Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (54 page)

BOOK: Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine
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UAG → failure of kidneys to secrete NH
4
+ Ddx: distal or hypoaldo RTA, early renal failure
nb, plasma K usually ↓ in distal and ↑ in hypoaldo RTA
• UAG evaluation assumes Pt volume replete (U
Na
>25) & no AG met. acid. (which causes
UAG due to excretion of organic anions)

Renal tubular acidoses (RTAs)
(
JASN
2002;13:2160;
Int J Clin Pract
2011;65:350)


Proximal
(Type II): ↓ proximal reabsorption of HCO
3
1° (Fanconi’s syndrome = ↓ proximal reabsorption of HCO
3
, PO
4
, glc, amino acids), paraprotein (multiple myeloma, amyloidosis), meds (acetazolamide, heavy metals, ifosfamide), renal transplant, ↓ Vit D, NRTIs

Distal
(Type I): defective distal H+ secretion
1°, autoimmune (Sjögren’s, RA), nephrocalcinosis, meds (ampho, Li, ifosfamide); normally a/w ↓ K; if with ↑ K → sickle cell, obstruction, SLE, renal transplant

Hypoaldo
(Type IV): ↑ K → ↓ NH
3
synthesis/delivery → ↓ urine acid carrying capacity
↓ renin: diabetic nephropathy, NSAIDs, chronic interstitial nephritis, HIV
normal renin, ↓ aldo synthesis: 1° adrenal disorders, ACEI, ARBs, heparin
↓ response to aldosterone
  meds: K-sparing diuretics, TMP-SMX, pentamidine, calcineurin inhibitors
  tubulointerstitial disease: sickle cell, SLE, amyloid, diabetes
• Combined (Type III): rarely discussed or clinically relevant, also called juvenile RTA, has distal & proximal features, can be due to carbonic anhydrase II deficiency
Figure 4-2 Approach to metabolic acidosis

Treatment of severe metabolic acidoses (pH <7.2)
(
Nat Rev Nephol
2012;8:589)

• DKA: insulin & IVF; AKA: dextrose, IVF, replete K, Mg, PO
4
as needed
• Lactic acidosis: treat underlying condition, avoid vasoconstrictors
• Renal failure: hemodialysis
• Methanol & ethylene glycol: early fomepizole, vit. B
6
(ethylene glycol), folate (methanol), hemodialysis (esp. if late presentation) (
NEJM
2009;360:2216)
• Alkali therapy: NaHCO
3
(eg, three 50-mmol amps in 1 L D
5
W) to get serum HCO
3
>8 and pH >7.2 (estimate mmol of HCO
3
needed as 8-[HCO
3
]
serum
× wt × 0.5) side effects: ↑ volume, ↑ Na, ↓ ICa, ↑ P
a
CO
2
(& ∴ intracellular acidosis), overshoot
No proven benefit in lactic acidosis or DKA (
Annals
1986;105:836 & 1990;112:492)
• THAM (proton acceptor) in Pts w/ ↑ P
a
CO
2

METABOLIC ALKALOSIS

Pathophysiology

• Saline-responsive etiologies require
initiating event
and
maintenance phase

Initiating event:
gain of HCO
3
or loss of acid
loss of H
+
from GI tract or kidneys
exogenous alkali
: iatrogenic HCO
3
administration, milk alkali syndrome
contraction alkalosis
: diuresis → excretion of HCO
3
-poor fluid → extracellular fluid “contracts” around fixed amount of HCO
3
→ ↑ HCO
3
concentration
posthypercapnia
: respiratory acidosis → renal compensation with HCO
3
retention; rapid correction of respiratory disorder (eg, with intubation) → transient excess HCO
3

Maintenance phase
volume depletion
→ ↑ proximal reabsorption of NaHCO
3
and ↑ aldosterone (see next)
hyperaldosteronism
(either 1° or 2°) → distal Na reabsorption in exchange for K+ and H+ excretion (and consequent HCO
3
retention)
hypokalemia
→ transcellular K+/H+ exchange; intracellular acidosis in renal proximal tubular cells promotes bicarbonate reabsorption and ammoniagenesis

Workup

• Check
volume status
and
U
Cl
U
Cl
<20 mEq/L → saline-responsive
U
Cl
>20 mEq/L → saline-resistant (unless currently receiving diuretics)
(U
Na
unreliable determinant of volume status as alkalemia → ↑ HCO
3
excretion → ↑ Na excretion; negatively charged HCO
3
“drags” Na+ along)
If U
Cl
>20 and volume replete, ✓
blood pressure
Figure 4-3 
Approach to metabolic alkalosis

Treatment of severe metabolic alkalosis (pH >7.6)

• If volume depletion: d/c diuretics and correct volume deficit with isotonic saline If cardiopulmonary disease precludes hydration, can use KCl, acetazolamide, HCl • If NGT drainage that cannot be stopped: PPI • Hyperaldosteronism: treat underlying condition

RESPIRATORY ACIDOSIS

Etiologies


CNS depression
: sedatives, CNS trauma, O
2
in chronic hypercapnia (↓ hypoxemic drive), central sleep apnea

Neuromuscular disorders
: myasthenia gravis, Guillain-Barré, poliomyelitis, ALS, muscular dystrophy, severe hypophosphatemia, high spinal cord injury, drugs (paralytics)

Upper airway abnormalities
: acute airway obstruction, laryngospasm, obstructive sleep apnea, esophageal intubation

Lower airway abnormalities
: asthma, COPD

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