I’m gonna write a book.
Actually I’m going to rewrite an old book. The Fluid, Electrolyte and Acid-Base Companion
Since 1999 I have:
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:
So I’m going to write a book.
So it begins.
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
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
Polyuria, polydipsia
The set up
Patient is the ICU, you receive a consult for hypernatremia resistant to therapy for three days.
Na 174Cl 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)
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%.
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.
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.
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
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.
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.
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
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:
- chloride intoxication
- GI losses
- 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.
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
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| 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.
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.
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.
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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.
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.
Coal Miner
The set up
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| Picture by Nicolas Holzheu |
Coal miner presents to the ED with fever and vomiting
pH 7.23
pCO2 67
pO2 88
pCO2 67
pO2 88
Na 144
Cl 96
BUN 8
Cl 96
BUN 8
K 3.2
Bicarb 27
Creatinine 0.6
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!