Acid/Base
Saleem Bharmal
1/6/2009
HPI:
• 75 year old M with PMHx of DM, HTN, CKD (baseline Cre 3.0),
bladder cancer s/p resection and orthotopic neobladder who was
initially admitted for workup of intermittent chest pain.
• On admission labs patient was noted to be in acute on chronic renal
failure with a Cre of 4.9 and was noted to have a serum HCO3 of 7.
• Patient at time of admission described some shortness of breath
and weakness. He denied any diarrhea, recent illness or
nausea/vomiting.
• He did state that he his urine contained more mucous which in the
past represented possible infection of the neobladder. Patient wife
straight cath neobladder daily and flushes it.
• Per patient wife he has a night bag to collect urine and is usually full
in the AM, but she noticed over the last few night the amount of
urine in the bag has progressively declined.
Past Medical History
•
•
•
•
•
IDDM
CKD stage IV, baseline Cre 3.0
Bilateral Renal Artery stenosis; s/p RAS stent to R
CAD s/p stent
S/P bladder resection for neoplasm and
orthotopic neobladder
• Anemia
• COPD (FEV1 65%)
• Hyperlipidemia
Outpatient Medications
•
•
•
•
•
•
•
•
Aspirin
Plavix
Imdur
NPH
Diltiazem
Labetalol
Ranitidine
Valsartan
•
•
•
•
•
•
•
Repaglinide
Albuterol
Spiriva
Vit D
Zocor
KCL 20meq daily
Lasix 20mg daily prn
(for leg swelling)
Physical Exam
T 97.2 P 87 BP 157/55 R 16 O2Sat 97% Wt 66 kg
Gen: Elderly male in NAD. Pt did not appear short of
breath of tachypnic
HEENT: MMM, no elevated JVD appreciated
Heart: S1/S2 no murmurs
Pulm: Clear to auscultation b/l, no crackles or wheeze
Abd: soft, NT ND; + bowel sounds, medial surgical scar
well healed
Ext: +1 pitting edema in LE bilaterally up to the knees
Neuro: AAOx3
Admission Labs and Studies
• WBC 10.7/HGB 8.3/HCT 25.7/PLT 99
• Na 140/K 4.7/CL 119/HCO 7/BUN 103/Cre 4.9/Gluc 112/Ca 8.0
• Anion Gap: 14
• Urinalysis: Yellow/clear/neg gluc/neg bili/neg ketones/
SG 1.011/trace blood/pH 7.0/prot 30/neg nit/+ leuk/4-8 WBC/1-3 RBC
• CXR: No evidence of focal consolidation, vascular congestion, or
pleural effusions
Brief Hospital Course
• Once admission labs were obtained ABG was
drawn which revealed:
ABG: 7.11/20.0/157/HCO3 6.0/lact 0.3
(This shows a primary metabolic acidosis with
appropriate respiratory compensation)
Brief Hospital Course
• Given the elevated creatinine patients ARB and
lasix were held.
• He had urine electrolytes sent as well as renal
ultrasound done:
Urine: Na 18 K 40 Cl 8 Cre 95 Osmolality 327
Calculated urine anion gap: (18+40) – (8) = + 50
• Renal U/S: No hydronephrosis; R 10cm L 9.6cm
Brief Hospital Course
• Given the low urine Na and decreased urine
output it was suspected that patient’s acute on
chronic renal failure could be secondary to
prerenal azotemia from intravascular volume
depletion.
• Patient was started on 3amp NaHCO3 in d5W
(134 meq NaHCO3) at 75ml/hr and started on
bicitra tabs 30ml po bid. NaHCO3 gtt was then
increased to 125ml/hr and Bicitra increased to
30ml q6.
Brief Hospital Course
• With IVF his Cre improved and returned to
baseline of 3.0 over 3 days. HCO3 gtt was
stopped after two days and serum HCO3
increased to 20. He was maintained on oral
Bicitra.
• A urine culture was sent, given WBC on U/A and
increased mucosal discharge from bladder, which
grew back positive for Klebsiella Pneumoniae
Differential of etiology of metabolic
acidosis
• Patient from, previous labs, at baseline appeared to have
an underlying metabolic acidosis with a serum HCO3
between 15-18. He was also noted to have a chronic
hypokalemia requiring him to take KCL supplementation.
• Patients underlying metabolic acidosis could be from CKD,
neobladder, Type I RTA (not type II RTA as urine pH 7.0
prior to getting HCO3 load).
• During admission patient had a more severe metabolic
acidosis than his baseline which could be attributed to
acute renal failure and or UTI in setting of neobladder.
Neobladder and other urinary
diversion and reconstructions
• Ureterosigmoidostomy: First surgical technique used, ureters are
implanted into the sigmoid colon and the anal sphincters were relied upon
to provide continence. No longer used as complications include chronic
UTI and decline in renal function, hyperchloremic acidosis, and
development of secondary cancers in the sigmoid colon
• Ileal loop conduit: Urine is directed from the ureters through a segment
of isolated ileum to the surface of the abdominal wall. Urine is collected
continuously via ostomy.
• Orthotopic neobladder: Internal reservoirs that are connected to the
native urethra and rely upon the external striated sphincter for
continence. Reservoirs are constructed from a segment of detubularized
intestine (usually ileum) anastomosed to the native urinary outflow tract
Metabolic Acidosis from Ureteral
Diversions
•
Hyperchloremic metabolic acidosis can result from reabsorption of excreted
metabolites through the intestinal mucosa.
•
Colon has an anion exchange pump with luminal chloride being reabsorbed as
bicarbonate is secreted
•
Colon can also absorb ammonium, which is derived both from the urine and from
urea-splitting bacteria.
•
This patient was found to have Klebsiella UTI which can cause hydrolysis of urea
into ammonium and hydroxyl ions.
•
Severe acidosis is a major problem usually only for ureterosigmoidostomy. It is less
frequent in the other procedures because they limit the amount of time that urine
is in contact with bowel mucosa.
•
In one series of 363 men with ileal neobladders, only 1 percent developed severe
metabolic acidosis, although nearly one-half required some form of alkalinizing
treatment due to mild acidosis.
Utility of Urine Anion Gap in this
situation?
Urine: Na 18; K 40; Cl 8
Calculated urine anion gap ([Na])+([K])-[Cl]: (18+40) – (8) = + 50
Urine anion gap =
unmeasured anions – unmeasured cations
• In the setting of metabolic acidosis excretion of NH4+ (unmeasured
cation) should increase if renal acidification is intact resulting in a
negative value.
• Urine anion gap that is positive in a setting of non (high) anion gap
acidosis suggests impaired H+ and NH4+ excretion which can be
seen in renal failure, or type 1 and type 4 RTA
Utility of Urine Anion Gap in this
situation?
• However in this case measurement of urine anion gap could be
misleading because patient has neobladder and also may have had
volume depletion.
• Volume Depletion: Volume depletion causes increased proximal Na
retention. This causes decreased distal Na+ delivery to which
impairs distal acidification (similar to Type I RTA). Distal delivery of
Na+ can be reabsorbed by principal cells and can cause an
electronegative luminal gradient which promotes H+ secretion.
• Neobladder: Colon has anion exchange pump with luminal chloride
being reabsorbed as bicarbonate is secreted. This may result in
lower urine Cl measurement which would give you a positive urine
anion gap and may also explain the elevated urine pH in setting of
metabolic acidosis.
Worsening metabolic acidosis in
setting of renal failure
• Decreased GFR results in decreased titratable
acid in the urine
• Decreased ammonia production and
ammonium excretion
• Impaired ability of HCO3 reabsorption