that their bodies are used to higher than normal glucose concentrations, symptoms can start at 78 mg/dL which is considered a normal glucose concentration for most people.


Source

Mattu, A. et al.  Avoiding Common Errors in the Emergency Department.  2010.

10 day old neonate presents with lethargy. Glucose 35. What should be the concentration and dose of dextrose administered?

5 cc/kg of D10 for neonates

2cc/kg of D25, if toddler
1 cc/kg of D50, if older child

Note, the product of the cc/kg and D% equals 50!  ie. 5 x 10, 2 x 25, and 1 x 50.


Source

The Pediatric Emergency Medicine Resource, 4th ed.

Pheochromocytoma: add this one to your differential for orthostatic hypotention

Huh?  Yeah, that's what I said to myself initially too but there's a case presentation of a pheo presenting with orthostatic hypotention in this week's New England Journal of Medicine.  This supposedly occurs because the pheo causes down-regulation of the receptors in the sympathoadrenal system which is responsible for maintaining cerebral perfusion in the upright posture.  Makes sense I suppose.

Causes of orthostatic hypotention:

• volume depletion
• autonomic neuropathy (parkinsonism, diabetic neuropathy)
• pharmacologic blockade of receptors used by the sympathoadrenal system 
• down-regulation of these same receptors because of chronic exposure (pheochromocytoma)

Source

Samuels, M. et al.  "Case 14-2010: A 54-Year-Old Woman with Dizziness and Falls"  N Engl J Med 2010.

Which hyperkalemic patients need admission to a telemetry monitored bed?

• K > 6.5
• EKG changes secondary to hyper-K

Source

Chen, E and Hollander, J. "When Do Patients Need Admission to a Telemetry Bed?" Journal of Emergency Medicine. 2007.

How can the risk of developing cerebral edema during the treatment of pediatric DKA be decreased?

• rehydrate but don't over do it
• do not give an initial bolus of insulin
  
• delay insulin drip administration for one hour or more after initiation of fluid therapy
• avoid bicarbonate therapy if possible
  

The mechanisms responsible for cerebral edema are poorly understood. It is generally believed that cerebral edema is related to the management of DKA and several factors, noted above, have been implicated but none has been definitively proven.

Source

Jeha, G. and Haymond, M. "Cerebral edema in children with diabetic ketoacidosis" Up to Date. 12 Jan 2009.

Jeha, G. and Haymond, M. "Treatment and complications of diabetic ketoacidosis in children" Up to Date. 15 Oct 2009.

What is the maximum recommended rate of IV potassium repletion?

• 10 to 20 meq/h
• but can increase to as high as 40 to 100 meq/h for those with paralysis or life-threatening arrhythmias
  

Of note, potassium concentrations > 60 meq/L should be administered through a central line given the pain that can be caused when given through a peripheral vein.


Source

Rose, B. MD. "Clinical manifestations and treatment of hypokalemia" Up to Date. 24 Jan 2009.

How quickly should hyponatremia be corrected?

Patients with plasma sodium concentrations below 115 meq/L with mild symptoms (fatigue, dizziness, confusion, lethargy, muscle cramps, gait disturbances) should have their sodium gradually corrected, not to exceed 10 - 12 meq/L over the first 24 hours to avoid osmotic demyelination.

More aggressive initial correction, at a rate of 1.5 - 2 meq/L per hour for the first 3 to 4 hours, is warranted in patients with seizures or other severe neurologic abnormalities (ie coma). However, the plasma sodium concentration should probably still be raised by less then 10 - 12 meq/L in the first 24 hours.

Source

Rose, B. MD "Treatment of hyponatremia" Up to Date. 12 May 2008.

Does random plasma glucose of 185 mg/dL = diabetes?

No.

The ADA defines diabetes as one of the following which must be reproducible on subsequent testing:

• random plasma glucose > 200 mg/dL in the presence of diabetic symptoms.
  
• fasting plasma glucose > 126 mg/dL
• 2 hour plasma glucose > 200 mg/dL with oral glucose tolerance test
  

Source

McCulloch, D. "Diagnosis of diabetes mellitus" Up to Date. May 2009.

Should thyroid function tests be routinely checked in critically ill patients?

No.

Thyroid function tests are often "messed up" in critically ill patients and these results often have no clinical significance. This phenomenom is called nonthyroidal illness or sick euthyroid syndrome.

Consider thyroid function testing only when there is super high clinical concern for thyroid dysfunction ie myxedema coma or hyperthyroid storm. Even in these cases however, treatment should be initiated based on clinical presentation and severity of illness, not on the results of thyroid function tests which may take hours to result.


Source

Irwin & Rippe's Intensive Care Medicine, 5th ed.

Sabatine, M. Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine. 3rd ed.

Does thyroiditis cause neck pain?

It can. In fact, pain or no neck pain is one of the key symptoms in helping identify the etiology of the thyroiditis. Here's an algorithm from American Family Physician:

click to enlarge

Source

Bindra, A and Braunstein, G. "Thyroiditis" American Family Physician. 15 May 2006.

Name three metabolic abnormalities that can ensue after initiation of spironolactone (aldactone)? What is the mechanism?

1. Hyperkalemia
2. Hyponatremia
3. Metabolic acidosis



Mechanim: Spironolactone blocks aldosterone at its receptor sites in the distal renal tubules, increasing sodium excretion while conserving potassium and hydrogen ions.


Source

Spironolactone: Drug information. Lexi-Comp.

How aggressive should hyperkalemia treatment be for a K of 5.3? 6.0? 6.5? 7.0?

The normal range for potassium is 3.7 to 5.2 mEq/L.

Not all hyperkalemic patients require the Full Monty treatment package including calcium insulin, glucose, beta-2 adrenergic agonists, diuretics, sodium bicarbonate, cation exchange resin and dialysis. There's a continuum of treatment which becomes more aggressive as the K gets higher, symptoms of hyper-K are manifest, EKG changes develop and the rate of rise increase.

Generally speaking,

1. K above 7.0, severe muscle weakness or marked EKG changes require immediate, aggressive treatment

2. K around 6.5 in asymptomatic patients with no EKG manifestations of hyperkalemia can be treated with a cation exchange resin

3. K < 6 can often be treated with a low K diet, +/- diuretics.

In all cases, find and reverse the underlying cause.


Source

Rose, B. "Clinical manifestations and treatment of hyperkalemia" Up to Date. 16 April 2008.

Did you know that eating too much black licorice can cause ventricular tachycardia?

According to a case report in the Lancet it can by inducing hypokalemia. We're not talking about a couple pieces of licorice a day here but more like 250-500 g a day for several years.

For those interested, here are the mechanistic details:

click image to enlarge

Source

Gerritsen, K. et al. "An unusual cause of ventricular fibrillation." Lancet. v 373. 28 March 2009.

When treating diabetic ketoacidosis, when should potassium supplementation be initiated? Insulin drip stopped? Dextrose added to the fluids?

A one minute DKA treatment primer ....

1. Rule out precipitants

2. Aggressive hydration

NS 10-14 ml/kg/hr tailored to cardiovascular status

3. Insulin

10 U IV push followed by 0.1 U/kg/h, continue drip until anion gap normal. If glucose < 250 and anion gap still high, add dextrose to IV fluid and continue the insulin drip. Once anion gap normal, transition to SC insulin.

4. Electrolyte repletion

Potassium: add 20-40 mEQ/L IV fluid if serum K < 4.5, cautious K repletion recommended in those with renal failure

Phosphate: replete if < 1


Source

Sabatine, M. MD. Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine. 3rd edition

Which foods have the highest potassium content and should be avoided in those suseptible to hyperkalemia?

Highest content (> 25 mEq/100 g)

• dried figs
  
• molasses
• seaweed
  

Very high content (>12.5 mEq/100 g)

• dried fruits (dates, prunes)
• nuts
  
• avocados
• bran cereals
  
• wheat germ
  
• lima beans
  

High content (>6.2 mEq/100 g)

• vegetables (spinach, tomatoes, broccoli, beets, carrots, cauliflower, potatoes)
• fruits (bananas, cantaloupe, kiwis, oranges, mangoes)
• meats (ground beef, steak, pork, veal, lamb)

Source

Gennari, F. MD. Hypokalemia. N Engl J Med 1998; 339 (7): 451-458.

Can you list 11 causes of hyperkalemia? Here are 2 freebies to start: Renal failure and hemolysis ...

1. Renal failure


2. Pseudohyperkalemia ie hemolysis


3. Acidosis


4. Insulin deficiency


5. B-blockers


6. Digoxin toxicity


7. Massive cellular necrosis (tumor lysis, rhabdo, ischemic bowel)


8. Hyperkalemic periodic paralysis


9. Decreased affective arterial volume (CHF, cirrhosis)


10. Excessive K intake


11. Hypoaldosteronism (secondary to decreased renin production - diabetic nephropathy, NSAIDS; or decreased aldosterone synthesis - primary adrenal disorder, ACE inhibitor, ARBs; or decreased response to aldosterone from meds such as K-sparing diuretics, TMP-SMX)

Source

Sabatine, M. MD. Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine. 3rd ed. 2008.

ED approach to hypotonic hyponatremia ...

If super low and super symptomatic, give hypertonic saline.

If not super low and not super symptomatic, assess volume status (history, vitals, orthostatics, JVP, skin turgor, mucous membranes, peripheral edema, BUN, Cr) and

• if hypovolemic (thiazides, mineralcorticoid deficiency, diarrhea, vomiting) initiate mild IV hydration w/ NS to decrease ADH production OR


• if euvolemic (SIADH, polydipsia)) or hypervolemic (CHF, end stage kidney failure, cirrhosis), initiate free water/fluid restriction

This empiric approach will generally get patients headed in the right direction until evaled by the internists and/or nephrologists. For those that are more ambitious feel free to send off urine 'lytes and osmoles.

Source

Sabatine, Marc MD. Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine. 3rd ed. 2008.