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I’m gonna write a book.

Actually I’m going to rewrite an old book. The Fluid, Electrolyte and Acid-Base Companion was published in 2000 but went to the printer in 1999. This book on the physiology underlying common clinical electrolyte problems was written by two residents, one in internal medicine, one in Med-Peds.

Since 1999 I have:

  • Done a year of pediatric critical care as part of Riley Children’s Hospital’s Newborn transport team

  • Completed a 2 year fellowship in Nephrology at the U of Chicago

  • Written a textbook chapter in Intensive Care in Nephrology on calcium, phosphorous and magnesium

  • Written a chapter in Principles of Critical Care, Third Edition on electrolyte issues in critical care

  • Written a review article on magnesium

  • Worked as part of the faculty for St John Hospital’s Nephrology Fellowship Program since 2003

    • So in the last nine years my knowledge and teaching sophistication on electrolytes has exploded. All this time I have been thinking about rewriting this book:

  • Fixing it

  • Adding an evidence based medicine perspective

  • Removing some of the esoteric chapters which add to the length without helping the student

  • Add resources to make it a better resource for teaching on rounds

  • Make it relevant in web based world (Think optimized for iPhone)

  • Complete revamp of Sodium with electrolyte free water

  • Finish the job we started by adding calcium, magnesium and phosphorous

    • So I’m going to write a book.
    So it begins.

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    Lecture Schedule

    March 21 Providence MS3: Acid-Base

    February 28 Providence MS3: Sodium

    January 24 Providence MS3: Body Water
    January 3 St John Hospital Residency: Potassium

    2014

    December 12 St John Nephrology Fellowship: ASN Kidney Week: reviewed.
    December 11 Mclaren Macomb: potassium and alkalosis
    December 6 St John Hospital Residency: AKI
    December 5 St John Nephrology Fellowship: NephSAP

    November 26 Providence Hospital Internal Medicine: Potassium
    November 22 Providence MS3: Acid-Base
    November 13 Mclaren Macomb: Potassium
    November 8 ASN Kidney Week, NephMadness
    November 7 ASN Kidney Week, Introduce KDIGO Mobile App

    October 24th St. John Hospital MS3: Acute renal failure
    October 22nd: Providence Hospital Internal Medicine residency: Acute Kidney Injury
    October 17th St John Nephrology Fellowship: Fellow level hyponatremia part 2
    October 10th St John Nephrology Fellowship: Fellow level hyponatremia part 1
    October 9th Mclaren Macomb: Acute Kidney Injury
    October 3 St John Nephrology Fellowship: NephSAP Fluids and Electrolytes

    September 27 ACP of Michigan: Uric Acic, Hypertension and Gout
    September 17 Beaumont Hospital and Medical Center: Acid Base
    September 11 Mclaren Macomb: Fluids and Electrolytes
    September 12 Providence Hospital MS3: Acid-Base
    September 6 St John Hospital Residency: Sodium

    August 29 St John Nephrology Fellowship: Anemia
    August 27 Oakland University Beaumont School of Medicine 2nd years: Potassium, alkalosis and secondary hypertension
    August 27 Providence Hospital Internal Medicine residency: Acid-Base
    August 19: Oakland University Beaumont School of Medicine 2nd years. Acid Base
    August 15 Oakland University Beaumont School of Medicine 2nd years. Na and water TBL
    August 3 Providence Hospital MS3: Sodium
    August 2 St John Hospital Residency Acid Base

    July St John Hospital Residency
    July Providence Hospital

    June 14 Providence Hospital MS3: Potassium
    June 11 St. John Hospital MS3: Acid-Base

    May 16 St. John Hospital MS3: Fluids and Electrolytes
    May 13 William M. Davidson Medical Education Week: NephMadness recap
    May 10 Providence Hospital MS3: IVF and sodium
    May 8 Mclaren Macomb: NAGMA
    May 3 St John Hospital internal medicine residents: Board review
    May 2 Providence Hospital Grand Rounds: Social Media in Health Care

    April 23 St John Hospital ID Fellowship: HIV and the Kidney
    April 12 Providence Hospital MS3: Acid-Base
    April 10 Mclaren Macomb: Acid-Base part 2
    April 9 St John Hospital MS3: Acute Renal Failure
    April 5 St John Hospital internal medicine residents: Metabolic alkalosis

    March 22 Gift of Life Minority Organ and Tissue Transplant Education Program: Social Media in Transplant
    March 15 Providence Hospital MS3: Potassium
    March 14 St John Hospital internal medicine residents: How to give a Lecture Lecture
    March 21 St. John Hospital MS3: Acid-Base
    March 13 Mclaren Macomb: Acid-Base
    March 1 St John Hospital internal medicine residents

    February 15 18 Providence Hospital MS3: Fluids and Electrolytes
    February 14 St. John Hospital MS3: Fluids and Electrolytes
    February 13 Mclaren Macomb: Hyponatremia

    January 18 Providence Hospital MS3: Acid-Base
    January 17 St John Hospital MS3: Acute Renal Failure
    January 9 Mclaren Macomb: IV Fluids
    January 3 St John Hospital Nephrology Fellowship: NephSAP divalent ions part 2

    2013

    December 13 St John Hospital Nephrology Fellowship: NephSAP divalent ions part 1

    December 11 St. John Hospital  MS3: Acid-Base
    December 7 Providence Hospital MS3: Sodium and Water
    December 6 St John Hospital Nephrology Fellowship: Renal Week Recap

    November 27 St John Hospital and Medical Center Grand Rounds: Medicine and Social Media
    November 13 St. John Hospital  MS3: Fluids and Electrolytes
    November 9 Providence Hospital MS3: Potassium
    November 9 St John Hospital internal medicine residents: Diabetic Nephropathy, A New Hope

    October 24-28 Michigan State Medical Society: Diabetic Nephropathy, A New Hope
    October 24 Providence Hospital MS3: Acid-Base
    October 26 Providence Hospital MS3: Sodium and Water
    October 9 St John Hospital MS3: Acute Renal Failure

    September 11 St. John Hospital third year medical Students: Fluids and Electrolytes
    September 7 St John Hospital internal medicine residents: Non-Anion Gap Metabolic Acidosis

    August 31 Oakland University Beaumont School of Medicine 2nd years. PBL: Glomerular Disease
    August 24 Oakland University Beaumont School of Medicine 2nd years. PBL: Acute and Chronic Kidney Disease
    August 21 Oakland University Beaumont School of Medicine 2nd years, Acid-Base
    August 20 Oakland University Beaumont School of Medicine 2nd years, Potassium Balance Disorders
    August 17 Oakland University Beaumont School of Medicine 2nd years. PBL: Sodium and water

    August 16 Providence Hospital 3rd year medical students: Potassium
    August 3 St John Hospital internal medicine residents: Acute Kidney Injury
    August 2 St John Hospital Nephrology Fellowship: Anemia and lack of placebo controlled trials
    August 1 Providence Hospital internal medicine residents: Acute Kidney Injury

    July 25 St Mary Hospital Grand Rounds: Acute Renal Failure, an update
    July 24 St John Hospital internal medicine residents: Acid-Base
    July 19 Providence Hospital 3rd year medical students: Sodium
    July 17 Providence Hospital internal medicine residents: Water, IV Fluids, Sodium, Diuretics

    July 13 Providence Hospital 3rd year medical students: Acid-Base

    July 10 St John Hospital third year medical Students: Acute Renal Failure
    July 3 St John Hospital internal medicine residents: Water, IV Fluids, Sodium, Diuretics

    June 12 St John Hospital third year medical Students: Acute Renal Failure
    June 8 Providence Hospital 3rd year medical students: Potassium

    May 24 Providence Hospital 3rd year medical students: Sodium
    May 15 St. John Hospital third year medical Students: Fluids and Electrolytes
    May 4 St John Hospital internal medicine residents: Renal Anemia

    April 19 Providence Hospital 3rd year medical students: Acid-Base
    April 18 Providence Hospital Resident Reasearch Day: Judge
    April 10 St John Hospital third year medical Students: Acute Renal Failure
    April 6 St John Hospital internal medicine residents: HIV associated nephropathy

    March 20 St. John Hospital third year medical Students: Fluids and Electrolytes
    March 13 St. John Hospital third year medical Students: Acid-Base
    March 2 St John Hospital internal medicine residents: board review

    February 24 UIC/Advocate Christ Medical Center Residents: Non-Anion Gap Metabolic Acidosis
    February 10 Providence Hospital 3rd year medical students: Potassium
    February 9 Providence Hospital 3rd year medical students: Sodium and Water
    February 3 St John Hospital internal medicine residents: Tolvaptan is effective in which patient and metabolic alkalosis
    February 2 St John Hospital Nephrology Fellowship: Board Review NephSAP CKD and Progression part 2

    January 19 St John Hospital Nephrology Fellowship Initiation of Dialysis
    January 17 St John Hospital third year medical Students: Acute Renal Failure
    January 12 Providence Hospital 3rd year medical students: Acid-Base
    January 5 St John Hospital Nephrology Fellowship: Board Review NephSAP CKD and Progression part 1

    2012

    December 13 St. John Hospital third year medical Students: Acid-Base
    December 8 St. Mary’s Hospital in Saginaw: Fructose, CKD and Hypertension
    December 2 St John Hospital internal medicine residents: Severe lactic acidosis and electrolyte disorders of the drunk.

    November 29 Providence Hospital 3rd year medical students: Potassium
    November 17 Providence Hospital 3rd year medical students: Acid-Base
    November 15 St John Hospital third year medical Students: Fluid and Electrolytes
    November 15 St John Hospital and Medical Center Grand Rounds: Diabetic Nephropathy, an Update
    November 11 U of C Alumni Reception. Marriott. 6:45pm
    November 11 Blogger get together McGillins Olde Ale House. 8pm
    November 11 AJKD Editorial Board Meeting Franklin 4 Room Marriott. 12:45-1:45
    November 4 St John Hospital internal medicine residents: Non-anion gap

    October 28 Providence Hospital 3rd year medical students: Sodium and Water

    October 27 Providence Hospital Grand Rounds: Anemia and lack of placebo controlled trials

    October 26 Michigan State Medical Society: Fructose, CKD and Hypertension
    October 25 Providence Hospital Residency Program: What’s New in Potassium
    October 22 Lupus Alliance of America: Panel discussion
    October 20 Providence Hospital 3rd year medical students: Acid-Base

    October 12 St. Mary Mercy Hospital: Fructose, CKD and Hypertension

    October 11 St John Hospital third year medical Students: Acute Renal Failure
    October 6 St John Hospital Nephrology Fellowship: Dialysis Kinetics

    September 30 Providence Hospital 3rd year medical students: Acid-Base
    September 22 St John Hospital Nephrology Fellowship: Physiology of Sodium and Water Handling
    September 20 Royal Oak Beaumont Internal medicine residency: Acid-Base Disorders
    September 13 St John Hospital third year medical Students: Acute Renal Failure
    September 2 St John Hospital internal medicine residents: Potassium

    August 30th Providence Hospital Residency Program: Potassium
    August 26th Providence Hospital 3rd year medical students: Acid-Base

    August 9th St John Hospital third year medical Students: Fluid and Electrolytes
    August 5 St John Hospital internal medicine residents: Acid Base

    July 26th St John Hospital third year medical Students: Acid-Base
    July 22nd Providence Hospital 3rd year medical students: Fluids and Electrolytes
    July 22nd St John Hospital internal medicine residents: Acute renal failure
    July 21st Beaumont Family Practice Residency: Acute renal failure
    July 21st St John Hospital Nephrology Fellowship: Anemia and lack of placebo controlled trials
    July 19th Providence Hospital Residency Program: Body water, IV fluids and diuretics
    July 1st St John Hospital internal medicine residents: Body water, IV fluids, diuretics and dysnatremia

    June 14th St John Hospital third year medical Students: Acid-Base
    June 9th: Abbott pharmaceuticals secondary Hyperparathyroidism: FGF-23
    June 8th: St John Hospital and Medical Center: Update in CKD: Anemia
    June 3rd: St John Hospital internal medicine residents: a case of Milk-Alkali syndrome and Fructose, Hypertension and Uric Acid
    June 2nd: St John Hospital Nephrology Fellowship Program: NephSAP Fluids and Electrolytes
    June 1st: Grand Rounds Beaumont Hospital: Fructose, Hypertension and Uric Acid

    May 26th St John Hospital Nephrology Fellowship Program: Hyponatremia
    May 17th St John Hospital third year medical Students: IVF and Hyponatremia
    May 6th St John Hospital internal medicine residents: Nephrology board review
    May 2nd: Michigan CRN meeting: Fructose, Hypertension and Uric Acid

    April 29th: Providence Hospital third year medical students: Sodium in the morning, potassium at 11
    April 20th: Providence Hospital third year medical students: Acid-Base
    April 18th: St John Hospital cardiology fellows: Cardiorenal Syndrome
    April 14th: Beaumont Gross Point family practice residents: IVF and Sodium Part 1
    April 12th: St John Hospital third year medical Students: Acute Renal Failure
    April 8th: St John Hospital internal medicine residents: How to give a lecture: Keynote Tutorial

    March 29th: Providence Hospital internal medicine residents: hypernatremia and hypercalcemia
    March 17th: St John Hospital third year medical Students: Acid-Base
    March 4th: St John Hospital internal medicine residents: Cardiorenal Syndrome

    Feburary 18th: Providence Hospital third year medical students: Potassium
    Feburary 16th: Providence Hospital third year medical students: IVF and Na

    Feburary 11th: Providence Hospital third year medical students: Acid Base
    Feburary 8th: Providence Hospital internal medicine residents: Hyponatremia, hypokalemia

    January 18th: St John Hospital Grand Rounds: Dialysis for the internist, an update

    2011

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    Polyuria, polydipsia

    The set up

    Patient is the ICU, you receive a consult for hypernatremia resistant to therapy for three days.

    Na 174
    Cl 128
    BUN 38

    K 3.2
    HCO3 27
    Cr 1.6
    glucose 128

    urine lytes:
    Na 56
    K 12
    Body weight 45 kg
    urine output 2,800

    Step one


    Calculate the fluid deficit:
    We assume the increase in sodium is entirely due to loss of water. If the patient is hypotensive, tachycardic orthostatic or has other clues that he maybe volume depleted, the situation is more complex. We calculate the percentage that the sodium is elevated above an imagined “ideal sodium.” Many equations use 140 as the idealized sodium, I tend to use 145. The percentage the sodium is above the ideal is identical to the percentage of the total body water that is needed to lower the sodium to the target level.

    174-145 / 145 = 0.2 (the sodium is 20% above 145)

    Multiple that by the estimated total body water (weight x % body water) = 5.4 liters

    I used 60% for estimated total body water. The patient looks like a young boy. Rose suggests lowering the estimated % body water by 10% so 50% would be okay also. In the elderly and obese this number can go below 50%. 

    Step two


    Going from 174 to 154 is too much change in 24 hours. The speed limit is 12 mmol/L/day so we will target a change from 174 to 162.

    I use a modified water deficit formula. I divide 12 (the change in sodium we are looking for) by the target sodium (current sodium minus 12):

    12/(174-12) = 0.08 x total body water = 2.0 liters or just over 80 mL/hour


    Step three

    Calculate the electrolyte free water clearance. The reason the ICU team repeatedly failed to correct the sodium is that they corrected the deficit without accounting for the ongoing water losses. In this case it is renal losses. If you just add the urine volume to the water deficit you will over estimate the amount of water needed because the urine contains sodium and potassium. To account for the electrolyte content of the urine we calculate the free water clearance.

    Urine Na + K divided by the serum Na will give the ratio of urinary electrolytes to serum solute. 
    56 + 12 / 174 = 39%
    The urine has 39% electrolyte content of plasma, another way of thinking about this is that 39% of the urine volume is isotonic and the remainder (61%) is pure water. The 61% is what we are interested in; multiply the urne output by 61% this is the volume of water we need to give the patient to account for his ongoing renal losses. 
    Then multiply this by the urine output (2,800) to get the electrolyte free water clearance, 1705 ml. This is another 71 mL/hour

    Wrap up

    Final fluid orders: 154 mL/hour of water, this can be given as D5W in the IV or preferably oral flushes. This calculation does not insensible losses.


    Posted on

    More metabolic acidosis than you can shake a stick at…

    The set up

    28 year old under going treatment for metastatic testicular cancer presents with a history of recurrent kidney stones.

    pH 7.13
    pCO2 22
    pO2 96

    Na 138

    Cl 114
    BUN 14

    K 3.2
    HCO3 8
    Cr 1.0
    glucose 96

    urine lytes:
    Na 56
    Cl 78
    K 12
    Measured osmolality 292

    Step one


    Determine the primary acid-base disorder. The pH, bicarbonate and pCO2 are all moving in the same direction (down in this case). When all the Henderson-Hasselbalch variables are moving in the same direction (up or down) the primary disorder is metabolic. The pH is decreased so this is a metabolic acidosis. 

    Step two


    Is the compensation appropriate, or do we have a primary respiratory disorder as well as a metabolic acidosis? 
    We use Winter’s Formula to get the predicted pCO2 based on the bicarbonate.
    1.5 x bicarbonate + 8 = 
    1.5 x 8 +8 = 20

    His actual pCO2 is 22 which is close enough, so a pure metabolic acidosis with appropriate respiratory compensation.

    Step three

    If there is a metabolic acidosis is there an anion gap?
    138 – (114 +8) = 16
    Yes, this is an anion gap metabolic acidosis.

    Step four

    If there is an anion gap, is there an osmolar gap? I usually don’t bother to look for an posmolar gap uness the patient is particularly toxic with a large anion gap, neither of which describe Lance, but since the information includes the measured osmolality we should check this. You know, Chekhov’s gun and all.
    2 x Na + Glucose / 18 + BUN / 2.8 + Ethanol / 4.6 = calculated osmolality
    2 x 138 + 96 / 18 + 14 / 2.8 + 0 / 4.6 = 286
    Osmolar gap = measured osm – calculated osm

    Osmolar gap = 292 – 286 = 6

    This is a normal osmolar gap. Poor foreshadowing by the question writer.

    Step five

    If there is an anion gap, what was the bicarbonate before the anion gap? To calculate the bicarbonate before, take the anion gap, subtract 12 and add that to the current bicarbonate:

    Bicarbonate before the anion gap = Bicarbonate + (Anion gap -12)

    Bicarbonate before the anion gap = 8 + (16 –12)
    Bicarbonate before the anion gap = 12

    So the bicarbonate before the anion gap was 12 indicating a large non-anion gap metabolic acidosis and a relatively mild anion gap metabolic acidosis.

    Step six

    If there is an NAGMA, what is the urinary anion gap? What does it mean? The patient has a NAGMA as discovered in step 4. The differential of NAGMA is:

    1. chloride intoxication
    2. GI losses
    3. RTA

    The patient doesn’t seem to be suffering from chlorine gas intoxication or have an isotonic saline drip running so number one is not likely.

    The low potassium could indicate GI losses as well as type 1 or 2 RTA. The urine anion gap in the face of severe metabolic acidosis will help here. In GI losses and chloride intoxication the urine amnion gap will be negative, in RTA it should be positive.

    Urine anion gap = (Na + K) – Cl

    Urine anion gap = (56 + 32) – 78

    Urine anion gap = + 10

    The positive anion gap indicates a lack of NH4+ in the urine. In diarrhea, the kidney will up ammonium excretion to get rid of the acid load. The increase cation load in the urine will be balanced by an increased in chloride in the urine. The increase Cl– will make the urine anion gap negative (in reality it is an unmeasured cation, or a positive cation gap, but by convention we use an anion gap). The positive urinary anion gap is the face of a severe acid load indicates a renal tubular acidosis.

    Put it all together

    This patient has a well compensated metabolic acidosis. The metabolic acidosis is partly anion gap and non-anion gap. The non-anion gap is a distal RTA. The AGMA may be a lactici acidosis from the neoplasm as these are not uncommon in metastatic neoplastic disease.

    The chief complaint of kidney stones points to type 1 RTA. Patients with testicular cancer receive platinum-containing chemotherapy. Platinum can cause proximal or distal RTA. However, proximal RTA is not associated with kidney stones. So I suspect this  is classic distal RTA due to platinum.
    Posted on

    Patient with a Liddle problem

    The Set Up

    42 year old African American woman presents with muscle weakness and palpitations. Her blood pressure is 180/110. Her hypertension has been documented since age 16.

    Her sister has a history of hypokalemia and hypertension. Three of her six kids, all of which are younger than 20 have hypertension.

    Na 144
    Cl 96
    BUN 14

    Photo: Creative Commons/Paleontour

    K 2.7
    Bicarb 42
    Cr 0.8

    ABG
    pH 7.54
    pCO2 51
    paO2 97

    Step one


    What is the primary acid-base disturbance.
    pH is elevated, so its an alkalosis. The pH, pCO2 and HCO3 are all going up (same direction) so it is a metabolic condition. Metabolic alkalosis.

    Step two


    Is compensation appropriate.
    To find the target pCO2 add two thirds of the delta bicarb to a normal pCO2 of 40 mmHg.

    Her bicarb is 42, and the delta (42 – normal bicarb of 24) = 18.
    Two thirds of 18 is 12.
    40 + 12 = 52 mmHg.

    Actual pCO2 is 51, so we are in the house, pCO2 is appropriate for a serum bicarbonate of 42, no second primary disorder affecting compensation.

    Step three


    What is the differential of hypokalemia, metabolic alkalosis and abnormal blood pressures?

    Hypokalemnia and metabolic alkalosis is an important pattern. The first concept that medical students invariably want to lean on is the intracellular exchange of hydrogen and potassium. When there is hypokalemia, potassium flows from the cells. To maintain electroneutrality hydrogen goes into the cells. The certainly is operating in these cases, however a model that looks at changes in total body potassium is much richer.

    The reason that metabolic alkalosis and hypokalemia can walk together is that they both are responces to hyperaldosteronism. The increased aldosteronism can be primary, secondary or unusual.

    • Secondary hyperaldosteronism. Patients with GI losses, diuretics or other causes of volume depletion will upregulate their aldosterone. Aldosterone will fight the volume depletion by reabsorbing sodium in the principle cells, flowing down its concentration gradient through the eNAC. Aldosterone increases the number and activity of the eNAC channels (it also increases the number and activity of the potassium channels and the Na-K-ATPase).
      • Volume deficiency
      • Renal artery stenosis decreases renal blood flow and induces a secondary hyperaldosteronism
    • Primary hyperaldosteronism. This is major cause of hypertension. Patients can have metabolic alkalosis and hypokalemia. If your patient has hypokalemia and alkalosis, definatly pursue primary hyperaldo, but do not rule out primary hyperaldo if you don’t have the electrolyte abnormality. Most patients with pimary hyperaldo do not have the typical electrolytes.
    • Unusual: one conditions to remember that cause metabolic alkalosis and hypokalemia:
      • Liddle syndrome. Patients have a mutation at 16p12 that encode the beta and gamma subunits of the eNAC. The eNAC is no longer sodium selective and is always open. The sodium reabsorption causes hypertension. The eNAC channel also increases potassium and hydrogen secretion.
      • The functional opposite of Liddle syndrome is Pseudohypoaldosteronism type 1. Here mutations to the alpha, beta or gamma subunits results in resistance to the effects of aldosterone. Patient have sodium wasting and hyperkalemia. There is an autosomal recessive and autosomal dominant form.
      • Licorice and SAME (Syndrome of Apparent Mineralocorticoid Excess) The structure of cortisol and aldosterone are almost identical and the mineralocorticoid receptors in the principle cells are unable to differentiate between these molecules. This means that cortisol can activate the mineralocorticoid receptors. This is made worse by the fact that cortisol typically is found at concentrations a 1000-fold higher than aldosterone. To prevent cortisol from acivating the mineralocorticoid receptors, cortisol is rapidly metabolised by 11-beta-hydoxysteroid dehydrogenase. If this enzyme is absent (SAME) or inhibited (licorice ingestion) you can get wildly up-regulated mineralocorticoid activity with simultaneous suppression of aldosterone.
    1. Sodium is reabsorbed through the ENaC. Sodium moves
      down its concentration gradient.
    2. The movement of sodium is electrogenic and results in
      a negative charge in the tubule.
    3. Chloride in the tubule can be reabsorbed paracellularly.
      The more chloride that is reabsorbed the less potassium
      is secreted.
    4. Potassium flows down an electrical and chemical gradient into the tubule.

    Step four


    The family history shows first degree relatives with a similar condition. This suggestes autosomal dominant transmission. This is consistant with Liddle syndrome.

    Step five

    Next steps in the diagnosis. Though the genetics are suggestive of autosomal dominant transmission, Liddle Syndrome is very uncommon while primary hyperaldosteronism is relatively common. A serum aldosterone level will separate these patients neatly. In Liddle Syndrome the aldosterone is suppressed, while in primary hyperaldosteronism it is up regulated. Genetic testing is available to confirm the diagnosis.

    See these posts at the Renal Fellow Network for additional information.

    Posted on

    Osmolar Gap

    The set up

    Patient without a significant medical history is admitted to the hospital comatose. The immediate differential includes alcohol ingestion

    Na 140
    K 4.0
    Cl 99
    HCO3 25
    BUN 38
    Cr 0.7
    Glucose 90
    ABG:
    7.34 / 47 / 167
    Ethanol 574 mg/dL
    Serum osmolality 442

    Step one

    What is the primary acid-base disorder:
    The pCO2 is up and so is the bicarb, so this is respiratory acidosis.

    Step two

    Is the compensation appropriate:
    for every 10 the pCO2 is increased the bicarb should rise 1 if the disease is acute and 3 if it is chronic. In this case we presume the respiratory disorder is due to the intoxication so it is acute, so the bicarb should rise 0.7 or close to one because the pCO2 is 7 above 40 (normal). The actual bicarbonate is 25 so this is an appropriately compensated acute respiratory acidosis.
    If this patient had chronic respiratory acidosis, then the bicarbonate should rise to 26 (0.7 x 3 =2.1).

    Step three

    Is there an anion gap?
    140 – (99+25) = 16. Yes. But it is very small.

    Step four

    Is there an osmolar gap?
    Calculated osmolality = 2 x Na + Glucose / 18 + BUN / 2.8 + Ethanol / 3.7
    2×140 + 90/18 + 15/2.8 + 574/3.7 = 280+5+5.4+155 = 445.5
    Osmolar Gap = Measured Osm – Calculated osmolality
    Osmolar Gap = 442 – 445 = -3

    Step five

    No significant anion gap and no osmolar gap means that this is just ethanol toxicity.
    Many medical calculators use 4.6 as the divisor for the osmolar gap. However empiric data shows that ethanol does not act as ideal solute and the divisor should be 3.7. If you use 4.6 the osmolar gap comes out to be: 442 – 415 = 26.

    Step six

    This is simple alcohol intoxication. No indication for fomepizole or dialysis. Ethanol is highly dialyzable. The indications for dialysis is hemodynamic instability despite pressers and volume resuscitation. This patient has depressed mental status and depressed respiration. The treatment for this is supportive care, not dialysis.
    Posted on

    Coal Miner

    The set up

    Picture by Nicolas Holzheu

    Coal miner presents to the ED with fever and vomiting

    pH 7.23
    pCO2 67
    pO2 88
    Na 144
    Cl 96
    BUN 8
    K 3.2
    Bicarb 27
    Creatinine 0.6
    glucose 128

    Step one: determine the primary disorder

    the pH is down, the HCO3 and CO2 are up so this is a respiratory acidosis

    Step two: check to see if the compensation is appropriate

    The CO2 is 67, since his chief complaint is not respiratory and he is a coal miner we will assume black lung and chronic COPD. So we will use the estimate for chronic respiratory acidosis
    67 is almost 30 above normal pCO2, and for every 10 the CO2 rises the HCO3 should go up 3 (1 is this was acute). So a pCO2 of 67 should have a HCO3 of 2.7 x 3 = 8.1 above a normal bicarb of 24 = 32.1.
    His actual bicarb is 27 so he has an additional metabolic acidosis (bicarb lower than predicted means metabolic acidosis).

    Step three: if there is a metabolic acidosis what is the anion gap

    The patient has a metabolic acidosis, so the anion gap is relevant. We calculate it and it is 21.

    Step four: if there is an anion gap, calculate the bicarbonate before

    The patient has an anion gap so to calculate the bicarbonate before the anion gap we subtract 12 from the calculated anion gap and add the difference to the current bicarbonate:
    21-12 = 9 add that to the bicarbonate of 27 to get a bicarbonate of 36. This is higher than the predicted compensated bicarbonate from step two (32.1) so the patient has an additional metabolic alkalosis.

    Final step: put it all together

    The patient has black lung and COPD. His largest acid-base disorder is chronic respiratory acidosis. He does have an acute illness. This illness is causing an anion gap metabolic acidosis. Sepsis and multi organ failure does this. Prior to developing the anion gap the vomiting caused a metabolic alkalosis.
    Its a triple disorder!