Download Attending Version: Complications of Dialysis in Patients with Kidney

Attending Version
Complications of Dialysis in Patients with Kidney Failure
Created by Dr. Patrick Moran
Objectives:
1.
2.
3.
4.
List the action plan for the 5 stages of chronic kidney disease.
List 5 indications for dialysis in patients with chronic kidney disease.
Name and discuss 5 complications associated with dialysis in kidney failure.
List 2 labs and 1 study in the work-up and management of altered mental
status in a dialysis patient.
References:
1. Levey, A.S., et. al. The National Kidney Foundation Practice Guidelines for Chronic
Kidney Disease: Evaluation, Classification, and Stratification. Ann Intern Med.
2003;139:137-147.
2. Brouns R, De Deyn PP. Neurological complications in renal failure: a review. Clin
Neurol Neurosurg. Dec 2004;107(1):1-16.
3. Pastan S, Bailey J: Dialysis therapy. N Engl J Med 1998 May 14; 338(20): 1428-37.
4. Yu HT: Progression of chronic renal failure. Arch Intern Med 2003 Jun 23; 163(12):
1417-29.
5. Foley RN, et. al. Clinical epidemiology of cardiovascular disease in chronic renal
disease. Am J Kidney Dis 1998;32(5 suppl 3):s112-9.
6. United States Renal Data System: III. Treatment modalities for ESRD patients. Am J
Kidney Dis 1999 Aug; 34(2 Suppl 1): S51-62.
7. Bailie, G. et. al. Chronic Kidney Disease 2006: A Guide to Select NKF-KDOQI
Guidelines and Recommendations. Edited by Nephrology Pharmacy Associates, Inc
2006.
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CASE
HPI: A 58 yo male with a history of DM-II, HTN and ESRD is admitted from the ED
for AMS. The patient has been on hemodialysis q Monday/Wednesday/Saturday for the
past 5 months. He had a portacath placed 3 months ago. The patient’s family reports that
everything appeared normal when he returned from dialysis earlier in the day. Then, this
afternoon, the patient began to behave erratically – talking to himself and not focusing on
conversations or tasks. Other than his AMS today, the patient has tolerated dialysis well
and leads an active lifestyle. At the bedside, the patient does not currently have any
complaints, but is notably distracted and incoherent.
PMHx:
1) Kidney failure from diabetic nephropathy
2) DM-II, now improved control with insulin (last A1c = 9.2 two months ago)
3) HTN
4) Dyslipidemia
5) OSA, uses CPAP intermittently at night
Family Hx: Mother - DM-II, HTN; Father - HTN, AMI @ 52 yo; Sister - DM-II, HTN
Social Hx: Lives with wife and son. Denies using ETOH, tobacco or illicit drugs.
Medications:
1. Lantus
2. ACEi
3. Metoprolol
4. Atorvastatin
5. Calcium carbonate supplements
Allergies: NKDA/NKA
PE: VS: T 99.1, HR 96, BP 96/70, RR 20, O2 sat 93%
Gen: Mildly agitated
HEENT: NCAT, MMM
Pulm: CTA bilat
CV: RRR, 2/6 SEM @ LLSB, no abd/carotid bruits, carotid pulse 2/4 bilat, dorsalis
pedis 1/4 bilat
Abd: Obese, +BS, soft, nondistened, nontender in 4 quadrants, no peritoneal signs
Ext: 1+ pretibial pitting edema bilat, no cyanosis
Derm: No rashes, no erythema, warmth, or tenderness at portacath-site (left chest )
Neuro: CN II-XII intact bilat, pt not able to follow commands
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1. What factors could contribute to patients’ altered mental status?
- Kidney failure on dialysis (electrolytes/fluid
shifts/anemia/uremia/pericarditis/acid-base),
- Comorbidities in PMHx (cardiovascular risks-ACS/CHF/Stroke; OSAacidosis/Pulm HTN),
- Vascular access (bacteremia/sepsis),
- DM-II on metoprolol (altered vitals),
- On insulin with ESRD (hypoglycemic),
- Family hx AMI (Father@ 52 yo).
- CO2 narcosis (pt with chronic OSA, may or may not be using CPAP).
- Acute toxic ingestions / illicit drugs / prescription drugs
2. What is the differential diagnosis at this point?
- Sepsis, AMI, CHF, electrolyte imbalance, fluid shifts, hypoglycemia, uremia,
acidosis, disequilibrium syndrome and drug ingestion.
3. What is your next step in management?
- Labs (CBC, Electrolytes, Cardiac enzymes, blood cultures, UDM-if pt still
urinating)
- Studies (head CT, EKG, CXR)
Discussion Outline:
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1. Classification of Chronic Kidney Disease (CKD):
Defined as either GFR <60 mL/min/1.732 for 3 or more consecutive months or kidney
damage. Kidney damage is defined as the presence of pathologic abnormalities or
markers of damage, including blood/urine tests, or imaging studies.
Table 1: National Kidney Foundation: Stages of Chronic Kidney Disease and Action Plan*.
Stage
Description
GFR
Action
(mL/min/1.732)
At increased risk
≥60 (with risk
Screening; chronic kidney disease
-factors)
reduction
Kidney damage with normal or
≥90
Diagnosis and treatment of
1
increased GFR
comorbid conditions, CVD risk
reduction
Kidney damage with mild
60-90
Estimating rate of progression
2
decreased GFR
Moderately decreased GFR
30-59
Eval and treatment of
3
complications
Severely decreased GFR
15-29
Preparation for kidney
4
replacement therapy
Kidney failure
<15 (or dialysis)
Kidney replacement/dialysis
5
*The level of kidney function (GFR), regardless of diagnosis, determines the stage of chronic
kidney disease according to the Kidney Disease Outcomes Quality Initiative (KDOQI) chronic
kidney disease classification (level A recommendation).
2. Indications for dialysis:
According to the Kidney Disease Outcomes Quality Initiative (KDOQI), dialysis should
be started when:
- GFR <10 mL/min/1.732 (Diabetics GFR <15),
- Serum Cr ≥8 mg/dL (Diabetics Cr ≥6)**,
- Uremic symptoms appear (ie; pericarditis, encephalopathy, coagulopathy),
- Fluid overloads are unresponsive to diuresis,
- Refractory hyperkalemia,
- Severe metabolic acidosis (pH <7.20)
(**Serum Cr alone should not be used to assess kidney function – level A
recommendation)
3. Complications associated with dialysis and kidney failure:
Hyperkalemia:
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K+ balance normally remains intact in chronic renal failure until the patient’s GFR is
<10-20 mL/min/1.732. It is the most common electrolyte abnormality and can cause lifethreatening arrhythmias. Treatment options include calcium carbonate/chloride, binding
resins, insulin/glucose, bicarbonate, or Albuterol nebs as needed.
Hyponatremia:
In dialysis patients, hyponatremia is usually a dilutional effect, after increased fluid
intake while on sodium restriction. It can cause AMS and seizures. Use diuretics only if
patient still has some ability to produce urine. If not, then treat with dialysis.
Hyperphosphatemia/Hypocalcemia:
Disordered metabolism of phosphorus, calcium, and bone is referred to as renal
osteodystrophy (ie; osteitis fibrosa cystic/osteomalacia). It usually begins when GFR
<20 mL/min/1.732. It can cause bony pain, fractures, and muscle weakness. Treat with
phosphorus-binding agents.
Acid/base disorders:
Damaged kidneys are not able to excrete the H+ ions that are regularly generated by
metabolism (ie; metabolism of proteins). The normal buffering systems of the kidney (ie;
NH3, HCO3-) are also reduced. The resultant metabolic acidosis has to be buffered by the
calcium carbonate and calcium phosphate that is stored in the bone, which, in turn,
exacerbates renal osteodystrophy. This state is often worsened by co-morbidities that
produce acidosis (ie; COPD, OSA, infection, etc). It can present as hyperpnea. Treat
with sodium bicarbonate or, if pH <7.20, with dialysis.
Anemia:
Characteristically normochromic/normocytic because it is primarily caused by a
decreased production of erythropoietin by damaged kidneys. Also, patients can have iron
deficient anemia. It present as generalized fatigue, however, it also increases the risk of
CHF and AMI in these patients.
Infection of vascular access: Usually present with local signs/symptoms such as pain,
redness, warmth, or fluctuance around access site. However, fever and sepsis may be
present without local signs. Take blood cultures and treat empirically if signs of sepsis.
Cardiovascular:
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1. Hypertension/hypotension: Results from alternating periods of sodium and water
retention (ie; between dialysis sessions), and periods of considerable diuresis (ie;
during and post-dialysis). These varying states of intravascular volume place
patients at increased risk for CHF, syncope, and AMS.
2. Pericarditis/pericardial effusion: Results from uremia. Can present as pleuritic
chest pain, weakness, syncope, or dyspnea. It can lead to cardiac tamponade.
Must be treated with dialysis.
3. Myocardial injury/infarction: More common in patients with ESRD. Can present
with chest pain or atypically, such as in diabetics, with hypotension and AMS.
Treated as non-dialysis patients with attention to drug selection and dosing.
Neurologic complications:
Uremic encephalopathy typically occurs when the GFR is <15 mL/min/1.73 2. Tertiary
hyperparathyroidism and hypercalcemia are also thought to contribute to the degree of
encephalopathy. It presents as lethargy, AMS, or coma and it must be treated with
dialysis.
Hyperinsulinemia:
Patients with kidney failure have decreased renal insulin clearance. Because of this, they
often require decreased doses of hypoglycemic medications. If insulin therapy is not
monitored closely and adjusted, these patients can experience symptoms of hypoglycemia
(ie; AMS, palpitations/tachycardia – careful with Beta-Blockers masking cardiovascular
symptoms).
Dialysis dysequilibrium syndrome (DDS):
It is characterized by weakness, dizziness, headache, and, in severe cases, AMS. DDS is
thought to be caused by repeated fluid shifts and is a diagnosis of exclusion.
4. Workup and Management of AMS in dialysis patients:
- ABCs.
- Establish new vascular access.
- Basic labs: CBC with diff, Chem 10, Cardiac enzymes, Coags, Blood cultures,
CBG, UA/UCx (use a foley catheter to check for residual urine or for pyuria).
- Other labs to consider depending on patient presentation or 1st lab results: ABG,
lactic acid, albumin, LFTs, UDM.
- 12-lead ECG and cardiac monitoring (AMI, Arrhythmias, pericarditis).
- CXR (CHF, pericarditis, infection).
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-
-
Fluids: Usually not used unless patient in frank shock. Must thoroughly evaluate
cardiovascular and pulmonary status. Fluids may be administered in small 250cc
boluses. No LR due to K+ content.
Consult a nephrologist if the patient has: a need for urgent dialysis (see KDOQI
recommendations in section II); a significant drop in baseline renal function; signs
of infection, obstruction, or aneurysm/pseudo-aneurysm of vascular access.
Consider other causes of AMS if patient has specific risks (ie; a fall, history of
TIA, etc), or if initial workup for dialysis-related causes is negative. May require
CT of the brain or MRI.
Review Questions:
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1) Which one of the following statements about hypo- or hypernatremia is true?
A) A patient with frank symptoms of hypo- or hypernatremia should have his/her
serum sodium concentrations corrected over a few hours back to normal levels.
B) The brain fully compensates for hyponatremia within 2-4 hours by making
"idiogenic osmoles".
C) The symptoms of hyper- and hyponatremia are mainly due to central nervous
system dysfunction.
D) Hyponatremia due to SIADH is most often due to underlying kidney disease.
E) "Pseudohyponatremia" is as dangerous as true hyponatremia.
Answer: C
Symptoms are mainly due to CNS dysfunction because: Hypernatremia causes neuronal
shrinkage and altered membrane potentials in the brain and spinal cord. Hyponatremia
causes cerebral edema and puts pressure mainly on the brainstem structures. Answer A
is incorrect because the serum sodium in hypernatremia should be corrected over 48-72
hours. In hyponatremia, depending on acuity and etiology, it should be corrected over
24-72 hours. Answer B is incorrect because the brain makes "idiogenic osmoles" to
compensate for the brain's hypoosmolar state caused by serum HYPERnatremia. Answer
D is incorrect because SIADH is caused by the inability of the body to suppress the
secretion of arginine vasopressin from the posterior pituitary. Answer E is incorrect
because, in pseudohyponatremia, the aqueous phase is diluted by excessive proteins or
lipids. The TBW and total body sodium are not changed (ie; hypertriglyceridemia).
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2) 44 yo male with PMHx of ESRD, DM II, and Gout presents with a two day history of
progressive weakness in all 4 extremities. He reports “missing” his last dialysis
appointment 3 days ago. Physical exam is all within normal limits except for three
findings; Muscle strength 0/5 in lower extremities (LEs), 1/5 in upper extremities, and
DTRs in LEs 0/4. Notable labs: NA+ 132, K+ 6.8. ECG: PR interval=0.25, QRS=0.12,
with T-waves that are mildly peaked.
What is the next step in the management of this patient?
A) Kayexalate 25 g PO mixed with 100 mL of 20% sorbitol
B) Calcium chloride 5 mL of 10% sol IV over 2 min
C) Regular insulin 10 U regular insulin and 2 amps D50W IV bolus
D) Lasix 40mg IV-push
E) Urgent dialysis
Answer: B. Because of the ECG changes, calcium chloride should be administered first
because it has the fastest onset of action and because it has cardio-protective properties.
3) Which of the following is NOT an indication for urgent dialysis for a patient with
renal failure?
A. Asterixis and drowsiness
B. Pulmonary edema resistant to diuretics
C. Pericarditis
D. Serum creatinine of 12 mg/dL
E. Serum potassium of 7.8 mEq/L
Answer: D. Serum Cr alone should not be used to assess kidney function – level A
recommendation from the KDOQI.
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Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
_______________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
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