Pee Your Heart Out:
By Gruber
A Patient with chest and belly pain with bradycardia and hypotension
60 yo woman with sob, palpitations and chest pain while driving. Recently has had
decreased exercise tolerance. Pt also notes crampy abdominal pain H/o HTN,
takotsubo cardiomyopathy, anxiety
85/55, 35, 24, 99.7 98%
nervous, repeatedly wetting her lips, cracked lips
lungs clear bilat
abd: mild suprapubic tenderness
ext: no edema
neuro intact
CXR unremarkable
1st EKG:
EKG: afib with slow ventricular response at 44 bpm with competing junctional
pacemaker
What is the differential for this bradycardia and hypotension?
-inferior STEMI with 2nd or 3rd degree block but this is not evident on ekg
-ca ch blker od; beta blker od; dig od, clonidine od
-hyperkalemia oftentimes presents with bradycardia
-vasovagal but there is no indication of this here
-neurogenic shock but no paralysis noted
-pts oftentimes become bradycardic and hypotensive prior to arresting but pt doesn’t
appear that sick
Labs
Na 123 K 8.1 Cl 99 HCO3 12 BUN 40 Cr 2.8 Glu 453 wbc 3.2 H/H 9.8/29.7 platelet 189
alk phos 272, AST/ALT 170/161
Issue: is this K real? In view of elev creatinine and slow ekg, hyperK is real and needs
immediate treatment
Pt treated for hyperk with insulin, dextrose, albuterol and calcium but not given
kayexellate as unclear about etiology of abd pain and kayexellate can cause serious GI
problems in pts with abnormal bowel function
Bradycardia resolved and pt in sinus rhythm but K 6.5 when repeated at 3hr
Pt subsequently found to be bradycardic again and pt c/o worsening abdominal pain
Pt given repeat doses of ca chloride, insulin, dextrose and albuterol but K noted to be
7.7
Pt notes that she has not peed since arrival in ED
Foley inserted with 2.5 liter of urine and resolution of abd pain
-Urine with large protein, large glucose, Na 121 Urine creat 38 and FeNa 7.4%
-Repeat serum K 6.2
Causes of renal obstruction
-upper tract: cancer, bilateral stones, retroperitoneal path such as tumor or hematoma
Hydroureter and or hydronephrosis would be seen on ultrasound with upper
tract obstruction
-lower tract: prostate,cancer, stone in urethra, anticholinergics
Critical Action Missed: With new onset of elevated creatinine, urinary obstruction
should have been considered especially in a pt with abdominal pain.
1-Urinary obstruction is generally an easily correctable problem and early recognition
and treatment are critical to preventing permanent renal failure. However, it is
oftentimes missed on inital presentation as the pt may not complain of not urinating and
you may forget to ask about this
2-Urinary retention may present with what appears to be a surgical abdomen but turns
out to be urinary retention resolved with placement of a foley catheter.
3-The patient may also present with an unstable arrythmia due to hyperkalemia or a
change in mental status due to uremia from urinary retention
4-This pt’s recurrent hyperkalemia despite standard treatment did not resolve until the
obstruction was relieved. It is critical not to miss post-obstructive renal failure as it can
cause life threatening problems.
5- Always get urine from a patient with abdominal pain (with or without renal failure) and
either place a foley or preferably u/s the bladder to see if it is full or empty. You may
relieve the pt’s “acute abdomen” and avoid an unnecessary CT by decompressing the
bladder.
6. Whenever an unremarkable urine is noted in patient with renal failure, urinary
obstruction should be considered
7-Progression of renal failure from prolonged obstruction may present with indices
consistent with ATN with elevated urine sodium, depressed osmolality and elevated
fractionated excretion of sodium FeNa>1%
Issue: is there a danger if the pt puts out too much urine after foley placement
(post-obstructive diuresis)?
This complication of obstruction typically occurs when the obstruction has been
prolonged and has resulted in renal failure or significant volume overload. Some authors
recommend monitoring pts with prolonged obstruction for 4 hours minimum for
significant hourly urinary output (>200 cc per hour over input) after initial return. If this
degree of output continues, admission is recommended with volume replacement
adjusted hourly according to urine output.
Issue: is there an advantage to gradual decompression of the bladder in terms of
avoiding hypotension?
Christensen found that 50% of the decrease in bladder pressure occurs after removal
of the first 100ml and therefore concluded that gradual decompression is unjustified
Issue: Can rapid decompression of bladder cause hematuria?
-Gould found in dogs that hematuria strongly correlated with bladder wall damage
before relief of obstruction and not to rate of emptying bladder.
Issue: Do you need to order bloods and check urine on every pt with urinary
retention?
Prolonged urine stasis predisposes patient to UTI, urosepsis and renal failure. Most pts
with urinary retention present shortly after not being able to urinate and do not require
labs and treatment for uti. However, pts with longer or unclear duration of urinary
retention should have labs drawn to evaluate for infection and renal failure.
Issue: is it possible for patient to have renal injury with normal creatinine?
It is possible to overlook significant renal injury without information about the pt's
baseline bun and creatinine. A pt with a very low baseline creatinine level can lose more
than half of their functioning nephons before developing an elevated Cr level
Issue: how useful are ekgs in evaluating for hyperkalemia requiring intervention?
Ekg is often the fastest screening test for hyperkalemia assuming no IStat is done, but
the sensitivity of ekg for a K >6.5 is only 14-60%. Contrary to textbook teaching on ekgs
and hyperkalemia, oftentimes there is no stepwise progression on the ekg ie peaked T
going to PR to loss of P to widening of the QRS.. A pt with an extremely high K may go
from normal ekg to vtach or a slow sinusoidal rythm.
Conclusion: do not be dissuaded from significant hyperk because of normal ekg
Issue: how useful are fluids, atropine, pacing or pressors in treating bradycardia
caused by hyperkalemia?
These measures will not work in hyperkalemia related bradycardia. Think hyperkalemia
if these medications are not working when you are treating pt with bradycardia. Note
that albuterol may be used at 4-8 times the regular nebulizer dose in treating
hyperkalemia. Tachycardia associated with albuterol is not a problem here
Issue: is calcium and bicarb indicated for this pt?
Calcium is indicated as this pt has high potassium and signicant ekg findings including
bradycardia and loss of p waves and is hypotense. The effect of calcium begins within
minutes and lasts 30-60 minutes. CaCl is recommended in the pt with hemodynamic
compromise because it contains 3 times as much calcium as Ca gluconate and also is
available quicker as it doesn’t require to be metabolized by the liver
If there isnt a central or deep anticubital vein access to avoid the skin necrosis
complications of CaCl extravasation, you can give Ca gluconate while waiting to get
better access for CaCl in the unstable pt. Always test that the line is working well before
giving calcium
Ca gluconate is indicated in the stable or relatively stable pt with hyperkalemia(which is
most of the time. As we have found that Ca gluconate can cause skin necrosis
requiring a skin graft if the vein is intiltrated, I like to dilate the calcium with 100cc of NS
and give it over 5-10 minutes assuming the pt is in danger of volume overload. Do not
push Ca gluconate. You can repeat the Ca dose if ekg changes do not normalize in 3-5
minutes. Although you can push CaCl (preferably over a minute if pt isn’t in arrest), do
not push Ca gluconate as it can cause hypotension if given rapidly
Bicarbonate has been shown to be ineffective in the first 1-2 hours in the hyperkalemic
pt who does not have significant acidosis . One series showed ,that prolonged bicarb
therapy in a constant infusion over 5hrs only lowered the K at 4-6 hrs in mildly acidotic
pts and most of the decline in K was from extracellular volume expansion. There is
limited data suggesting that bicarb is beneficial in the acute treatment of hyperkalemia
in the pt with profound acidosis ie serum HCO3 1.5-7.5.
Issue: what is the correct dose of dextrose and insulin for hyperkalemic patients
who are on hemodialysis or with significant renal failure?
The usual 10 unit bolus of regular insulin along with one amp of D50 (25gm of glucose)
results in hypoglycemia in up to 75% of HD pts typically occurring about one hr after the
bolus. This drop in glucose may be due to the decrease in clearance of insulin in the
HD pt. To avoid this complication, up-to-date recommends that the D50 bolus be
followed by an infusion of D10 at 50-75ml/hr with close glucose monitoring. Nebulized
albuterol administered with insulin has been shown to attenuate the hypoglycemic effect
of insulin. Nebulized albuterol was equally as effective as insulin in lowering K and the
hypokalemic effects of the 2 drugs was additive. Thus, assuming no cardiovascular
contraindications to the tachycardia with albuterol, giving the 2 drugs together results in
greater reduction of hyperK and less hypoglycemia than giving insulin alone
Lowering the dose of insulin or giving the insulin more slowly is another option to avoid
hypoglycemia but the K lowering effect of insulin is greater at the higher insulin
concentrations achieved with bolus therapy. Lower doses of insulin should also be
considered in the pt with significant liver disease.
.
The effect of insulin begins in 10-20 minutes, peaks at an hour and lasts 4-6hrs thus
providing an important complement to the short acting calcium. Repeat measurements
of serum glucose and K should be done at about 1 hour after insulin is given.
Issue: is kayexellate indicated for the treatment of hyperkalemia?
Kayexellate (sodium polystyrene sulfonate-SPS) exchanges sodium for potassium and
binds it in the gut, decreasing K by approximately 0.5-1 mEq. Multiple doses of
kayexellate are usually necessary. Onset of action is about 2-24hrs after oral dosing so
you need to wait at least several hrs before repeating your K level
A laxative such as sorbitol is required to prevent constipation from kayexellate. SPS is
a brand name which includes sorbitol The osmotic diarrhea from sorbitol also
contributes to lowering the K. One study suggests that sorbitol alone is at least as
effective as kayexellate with sorbitol . .
Kayexellate with sorbitol has been associated with intestinal necrosis and other serious
GI complications and therefore the FDA advised against its use in pts without normal
bowel function. Abnormal bowel function includes post surgery pts, pts with abdominal
pain or tenderness, pts at risk for developing constipation or impaction including pts with
history of impaction, chronic constipation, IBD, ischemic colitis, previous bowel
resection or bowel obstruction. Abnormal bowel function also includes pts who have
received medications that may slow their bowel motility ie morphine that may increase
the duration of drug contact with the intestinal mucosa. The complication rate of
kayexellate was highest in renal transplant patients.
The sorbitol that is used with kayexellate has been implicated in cases of colonic
necrosis and the FDA recommended that SPS should no longer be given with sorbitol.
However, most hospital pharmacies stock SPS with sorbitol. There is evidence that
kayexellate alone can cause bowel necrosis. The FDA advises not giving repeated dose
of kayexellate in pts who have not had a bowel movement.
Any new onset of abdominal pain, change in the character of abdominal pain or GI
bleeding after Kayexellate with sorbitol or kayexellate alone should be thoroughly
evaluated for possible ischemia,ulcers, perforation or other complications of this
medicine.
Up-to-date recommends SPS in patients with potentially life threatening hyperkalemia
where dialysis is not readily available and other therapies to remove potassium such as
diuretics or rapid restoration of kidney function (foley in urinary obstruction, ) have failed
or are not possible. However, even in the above pts, kayexellate is contraindicated if
the pt is post-op, has ileus or is receiving opiates or has large or small bowel
obstruction. In the pt where urgent dialysis is planned, kayexellate will provide no
benefit as it takes at least 2 hrs to begin to work and will cause the unpleasant situation
of the pt being in dialysis with severe diarrhea from a medication she never needed.
In patients with less severe hyperkalemia, diuretic therapy, IVF if not fluid overloaded,
low K diet and removal of or discontinuation of potentially reversible causes such as an
angiotensin inhibitor may be sufficient without SPS. A laxative without sorbitol, K or
phosphorous such as lactulose or polyethylene glycol may be indicated as it is safer
and most probably as effective as Kayexellate in lowering K.
The delay in the onset of kayexellate argues against its use in pts with hyperkalemia
due to digoxin toxicity as the digibind will correct the poisoned Na/K pump and lower the
K before the kayexellate works.
In this patient, kayexellate was not given as there was question of whether pt had
normal bowel function and whether the post-renal obstruction may be a reversible
cause of the hyperkalemia. However, prolonged obstruction caused intrinsic
nephropathy and the patient required repeated dialysis.
Pearls and Pitfalls:
-In this case, the source of the pt’s renal failure and hyperkalemia was only noted later
in the ED course of her treatment when the pt volunteered the information that she
hadn’t peed for awhile.
-Do not forget to evaluate the patient with new onset or unknown onset of elevated
creatinine for post-renal obstruction.
-Always think hyperkalemia in the pt who presents with bradycardia especially in the pt
with abdominal pain
-In the pt with profound bradycardia or AVB, hyperkalemia is the dx until proven
otherwise
-Do not be lulled into false sense of security by a pt with very high K and a normal ekg
as the next ekg may be vtach/vfib or asystole
-Think post-renal obstruction if standard treatment of hyperkalemia is only transiently
successful.
-Do not use Kayexellate with or without sorbitol in patients without normal
bowel function
-Abdominal complaints after Kayexellate with or without sorbitol require thorough
evaluation
-After bladder decompression in pt with urinary retention of prolonged duration or
unclear duration, it is best to observe them for 2-3 hours to make sure that
postobstructive diuresis does not cause clinical deterioration
-Do not forget to do thorough neurologic exam to evaluate for spinal cord compression
as cause of urinary retention
-Refer all patients with urinary retention to urology for work up of cancer as cause of
obstruction
- Do not be dissuaded from diagnosis of hyperkalemia by a normal ekg as the ekg has
low sensitivity for hyperkalemia
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