the good, the bad, and the ugly bruce wall, md october 9 th, 2006

The Good, the Bad, and the Ugly

Bruce Wall, MD

October 9th, 2006

Case Presentation: admit 9/14/6

“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 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: 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

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:

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

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:

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:

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…

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

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:

A) Hyperkalemia

B) Increased plasma aldosterone levels

C) Increased delivery of sodium to distal tubule

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Hyperkalemia: definitions

TRANSIENT HYPERKALEMIA: likely from net release of K+ from cells (will review 12 different potential causes)

PERSISTENT HYPERKALEMIA: requires impairment of urinary K+ excretion (low aldosterone or low Na+ delivery)

Increased K+ release from cells:

(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)


(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:

(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


(4) TISSUE CATABOLISM:

Trauma, tumor lysis syndrome, acute hypothermia, and acute renal failure

(5) EXERCISE:

Very small effect (without ARF); K+ may rise during exercise and fall, post.


(6) Beta adrenergic blockade:

Therefore, beta agonists are used to Rx hyperkalemia

(see figure)


(7) DIGITALIS TOXICITY:inhibition of Na+-K+-ATPase pump

(8) HYPERKALEMIC form of PERIODIC PARALYSIS

point mutation in gene for alpha subunit of skeletal muscle sodium channel

(9) SUCCINYLCHOLINE


(10) Calcineurin inhibitors:Neoral® brand of cyclosporin and Prograf® brand of tacrolimus

Activate ATP dependent K+ channels (plus chronic renal disease)

(11) K+ based PCN: rarely in neonates (12) Stored RBC’s: rarely in CKD pts

REDUCED URINARY K+ Excretion: Persistent Hyperkalemia

HYPOALDOSTERONISM:multiple causes: deficiency and resistance

CKD: K+ excretion generally maintained in advanced CKD as long as both aldosterone secretion and distal flow are maintained

Reduced urinary K+ excretion: 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?

GI symptoms remains a mystery…

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

Case reports

Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole Alappan, et al, Ann Inter Med 1996 Feb 1

105 pts; serum K+ increased by 1.21mmol Worse in diabetics; worse if creat > 1.3mg%

Case reports

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:

Trimethoprim-induced hyperkalemia: An analysis of reported cases

Marinella: Gerontology 1999 Jul-Aug 45

Literature search: 9 cases; mean age 76; mean duration 10days; baseline creat 1; baseline K+ 4.55Mean peak K+ 7.0mmol/Lno deaths

Dr. Allison Liddell

Comments on Bactrim

One last thought on urinary K+

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

the good, the bad, and the ugly bruce wall, md october 9 th, 2006

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