SIMPLE ACID-BASE DISORDERS

PROBLEM 1 This 38-year-old man has been followed for several years with a diagnosis of chronic glomerulonephritis and gradually progressive azotemia. This admission was prompted by increasing weakness, lethargy and anorexia. Physical examination showed BP 170/110, T 98, R 22. Positive findings included a sallow complexion, GR II hypertensive retinopathy, a soft mid-systolic murmur along the left sternal border and moderate cardiomegaly. There were no rales, hepatomegaly or dependent edema. Laboratory studies showed: Na K C1 HC03 134 5.6 100 14 BUN Creat pH PCO2 159 mg% 18mg% 7.26 27

Urine showed 3+ protein, SG 1.012 and a variety of fine and granular casts. Questions:

1) What is the acid-base disturbance? Acidemic (pH 7.26) with a low HCO3 so definitely at least a metabolic acidosis. The patients anion gap is 134 (14 + 100) ie 20 so anion gap acidosis. In order to check for respiratory compensation you use the Winters equation. This formula is only applicable for respiratory compensation for a metabolic acidosis. The expected pCO2 = 1.5 HCO3 + 8 +/- 2 If the patients pCO2 is within the expected range then the comment is appropriate respiratory compensation or secondary respiratory alkalosis. In this case expected pCO2 is 1.5 (14) + 8 +/- 2 ie 27-31 so this patient has a compensated respiratory alkalosis. If the pCO2 had been lower than 27 then it would be a primary respiratory alkalosis ie overcompensated If greater than 31 then inadequate compensation ie primary respiratory acidosis

2) What are the underlying mechanisms accounting for this disorder? The kidney normally needs to replace the decrease in bicarbonate from metabolism by excreting acid with PO4 or NH4+ and bicarbonate is released into circulation. Normally the kidney needs to have net acid excretion or make new bicarbonate of about 1 meq/kg/day. In chronic renal failure the kidney is not able to make enough bicarbonate due to decreased number of functioning nephrons leading to decreased ammoniogenesis

PROBLEM 2 A 42-year-old known alcoholic is brought to the hospital in coma. Physical exam revealed an afebrile patient, BP 120/80, P 86 regular, R 24. The odor of ethanol was absent as was jaundice. Apart from mild hepatosplenomegaly and coma without localizing signs, his exam was negative. Retinal exam was not done. Laboratory data revealed: BUN Glu K HCO3 30 mg% 90 mg% 5.0 10 Creat Na C1 pH PCO2 1.5 mg% 140 105 7.26 23

Serum osmolality was 340 mosm% Serum ketones were negative

Questions: 1. What disease entities should one think of in the alcoholic with a high AG acidosis? Methanol metabolized to formic acid Ethylene glycol metabolized to oxalic acid Alcohol causing either a alcoholic lactic acidosis or alcoholic ketoacidosis. MUDPILES should be MUKPILES since the D is diabetic ketoacidosis but there is also alcoholic and starvations ketoacidosis.

2.

How does the serum osmolality help in the diagnosis?

The calculated serum osmolality = 2 Na + BUN/2.8 + glucose/18 With both methanol and ethylene glycol these are osmoles but not part of the calculated osmolality. You use the osmolal gap ie measured osmolality minus calculated osmolality. If it is increased then there is some unmeasured osmol In this case 340 296 = 44 and normal <10

3.

Suppose the urine sediment revealed many calcium oxalate crystals? What disease would this suggest and how should it be treated?

Ethylene glycol since metabolized to calcium oxalate 4. Why is it especially important to examine the fundi in this setting?

Methanol can cause blindness The treatment is to give alcohol to utilize alcohol dehydrogenase and dialyze

PROBLEM 3 A 23-year-old woman with no significant past medical history enters the hospital with a 5-day history of diarrhea. She denies any drug ingestion. Physical examination shows mild dehydration, mild bilateral lower quadrant tenderness and active bowel sounds. The following laboratory data were obtained:

BUN Na K C1 HCO3

35 140 3.6 115 15

Creatinine pH PCO2 UNA UCI UK

1.5 7.34 30 10 mEq/L 80 mEq/L 30 mEq/L

Urinalysis revealed clear, yellow urine without glycosuria or ketonuria, 1+ protein, SG 1.020 and a pH of 5. Urine sediment was unrevealing. Questions: 1. What is the acid-base abnormality and what is the differential diagnosis of such disorders?

Non anion gap metabolic acidosis with respiratory compensation. Winters formula expected pCO2 = 1.5 (15) + 8 +/- 2 = 30 34 so compensated metabolic acidosis. Most common causes are diarrhea and renal tubular acidosis 2. What is the most likely cause of the acid-base disorder in this patient and what is the mechanism by which it occurs? Loss of bicarbonate in the diarrheal fluid

3. What is the mechanism for the urine anion gap (UNa + UK UCI) of 40? The reason there is an increased chloride causing a negative urine anion gap is due to the fact the kidney is trying to compensate for the decreased bicarbonate by making bicarbonate due to increased ammoniogenesis. Ammonium NH4+ needs to be secreted with an anion which is chloride. This is why you have the negative anion gap

PROBLEM 4 JL is a 45 year old alcoholic who stopped drinking last week and has had frequent episodes of vomiting. He presents to the emergency room complaining of numbness and tingling of his mouth and fingers and generalized fatigue. BP 110/65 sitting, 95/56 standing, P 95 sitting, 110 standing. Apart from poor skin turgor, mild hepatomegaly, no edema, very mild hyperreflexia, his physical exam was negative. Chvosteks sign was positive and the BP cuff was inflated to a pressure midway between systolic and diastolic to check for a Trousseaus sign which was not elicited. Lab: Na K CI HCO3 BUN 127 2.5 75 40 30 Creatinine pH PCO2 1.2 7.59 43

Urine: Na 40, K 75, C1 2 mEq/L

Questions: 1. What is your acid-base diagnosis?

Metabolic alkalosis due to increased pH. The expected pC02 for metabolic alkalosis is variable ie 4-7 mm Hg for every 10 increase in HCO3. In this case HCO3 is increased 40-25 ie 15 so expect pCO2 to be increased 6 10 but most patients due to acutet illness do not decrease their alveolar ventilation to see that much of an increase in pCO2 as in this case. Officially since pCO2 is not increased as expected you can say primary respiratory alkalosis but normally not clinically important. 2. What is the pathophysiology of the disorder? Loss of acid in vomitus causes increased bicarbonate. Initially the bicarbonate exceeds the renal threshold and is lost with a cation either Na or K. Due to subsequent volume depletion leading to increased A2, aldosterone, catecholamines the patient is able to reabsorb more bicarbonate causing an increased bicarbonate in the blood. The urine chloride is low due to volume depletion ie the patient is trying to absorb as much sodium as possible with any anion. If the filtration of sodium bicarbonate is higher than reabsorption then bicarbonate will be excreted with cations sodium and potassium. This is one example of where urinary sodium is high but chloride is low. There should not be any ammonium since alkalemic and that shuts off ammoniogenesis. 3. What is the mechanism(s) to explain the low serum K? Mainly loss with bicarbonate in urine Increased aldosterone Intracellular shift due to alkalemia Minimal lost in the vomitus 4. What is the mechanism(s) to explain the decreased serum Na and how do you explain the urinary Na of 40 and the urinary CI of 2? Decreased serum sodium predominantly due to volume depletion leading to non osmotic release of ADH. Another contributing to the hyponatremia is decreased total body K causing water to leave intracellular space and go extracellular. The urinary sodium and chloride explanation is above

5.

How would you treat the patient and why?

Aggressive fluids ie normal saline and potassium. By giving fluids in form of normal saline that will restore volume and shut off non osmotic release of ADH. In addition the replacement of K will help the decreased serum sodium..You know when the patient is euvolemic ie when the kidney starts to excrete chloride

PROBLEM 5 A 58 year old man with a long history of smoking presents with increasing dyspnea and edema and is admitted. His exam is remarkable for BP 130/80, P 100, RR 20. His exam is remarkable for stigmata of chronic obstructive disease, JVP of 15 cm, a subxiphoid PMI, a pulsatile liver and 3+ edema. ABG on R.A.: pH 7.32, pCO2 60, pO2 50, HCO3 30. 1. What is the acid-base disturbance?

Chronic respiratory acidosis based on decreased pH increased pCO2 and renal compensation. Chronic respiratory acidosis is characterized by for every 10 increase in pCO2 the bicarbonate increases about 3.5 ie so in this case pC02 of 60 expect HCO3 to be increased (60-40) x .35 ie 7 so about 31 so close enough

He is given O2 and aggressive diuretics. Two days later his ABG on 2 L/m: pH 7.42, pCO2 65, pO2 60, HCO3 40. 2. What is the acid-base disturbance?

Since normal pH implies at least two disorders in this case chronic respiratory acidosis and primary metabolic alkalosis. You never respiratory of renal compensate to a normal pH

3.

What is the mechanism for the increased HCO3?

Serum HC03 = Total body bicarbonate/Volume of distribution. With diuretics by increasing distal delivery of Na that leads to increased secretion of H+ due to increased aldosterone but mainly you lose fluid that does not have bicarbonate so that leads to a decreased volume of distribution ie contraction alkalosis