Transcript The Good, the Bad, and the Ugly

The Good, the Bad, and
the Ugly
Bruce Wall, MD
October 9th, 2006
Case Presentation: admit 9/14/6
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“I am feeling tired every morning…”
HPI: 81 yo WM with HBP, remote tobacco,
and ASCVD. Complains of mid epigastric
‘discomfort’, with 15lb weight loss @ 6
months. Worse in the morning, better in the
afternoon. Denies ‘pain’, change in bowel
habits, blood in stool, or substernal
symptoms. Appetite is better in the afternoon.
No response to Reglan, PPI, or prn use of
Tums. Gastroenterologist admitted patient for
current symptoms, and noted @ K+ 7.2meq/L.
HPI: continued
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No recent exposure to ACE/ARB, NSAID’s, Diuretics,
(including aldactone, amiloride, or triamterene).
He denies any CURRENT voiding problems - S/P TURP in
April 2006, complicated by severe post operative
hyponatremia (resolved by discharge). Baseline CKD with
BUN 35mg%, Creatinine of 1.7mg%, both pre and post
prostate resection.
Repeat K+ level drawn confirmed the hyperkalemia.
Dietary intake of potassium likely quite low. No salt substitute.
No family history of unexplained hyperkalemia.
CT scan on admission, without contrast, was negative for
obstruction.
No history of extreme temperature or exertion
No subcutaneous Heparin exposure
Past History:
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Chronic Kidney Disease: “ CKD ”
Baseline creatinine of 1.7mg% - estimated
GFR: (140-age)/creat = 34.7ml/min
MDRD equation: ml/min/1.73sqmeters =
186 x (SCr)power-1.54 x (age)power-0.203
x (0.742) (female) X 1.21 (AfricanAmerican)
= 38.6ml/min/1.73sqmeters
Glofil ( Iodine 131 isotope): not done
Chronic Kidney Disease
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Stage I: > 90 ml/min
Stage II: 60 - 89 ml/min
Stage III: 30 – 59 ml/min
Stage IV: 15 – 29 ml/min
Stage V: < 15 ml/min
ICD9 codes: 585.1, etc…
Therefore this patient has stage III
disease
Past Medical History:
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1) Coronary artery disease, associated
with SSS, required previous stent
2) Hypertension, essential
3) BPH – S/P TURP June 2006
4) Gastritis – EGD biopsy January 2006
5) Villous adenoma – November 2004
History: continued
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Medications: ‘absolutely clueless’ –
Labetalol, Plavix, baby ASA, Lipitor,
& Procardia
Review of Systems: 80 pack year history
of smoking. Mid epigastric discomfort +/worsened after large meal. No evidence
of pancreatitis. No previous TIA or
classic claudication. Nocturia is minimal.
No bone pain or hypercalcemia.
Physical Exam:
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Height 5feet 6inches. Weight @ 130lbs. BP
120/66 P 80 regular R 16 unlabored
EKG contained P waves, and normal T’s
HEENT: mild wasting NECK: no bruits
LUNGS: slight prolonged expiration
HEART: RRR, no murmur, no tachy/brady
ABDOMEN: no bruits, non-tender, soft
EXTREMITIES: good pulses, no edema
NEURO/PSYCH: non-focal; poor historian
Laboratory exam:
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WBC 4K Hemoglobin 11.2gms Plts125K
Na+ 145 K+ 7.2 Cl- 105 HCO3 22 BUN
73 Creatinine 2.2 Mg++ 1.6
Blood cultures NEGATIVE
Urinalysis: 1+protein 1+leukocyte esterase
100 WBC’s/HPF 15-20 RBC’s/HPF
ESR 16
DIG level 1.9 LFT’s WNL
lipase 25 albumin 3.9 PSA 1.3
Stat renal sonogram negative for obstruction
No evidence of paraproteinemia / M spike
HYPERKALEMIA: input – output
= accumulation…
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Which is more efficient: ability of GI tract
to absorb water, or the ability of kidney to
excrete?
With normal renal function, most dietary
potassium is excreted in urine within 6-8
hours
Therefore, hyperkalemia is rarely caused
by dietary ingestion UNLESS low GFR
Therapy for hyperkalemia
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Do not forget hyperventilation
IV medications to drive K+ into cells
Diagnosis and correction of acidosis
Kayexalate therapy: PO vs Enema; case
reports of gastric rupture…
To Rx or not to Rx, that is the question
Is normal EKG, enough?
Causes of increased urinary K+
secretion:
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A) Hyperkalemia
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B) Increased plasma aldosterone levels
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C) Increased delivery of sodium to distal
tubule
©2006 UpToDate®
©2006 UpToDate® • www.uptodate.com
Licensed to Steven E. Rinner MD
SupportTag: [WEB006-66.141.170.183-1B815CF004-6]
Hyperkalemia: definitions
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TRANSIENT HYPERKALEMIA: likely
from net release of K+ from cells (will
review 12 different potential causes)
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PERSISTENT HYPERKALEMIA:
requires impairment of urinary K+
excretion (low aldosterone or low Na+
delivery)
Increased K+ release from cells:
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(1) PSEUDOHYPERKALEMIA:
- trauma during collection process
- spherocytosis
- leukocytosis > 150K
- thrombocytosis > 500K
- familial type of pseudohyperkalemia:
(likely from temperature dependent leak of
K+ that occurs after the collection)
Increased K+ release from cells:
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(2) METABOLIC ACIDOSIS:
related to requirement of cellular electroneutrality
0.6meq/L increase for every 0.1unit change in pH
less common in organic acidoses, i.e. lactic
acidosis and DKA (where K+ shift is actually
related to lack of insulin)
Increased release K+ from cells:
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(3) INSULIN DEFICIENCY &
HYPERGLYCEMIA
Relative decrease in insulin affects
transport of K+. This is an important
mechanism in DKA patients who may be
total body potassium depleted
©2006 UpToDate®
©2006 UpToDate® • www.uptodate.com
Licensed to Steven E. Rinner MD
SupportTag: [WEB006-66.141.170.183-1B815CF004-6]
Increased K+ release from cells:
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(4) TISSUE CATABOLISM:
Trauma, tumor lysis syndrome, acute
hypothermia, and acute renal failure
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(5) EXERCISE:
Very small effect (without ARF); K+ may rise
during exercise and fall, post.
Increased K+ release from cells:
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(6) Beta adrenergic blockade:
Therefore, beta agonists are used to Rx
hyperkalemia
(see figure)
©2006 UpToDate®
©2006 UpToDate® • www.uptodate.com
Licensed to Steven E. Rinner MD
SupportTag: [WEB006-66.141.170.183-1B815CF004-6]
Increased K+ release from cells:
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(7) DIGITALIS TOXICITY:
inhibition of Na+-K+-ATPase pump
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(8) HYPERKALEMIC form of PERIODIC
PARALYSIS
point mutation in gene for alpha subunit
of skeletal muscle sodium channel
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(9) SUCCINYLCHOLINE
Increased K+ release from cells:
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(10) Calcineurin inhibitors:
Neoral® brand of cyclosporin and
Prograf® brand of tacrolimus
Activate ATP dependent K+ channels
(plus chronic renal disease)
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(11) K+ based PCN: rarely in neonates
(12) Stored RBC’s: rarely in CKD pts
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REDUCED URINARY K+ Excretion:
Persistent Hyperkalemia
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HYPOALDOSTERONISM:
multiple causes: deficiency and
resistance
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CKD: K+ excretion generally maintained
in advanced CKD as long as both
aldosterone secretion and distal flow are
maintained
©2006 UpToDate®
©2006 UpToDate® • www.uptodate.com
Licensed to Steven E. Rinner MD
SupportTag: [WEB006-66.141.170.183-1B815CF004-6]
Reduced urinary K+ excretion:
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Chronic Kidney Disease – most consider
“multiple insults”
- oliguria
- dietary abuse
- crush injury
- medications
- decreased circulating volume
- acute rejection @ transplantation
- Lupus nephritis
- hyperkalemic form of type I RTA
What caused our patient’s
symptoms? Hyperkalemia?
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GI symptoms remains a mystery…
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Family members arrived with meds from home:
Bactrim DS BID for the 7 days
Trimethoprim 160mg / Sulfamethoxazole 800mg:
Indicated UTI, acute otitis, acute on chronic
bronchitis, shigellosis, PCP, and traveler’s
diarrhea
Contraindications: allergy, folate deficiency, CKD,
hepatic insufficiency, thiazides, MTX
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Case reports
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Hyperkalemia in hospitalized patients treated
with trimethoprim-sulfamethoxazole
Alappan, et al, Ann Inter Med 1996 Feb 1
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105 pts; serum K+ increased by 1.21mmol
Worse in diabetics; worse if creat > 1.3mg%
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Case reports
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Trimethoprim-sulfamethoxazole:
Hyperkalemia is an important complication
regardless of dose
Perazella et al; Clin Nephrol 1996 Sept
Increased incidence of hyperkalemia in
AIDS pts treated for PCP.
Trimethoprim acts like amiloride to reduce
urinary K+ excretion
Case reports:
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Trimethoprim-induced hyperkalemia: An
analysis of reported cases
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Marinella: Gerontology 1999 Jul-Aug 45
Literature search: 9 cases; mean age 76;
mean duration 10days; baseline creat 1;
baseline K+ 4.55
Mean peak K+ 7.0mmol/L
no deaths
Dr. Allison Liddell
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Comments on Bactrim
One last thought on urinary K+
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Urinary K+ excretion is of limited utility in
persistent hyperkalemia
Estimation of the transtubular potassium
concentration gradient (TTKG) will help separate
hypoaldosteronism from CKD or volume depletion
TTKG = [urine K / (urine osm/serum osm)] /
divided by the serum K+
Value < 7 suggestive of hypoaldosteronism, as
long as urine osm > serum osm, and U Na+ > 25