Acid base disturbances are major causes of ICU deaths
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Board Review
Acid Base Disorders
7/2/2013
Metabolic Acidosis
•Anion Gap Acidosis = decrease in bicarbonate
due to presence of unmeasured acid (lactate)
•Non-Anion Gap Acidosis = lack of bicarbonate
in which chloride increases to maintain
neutrality (Diarrhea)
Metabolic Acidosis
•Mixed Picture
–Calculate corrected bicarbonate
Corrected Bicarbonate = 24 –ΔAnion Gap
Measured > Corrected = Metabolic Alkalosis
Measured < Corrected = Normal Anion Gap Acidosis
Anion Gap Metabolic Acidosis
•Propofol-Related Infusion Syndrome
–IV dosing > 4 mg/kg/h for more than 48 hours can
induce lactic acidosis
–Also leads to rhabdomyolysis, hyperlipidemia, and J-
point elevation on EKG
•D-Lactic Acidosis
–Occurs in short bowel syndrome after bowel
resection; secondary to carbohydrate conversion to D-
lactate by flora in the colon
–Symptoms include: confusion, slurred speech, and
ataxia
Non-Anion Gap Metabolic Acidosis
•Use the Urine Anion Gap
–AG = Na + K –Cl
•AG Negative = presence of ammonium and
appropriate kidney response to metabolic
acidosis (Diarrhea)
•AG Positive = no ammonium and inadequate
kidney response to acidosis (RTA)
Type I RTA
•Impaired excretion of hydrogen ions
•Leads to urine pH > 6.0 and nephrocalcinosis
Type II RTA
•Reduction of bicarbonate reabsorption
•Bicarbonate eventually becomes reabsorbed
once serum level falls low enough
•Urine eventually becomes devoid of
bicarbonate and pH becomes < 5.5
(chronically)
Type IV RTA
•Usually associated with hypoaldosteronism
•Hyperkalemia
•Urine pH < 5.5
Metabolic Alkalosis
•Saline Responsive with decreased ECF and
intravascular volume (Vomiting, Diuretic use)
–Use normal saline
•Saline Responsive with Increased ECF and
decreased intravascular volume (CHF,
Cirrhosis)
–Use acetazolamide (blocks carbonic anhydrase
leading to blocked secretion of hydrogen ions
and increased excretion of bicarbonate)
A 56-year-old man is evaluated in
the emergency department after his
wife found him unconscious. She
reports that he has a history of
alcohol abuse. He is treated with
lorazepam, thiamine and 1 L of
D5/NS. Upon arrival, he has a
generalized seizure that resolves
spontaneously.
Laboratory studies:
Initial 30 Minutes Later
Blood urea
nitrogen
56 mg/dL (20
mmol/L)
42 mg/dL (15
mmol/L)
Serum creatinine
1.6 mg/dL (141
µmol/L)
1.5 mg/dL (133
µmol/L)
Electrolytes
Sodium
133 meq/L (133
mmol/L)
135 meq/L (135
mmol/L)
Potassium
3.5 meq/L (3.5
mmol/L)
3.4 meq/L (3.4
mmol/L)
Chloride
92 meq/L (92
mmol/L)
97 meq/L (97
mmol/L)
Bicarbonate
16 meq/L (16
mmol/L)
20 meq/L (20
mmol/L)
Ethanol
88 mg/dL(19
mmol/L)
-
Glucose
90 mg/dL(5.0
mmol/L)
102 mg/dL (5.7
mmol/L)
Osmolality 320 mosm/kg H
2O-
Arterial blood gas
studies (ambient
air):
pH 7.15 7.30
PCO
2 40 mm Hg (5.3 kPa)37 mm Hg (4.9 kPa)
PO
2
86 mm Hg (11.4
kPa)
92 mm Hg (12.2
kPa)
Urinalysis
pH 5.4; trace
protein; 1+
ketones; few
hyaline casts
Which of the following is the most
appropriate next step in
management?
A Fomepizole
B Hemodialysis
C Sodium bicarbonate
D Supportive care
•AG acidosis with respiratory acidosis (normal
PCO
2in setting of acidosis)
•Seizure related lactic acidosis with alcoholic
ketoacidosis
•Respiratory Acidosis secondary to postictal
state
•Improves with volume repletion and
supplemental glucose
•No osmolalgap when you add ethanol
–320-314 = 6 (no gap)
–No indication for fomepizoleif no osmolargap
(methanol or ethylene glycol ingestion)
•HD not indicated as no toxic ingestion is
suspected
•Sodium bicarbused only to keep pH > 7.15
A 42-year-old man hospitalized for recurrent variceal
bleeding is evaluated for severe metabolic alkalosis. He
has a 4-year history of alcoholic cirrhosis. He required
six units of packed red blood cells and four units of
fresh frozen platelets to maintain hemodynamic
stability.
On physical examination, temperature is normal, BP is
100/70 mm Hg, and HR is 96/min. Cardiopulmonary
examination is normal. Ascites is noted. There is 2+
presacral edema and 2+ leg edema.
Laboratory studies:
On AdmissionHospital Day 2
Serum
creatinine
1.2 mg/dL (106
µmol/L)
-
Electrolytes
Sodium
138 meq/L (138
mmol/L)
136 meq/L (136
mmol/L)
Potassium
3.8 meq/L (3.8
mmol/L)
5.0 meq/L (5.0
mmol/L)
Chloride
105 meq/L (105
mmol/L)
85 meq/L (85
mmol/L)
Bicarbonate
21 meq/L (21
mmol/L)
38 meq/L (38
mmol/L)
Urine chloride-
<5 meq/L (5
mmol/L)
(normal range
for men, 25-371
meq/L [25-371
mmol/L])
Arterial blood
gas studies
(ambient air):
pH - 7.52
PCO
2 -
48 mm Hg (6.4
kPa)
Which of the following is the
most appropriate management?
A Add acetazolamide
B Add furosemide
C Add isotonic saline
D Discontinue octreotide
•Metabolic alkalosis from metabolism of citrate
in blood products (increase bicarbonate)
•Impaired excretion of bicarbonate due to poor
renal perfusion from cirrhosis because of
increased proximal reabsoprtion of
bicarbonate
•Acetazolamide will improve both alkalosis and
volume retention
•Furosemide facilitates sodium chloride
excretion, not bicarbonate excretion
•Saline would worsen fluid status as patient has
increased ECF
A 23-year-old woman is evaluated in the
emergency department for a 2-month history of
progressive leg weakness. She reports no
diarrhea or weight loss. Medical history is
remarkable for Sjögren syndrome. She takes no
medications.
On physical examination, vital signs are normal.
Diffuse weakness is noted most prominently in
the legs, graded at 3/5.
Laboratory studies:
Albumin 4.5 g/dL (45 g/L)
Blood urea nitrogen13 mg/dL (4.6 mmol/L)
Calcium 9.1 mg/dL (2.3 mmol/L)
Serum creatinine 1.1 mg/dL (97.2 µmol/L)
Electrolytes
Sodium 141 meq/L (141 mmol/L)
Potassium 1.9 meq/L (1.9 mmol/L)
Chloride 117 meq/L (117 mmol/L)
Bicarbonate 14 meq/L (14 mmol/L)
Magnesium 2.2 mg/dL (0.91 mmol/L)
Phosphorus 3.5 mg/dL (1.13 mmol/L)
Total protein 8.9 g/dL (89 g/L)
Urine anion gap Positive
Urinalysis
Specific gravity 1.014; pH
7.0; no blood; trace
protein; no glucose; no
leukocyte esterase; no
nitrites
Which of the following is the most
likely diagnosis?
A Gitelman syndrome
B Distal (type 1) renal tubular
acidosis
C Laxative abuse
D Proximal (type 2) renal tubular
acidosis
•Normal AG and hypokalemia
•Inability to secret hydrogen ions = pH > 6.0
•Calcinosis
•Positive urine AG (no ammonium in the urine)
•Gitelman syndrome leads to metabolic
alkalosis and is associated with
hypomagnesemia
•Laxative abuse would have a negative urinary
AG (appropriate kidney response to acidosis)
•RTA Type II has urine pH < 5.5 (bicarbonate is
eventually reabsorbed once serum level has
fallen enough)
An 18-year-old woman is evaluated for a 6-
month history of progressive weakness and a
11-lb weight loss. She reports increased fatigue
and myalgiafollowing exercise during the past 2
months.
On physical examination, the patient is thin.
Temperature is 97.6 °F, BP is 110/60 mm Hg, HR
is 96/min. BMI is 18. The remainder of the
examination is unremarkable.
Laboratory studies:
Blood urea nitrogen 4 mg/dL (1.4 mmol/L)
Serum creatinine 0.5 mg/dL (44.2 µmol/L)
Electrolytes
Sodium 135 meq/L (135 mmol/L)
Potassium 3.1 meq/L (3.1 mmol/L)
Chloride 108 meq/L (108 mmol/L)
Bicarbonate 18 meq/L (18 mmol/L)
Urine studies:
Creatinine
120 mg/dL (normal range
for women, 15-327 mg/dL)
Sodium
22 meq/L (22 mmol/L)
(normal range for women,
15-267 meq/L [15-267
mmol/L])
Potassium
15 meq/L (15 mmol/L)
(normal range for women,
17-164 meq/L [17-164
mmol/L])
Chloride
45 meq/L (45 mmol/L)
(normal range for women,
20-295 meq/L [20-295
mmol/L])
Urea
112 mg/dL(normal range
for women, 132-1629
mg/dL)
Osmolality
290 mosm/kg H
2O (normal
range, 300-900 mosm/kg
H
2O)
Urinalysis
Specific gravity 1.012; pH
5.8; no blood, protein,
glucose, leukocyte esterase,
ketones, or nitrites
Which of the following is the
most likely cause of this
patient's acid-base disorder?
A Diuretic abuse
B Distal (type 1) renal tubular
acidosis
C Laxative abuse
D Surreptitious vomiting
•Normal anion gap metabolic acidosis
•Urine anion gap is negative ( 22 + 15 –45) = -8
•Bicarbonate loss exceeds increased
ammonium excretion
•Diuretic abuse and vomiting leads to
metabolic alkalosis
•RTA Type I would expect a positive urine anion
gap
A 42-year-old man is evaluated in the emergency
department for increased confusion. He has
psoriasis and was treated with cream and a body
wrap for 1 hour. He subsequently developed
nausea and vomiting. He reports hearing water in
his ears. He also has hypertension and type 2
diabetes mellitus complicated by proteinuria.
Medications are enalapriland metformin.
On physical examination, the patient is irritable,
anxious, and intermittently somnolent but easily
aroused. Temperature is 99.7 °F, BP is 160/100 mm
Hg, HR is 106/min standing, and RR is 20/min.
Laboratory studies:
Hemoglobin 14.4 g/dL (144 g/L)
Leukocyte count 6300/µL (6.3 ×10
9
/L)
Blood urea nitrogen 15 mg/dL (5.4 mmol/L)
Serum creatinine 1.3 mg/dL (115 µmol/L)
Electrolytes
Sodium 145 meq/L (145 mmol/L)
Potassium 3.6 meq/L (3.6 mmol/L)
Chloride 109 meq/L (109 mmol/L)
Bicarbonate 18 meq/L (22 mmol/L)
Glucose 158 mg/dL (8.8 mmol/L)
Lactic acid 7.2 mg/dL (0.8 mmol/L)
Osmolality 308 mosm/kg H
2O
Arterial blood gas studies
(ambient air):
pH 7.51
PCO
2 35 mm Hg (4.7 kPa)
PO
2 96 mm Hg (12.8 kPa)
Urinalysis
Specific gravity 1.024; pH
6.0; trace blood; 2+
protein; 1+ glucose; trace
leukocyte esterase; no
ketones, nitrites, cells, or
formed elements
Which of the following is the
most likely cause of this
patient's clinical presentation?
A Metformin toxicity
B Methanol toxicity
C Salicylate toxicity
D Sepsis
•Respiratory alkalosis
•Excessive decrease in bicarbonate (decrease
of more than 2 in bicarb when only 5 drop in
PCO
2)
•AG Metabolic acidosis also present
•Used oil of wintergreen (methyl salicylate)
•Mental status changes, nausea, fever,
vomiting and tinnitus
•Metformin Toxicity leads to lactic acidosis
(normal lactic acid level (6-16))
•Methanol poisoning leads to increased
osmolal gap (308-304 =4)
•Sepsis unlikely based on clinical picture and
absence of leukocytosis
A 41-year-old woman is evaluated during a follow-up visit for high blood
pressure. On physical examination, blood pressure is 162/100 mm Hg, which
is similar to the values measured at her initial visit. Other vital signs are
normal. BMI is 21.
Laboratory studies are normal.
Which of the following is the most appropriate next step in the management
of this patient's hypertension?
A Combination drug therapy
B Lifestyle modifications
C Single-drug therapy
D Reevaluate patient in 2 weeks
•Stage 2 HTN ( SBP > 160 or DBP > 100)
•Goal for this patient is 140/90
•If require reduction of SBP > 20 or DBP > 10,
combination therapy is recommended
•Can shorten time for needed for medication
adjustment
•Can increase likelihood of BP goal
An 81-year-old man is evaluated for progressive
fatigue. Nine months ago, he was diagnosed with
giant cell arteritis; at that time, prednisone,
omeprazole, risedronate, and vitamin D were
initiated. His symptoms improved, and the
prednisone was tapered. Five months ago he
began to feel more fatigued. Evaluation was
unremarkable other than the urinalysis, which
was positive for leukocytes and leukocyte
esterase. He was treated with ciprofloxacin
without improvement of his symptoms. A
subsequent urine culture was negative.
Laboratory studies:
Hemoglobin 10.7 g/dL (107 g/L)
Leukocyte count
8700/µL (8.7 ×10
9
/L)
(65% neutrophils, 23%
lymphocytes, 11%
monocytes, and 1%
eosinophils)
Platelet count 198,000/µL (198 ×10
9
/L)
Blood urea nitrogen51 mg/dL (18.2 mmol/L)
Serum creatinine
3.1 mg/dL (274 µmol/L)
(baseline: 1.1 mg/dL
[97.2 µmol/L])
Lactate dehydrogenase80 units/L
Urinalysis
Specific gravity 1.014; pH
6.0; trace protein; +
leukocyte esterase;
occasional leukocytes;
rare erythrocytes;
occasional hyaline casts
Which of the following is the most
likely diagnosis?
A Acute interstitial nephritis
B Acute tubular necrosis
C Glomerulonephritis
D Thrombotic thrombocytopenic
purpura
•Hypersensitivity to medication
•PPI is common
•Eosinophils on differential
•Leukocytes and possibly leukocytes casts with
negative culture
•ATN presents with muddy brown casts
•Can be induced by bisphosphonates
•Giant cell arteritis affects large blood vessels,
not usually small vessels of kidneys
•Would expect dysmorphic erythrocytes and
erythrocyte casts
•TTP would see thrombocytopenia and
microangiopathic hemolytic anemia
A 26-year-old man is evaluated in the emergency
department after being found on the floor in his
apartment by friends who had not seen him in several
days.
On physical examination, the patient is somnolent and
minimally responsive. Temperature is 37.2 °C (98.9 °F),
blood pressure is 92/54 mm Hg, pulse rate is 118/min, and
respiration rate is 14/min with 97% oxygen saturation on
ambient air. BMI is 25. Skin is mottled and edematous on
the posterior surface of the legs, buttocks, and back.
Neurologic examination reveals no focal or lateralizing
findings. The remainder of the examination is normal.
Laboratory studies:
Blood urea nitrogen 174 mg/dL (62.1 mmol/L)
Calcium 7.8 mg/dL (2.0 mmol/L)
Creatine kinase 125,000 units/L
Serum creatinine 8.3 mg/dL (734 µmol/L)
Electrolytes
Sodium 151 meq/L (151 mmol/L)
Potassium 5.8 meq/L (5.8 mmol/L)
Chloride 121 meq/L (121 mmol/L)
Bicarbonate 19 meq/L (19 mmol/L)
Glucose 94 mg/dL (5.2 mmol/L)
Phosphorus 8.5 mg/dL (2.75 mmol/L)
Urinalysis
Specific gravity 1.012; pH
6.5; 3+ blood; 1+ protein;
0-5 erythrocytes/hpf; 1-3
leukocytes/hpf; dark
granular casts
Toxicology screeningPending
Which of the following is the most
appropriate treatment for this patient?
A Hemodialysis
B Intravenous mannitol
C Rapid infusion of intravenous 0.9%
saline
D Rapid infusion of intravenous 5%
glucose