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Chapter 9: Fluid, Electrolyte, & Acid-Base Disorders

Chapter 9. Fluid, Electrolyte, & Acid-Base Disorders

A 28-year-old man with history of depression is found down and brought to the emergency department. He responds to voice, moves his extremities spontaneously, and opens his eyes to pain only. Initial vital signs: T 98.0°F, P 72, BP 118/65 mm Hg, RR 28 breaths/min, O₂ saturation 99% on a non-rebreather mask. Primary survey is within normal limits, secondary survey reveals only superficial abrasions. Initial laboratory data include

ABG: pH 7.36, Pco₂ 38 mm Hg, Pao₂ 173 mm Hg, HCO₃⁻ 20 mmol/L

CPK 125

Serum salicylate 824 mg/L (normal 30-300 mg/L)

Based on this patient’s history, examination findings and laboratory data, what is this patient’s acid-base derangement?

A. No disorder

B. Respiratory acidosis with appropriate renal compensation

C. Anion gap metabolic acidosis with appropriate respiratory compensation

D. Nonanion gap metabolic acidosis with appropriate respiratory compensation

E. Mixed metabolic acidosis and metabolic alkalosis

C. Anion gap metabolic acidosis with appropriate respiratory compensation. As above, values from an arterial blood gas are typically reported in this order: pH, pCO₂, paO₂, HCO₃⁻.

This patient's pH is normal, but near-acidotic. HCO₃⁻ and pCO₂ are both low. Decreased HCO₃⁻ will cause acidosis, while decreased pCO₂ will cause alkalosis, thus the patient's primary disorder is metabolic. His calculated anion gap is 22. pCO₂ is within the 36–40 mm Hg range of appropriate compensation predicted by1 Winter's formula, thus no concurrent respiratory disorder exists. Therefore, this patient has an anion gap metabolic acidosis with appropriate respiratory compensation. Respiratory compensation for metabolic disorders is rapid (note his hyperventilation), hence the normal pH.

If respiratory compensation were inappropriate, one would need to consider another, simultaneous process, in addition to alkalosis, eg, the respiratory acidosis which occurs in the later stages of salicylate poisoning, when central respiratory drive has been suppressed.

Note the patient's ΔΔ = 2.5. Considering this finding in isolation, one would conclude that the patient has a mixed anion-gap metabolic acidosis and metabolic alkalosis. This underscores the need to take into account all of the patient's data when making determinations of acid-base status. There is no additional evidence of a metabolic alkalosis, thus this additional disturbance is unlikely.

A 54-year-old alcoholic man is discovered to have a new gastric cancer. He reports 15 lb weight loss over the past month. Laboratory data includes an albumin of 2.4 g/dL, indicating significant longstanding malnutrition. Postoperatively, which of the following electrolyte derangements would be of initial concern, especially when he starts to eat or receive some other form of nutrition?

A. Hypophosphatemia

B. Hyperphosphatemia

C. Hypermagnesemia

D. Hyponatremia

E. Hyperkalemia

A. Hypophosphatemia. Refeeding syndrome occurs when a malnourished patient (eg, an elderly or alcohol-dependent patient, or a patient who has experienced recent weight loss) begins to consume calories or begins to receive intravenous glucose administration. Insulin levels rise, causing electrolytes which have shifted to the extracellular space during a period of starvation to shift back to the intracellular space for use in the construction of new proteins and cells. Refeeding also leads to increased intracellular requirements for PO₄³⁻ and Mg²⁺ due to increased ATP production and glucose metabolism, decreasing serum levels of these electrolytes even further. This all leads to hypokalemia, hypomagnesemia, and hypophosphatemia, any one of which may be fatal. For these reasons, electrolytes must be closely monitored and aggressively repleted in patients at risk for refeeding syndrome.

A 70-year-old man undergoes a laparoscopic cholecystectomy for acute cholecystitis. On postoperative day 1 he complains of light-headedness while attempting to transfer from his bed to a chair. His vital signs include T 99.1°F, P 82, BP 109/63 mm Hg, RR 14 breaths/min, O₂ saturation 99% on room air. The nurse informs you that he has had poor enteral intake since the operation, and his urine output has diminished to 10 mL/h. She also informs you that his intravenous access was lost soon after his surgery and was never reestablished. His BUN and Cr preoperatively were 16 mg/dL and 0.8 mg/dL, respectively. Laboratory data include

Urine Na 153 mmol/L Urine Cr 284 mg/dL

You suspect the cause of his orthostasis and oliguria is hypovolemia. Which of the following findings would most strongly confirm your hypothesis?

A. BUN:Cr ratio < 20

B. Fractional excretion of sodium (FENa) > 1%

C. FENa < 1%

D. Renal ultrasonography demonstrating normal kidney parenchyma and vasculature

E. Fractional excretion of urea nitrogen (FEUN) > 35%

C. FENa < 1%. In oliguric patients, FENa < 1% is indicative of pre-renal azotemia and intravascular volume depletion. BUN:Cr ratio > 20 is indicative of hypovolemia. FENa > 1% is indicative of intrinsic renal causes of oliguria, and should prompt workup including microscopic urine analysis and renal ultrasonography. Post-renal obstruction should be investigated if clinically suspected (eg, caused by benign prostatic hypertrophy in this 70-year-old male).

FENa is unreliable in patients taking diuretics. In such cases, FEUN should be calculated:

where U: urine, P: plasma, UN: urea nitrogen, BUN: blood urea nitrogen, Cr: creatinine.

Table 9–5.Common laboratory values distinguishing between oliguric pre-renal and intrinsic renal failure.

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Table 9–5. Common laboratory values distinguishing between oliguric pre-renal and intrinsic renal failure.

Test

Pre-renal value

Intrinsic renal value

Post-renal value

FENa

< 1%

≥ 1%

FEUN

< 35%

≥ 35%

BUN:Cr ratio

> 20

< 10

10–20

A 19-year-old woman arrives in the trauma bay after a helmeted motorcycle crash. She is hemodynamically unstable, and immediately taken to the operating room. Exploratory laparotomy reveals 3 L of hemoperitoneum, a grade 5 splenic laceration, and a grade 3 liver laceration. A splenectomy is performed and the liver laceration is packed. Inspection of the rest of the abdomen reveals no additional injuries. Two hours into the case anesthesia alerts you that her temperature is 93°F and her pH is 7.2; thus you decide to suspend the operation, leave her abdomen open, and admit her to the surgical intensive care unit (SICU) for resuscitation before returning to the operating room. Despite aggressive resuscitation with packed red blood cells (PRBCs) and other blood products, she remains hemodynamically unstable. Pelvic angiography reveals a bleeding right inferior gluteal artery, which is embolized. She is returned to the SICU for further resuscitation. You take over her care at this point, and notice that she has received 21 units of PRBCs, 19 units of fresh frozen plasma, and 20 units of platelets, but has not had her serum electrolytes checked in 5 hours. Which of the following electrolyte disorders is she most at risk for?

A. Hypocalcemia

B. Hypomagnesemia

C. Hyperkalemia

D. All of the above

E. None of the above

D. All of the above. Stored blood products are anticoagulated with trisodium citrate, which chelates Ca²⁺ from stored blood, disrupting the clotting cascade. In the setting of massive transfusion, such as this patient has undergone, normal hepatic metabolism of trisodium citrate may be overwhelmed, and Ca²⁺ (along with Mg²⁺) may be chelated from the blood, leading to hypocoagulability, hypocalcemia, and hypomagnesemia. Furthermore, stored pRBCs contain high levels of K⁺, the result of lysis of red blood cells. This is especially true of the older pRBCs often utilized in massive transfusion situations. For these reasons, serum electrolytes must be closely monitored and controlled in the setting of massive transfusion.

A 61-year-old woman undergoes a sigmoid colectomy for perforated sigmoid diverticulitis. Postoperatively she is transferred to the surgical intensive care unit, still intubated and mechanically ventilated. On postoperative day 3 she develops an ileus, and her orogastric tube is put to low wall suction. On postoperative day 8 she develops hypotension and tachycardia to 140 beats/min, and requires a norepinephrine infusion to maintain adequate mean arterial blood pressure. Laboratory data includes

ABG 7.32/40/154/20

What is the most likely explanation for her acid-base disorder?

A. AG metabolic acidosis with adequate respiratory compensation

B. Mixed metabolic alkalosis and AG metabolic acidosis

C. Metabolic alkalosis with respiratory compensation

D. Mixed metabolic alkalosis and respiratory acidosis

E. Mixed AG metabolic acidosis and respiratory alkalosis

B. Mixed metabolic alkalosis and AG metabolic acidosis. The patient is acidotic, with a normal pCO₂, low-normal HCO₃⁻, and high anion gap. Therefore, this patient has an anion-gap metabolic acidosis. Given the clinical circumstances, the most likely etiology of her metabolic acidosis is lactic acidosis caused by septic shock.

Note that the patient's pH is significantly below the lower limit of normal, despite the normal pCO₂ and low-normal HCO₃−. This should prompt concern for a mixed acid-base disorder. Her ΔΔ = 2, indicating a coexistent metabolic alkalosis. The several days of gastric suctioning provides a ready explanation for this component of her mixed acid-base disorder.

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Chapter 9: Fluid, Electrolyte, & Acid-Base Disorders

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