Presentation on theme: "Renal Failure Rebecca Burton-MacLeod R5, Emerg Med Nov 8 th, 2007."— Presentation transcript:
Renal Failure Rebecca Burton-MacLeod R5, Emerg Med Nov 8 th, 2007
Overview of RF Renal Failure Acute renal failure Chronic renal failure Acute on chronic renal failure
Acute renal failure 2 main renal physiological functions that are easily measured in ED: –Urine output –Excretion of water soluble waste products of metabolism Therefore, definition of ARF: –Decline in Cr clearance of 50% –Increase in serum Cr of 50% –Renal insult causing pt to require dialysis
ARF May have anuric (<100cc/24h), oliguric (<0.5cc/kg/h), or non-oliguric renal failure Mortality lower with non-oliguric renal failure; however, may still have renal failure with NORMAL urine output!!
Etiology Pre-renal (most common; 55% hosp pts) –Intravascular depletion (hemorrhage, dehydration, diuresis, GI losses, skin losses) –Vasodilation or dec cardiac output (sepsis, anaphylaxis, nitrates, antihypertensives, liver failure) Post-renal (obstruction anywhere along UT) –Renal calculi –Urethral valves –VUR –Cervical Ca or pelvic inflammation –Prostatic disease
Etiology: renal causes ATN (ischemia, rhabdo, toxins—contrast, aminoglycosides, NSAIDs, ACEi, ARBs, tacrolimus, cyclosporine, cisplatinum, heavy metals, ethylene glycol, cocaine) Interstitial insult (adverse drug rxn, often assoc with fever, rash, jt pain) Glomerular insult (glomerulonephritis) Vascular insult (renal art thrombosis or stenosis, renal vein thrombosis, scleroderma)
U/A Casts: –Hyaline—generally assoc with pre-renal or post-renal obstructive causes –RBC—always significant; assoc with glomerulonephritis –WBC—renal parenchymal inflammation –Granular—cellular remnants and debris –Fatty—nephrotic s/o or other nonglomerular renal disease
Urine lytes Urine Na Fractional excretion Na –(Urine Na x plasma Cr) / (plasma Na x urine Cr) –Affected if mannitol or loop diuretics administered Urine Na <20 and FENa <1% –Pre-renal failure, acute obstruction, contrast- induced ATN, rhabdo- induced ATN, nonoliguric ATN Urine Na >40 and FENa >1% –ATN, chronic obstruction, underlying CRF
Prevention Adequate volume replacement Foley/percutaneous nephrostomy Avoid nephrotoxic agents if possible, or else use OD dosing Renal-dosing dopamine in conjunction with lasix may aid in converting oliguric to non- oliguric RF Consider low-dose vasopressin in sepsis
Management of specific problems HyperPh: give oral Ca antacids which bind to Ph Symptomatic hypoCa: 10cc of 10% Cagluconate IV HyperK: if >6.5 and EKG changes…be aggressive! Volume overload: diuretics, nitrates, dialysis
Indications for dialysis with ARF Fluid overload in oliguric/anuric RF HyperK Severe acidemia Uremic encephalopathy Toxins: ethylene glycol, methanol, ASA, Li, theophylline
Prognosis in ARF If receive dialysis for ARF then 16% remain dialysis-dependent Also, 40% of pts develop CRF
Chronic renal failure Definition: –CRF—GFR <60cc/min, but decreased by <75% –ESRD—GFR <10cc/min, serious life- threatening complications without dialysis or transplant
Etiology DM (45%) Hypertension (30%, up to 40% in black popn) Glomerulonephritis Collagen vascular disease (SLE, scleroderma, Wagners) Hereditary (PCKD, Alports s/o) Obstructive uropathy (BPH, retroperitoneal tumor, nephrolithiasis) HIV Nephrotoxins (contrast, heroin, ampho B, aminoglycosides) Peds—reflux nephropathy
Complications Uremia Renal osteodystrophy Normocytic normochromic anemia Infections (impaired WBC function) GIB (stress ulcers and impaired hemostasis) Pericarditis (up to 20% of dialysed pts)
What ? Do you need to ask… Dry weight? Dialysis schedule? Form of dialysis (hemo, peritoneal)? Missed dialysis?
Mgmt of specific disorders Cases…
Case 1 68yo F with sharp lower abdo pain x2d, worsening. Small amount of blood in stool this a.m. You’re convinced you need a CT abdo. Speak to Radiol. They ask what her Cr is… ….long pause…..142…. Do you still want CT? What are your options?
Contrast nephropathy Risk factors—DM, underlyling renal d/o, amyloidosis, MM, hypo-proteinuric states, larger doses of contrast, repeat exposures to contrast <72hr, type of contrast NAC? Bicarb?
Papers… Several studies done looking at benefit of NAC vs. bicarb vs. saline for prevention of contrast nephropathy
N=264; received either bicarb infusion, or N/S infusion, or NAC and N/S infusion 6 hrs pre and post angio Baseline Cr 139 Change in Cr clearance significantly better with bicarb than with other regimens
DBRCT n=326 pts undergoing angio All had chronic renal disease Protocols: 1) N/S x12 hrs pre and post and NAC 2) bicarb x1h pre and 6h post and NAC 3) N/S and ascorbic acid and NAC All pts had NAC day prior to procedure and days after
Cont’d Outcome: –In N/S and NAC: 9.9% developed CN –In bicarb and NAC: 1.9% developed CN –In N/S and ascorbic acid and NAC: 10.3% CN –Bicarb and NAC significantly better in medium to high risk pts for CN
N=118 with Cr >110 Bicarb 3ml/kg/h x1h prior then 1ml/kg/h x6h post vs. N/S infusion as above Significantly greater nephroprotective effects from bicarb Postulated due to inc flow, local tubular alkalinization, partial correction of ischemic acidosis
Case 2 72yo M presents c/o chest pain, weakness. At triage, HR noted to be 32. Brought back to monitored bed. Hx of DM, hypertension, recent w/u for back pain Meds: metformin, lasix, propanolol, penicillin, one other med he can’t remember the name of…
HyperK in RF CaCl 5cc IV bolus, rpt q5min prn –?is he on digoxin? Bicarb 50meq IV, rpt x1 prn –Watch for volume overload!! Ventolin nebs, rpt or continuous Insulin—give 10-20U Hum R mixed with glucose –Use D20 or D50 to decrease volume Kayexalate, mixed with sorbitol –Watch for Na overload as exchanges K for Na IV diuretics –Only works if residual renal function! Dialysis!!!
How quickly will K drop? Insulin drops K by 1meq/L after 1h IV Ventolin drops K by 1.1meq/L after 15min Dialysis: –Hemodialysis—removes up to 50meq/h –Peritoneal dialysis—removes 15meq/h
Case 3 47yo F hemodialysis patient presents to ED c/o SOB Last dialysis 5d ago (missed one because travelling back from US); states weight up 6lbs O/e: HR 110, BP 145/87, sats 88% r/a Tachypneic, ++crackles to bilat lungs, elevated JVP You call her Nephrologist…waiting for them to get back to you… Plan?
Pulmonary edema Hemodialysis… Oxygen, sitting position Consider CPAP Nitrates: SL, IV or nitroprusside Lasix mg IV (for pulm vasodilation) +/- IV morphine Sorbitol 70% cc dose q20-60min (causes osmotic shift into gut) Hemodialysis…
Case 4 59yo M presents to ED c/o cough, SOB, fever x3d Mild chest pain, no abdo pain, no n/v PMHx: hemodialysis pt, DM, pacemaker O/e: HR 115, SBP 95, RR 30, sats 95% r/a Slight JVD, normal HS, lungs clear, abdo soft Investigations?
Case 5 You get a call from dialysis unit. They’re mid-way thru a run of HD with a pt who has now developed hypotension. They can’t get a hold of Nephro and are not sure what to do with the pt. You asked if they’ve slowed the rate and amount of ultrafiltration (duh!)… They want to send him down to ED…
Cont’d Before the pt even arrives, you’re thinking Ddx: –Hypovolemia (dialysis related, GIB, hemorrhage) –CV causes (MI, dysrhythmias, tamponade) –Lyte d/o (Ca, Mg, K) –Air embolism –Hypoxemia –Drugs (narcotics, antihypertensives, anxiolytics) –Hypersensitivity rxn (to ethylene oxide which sterilizes dialyzer, polyacrylonitrile in the membranes) –Autonomic neuropathy –Acetate-based dialysate
Mgmt of hypotension Obviously, decrease flow rate and amount of ultrafiltration N/S IV bolus: cc in small boluses of cc and frequently reassess! Try to figure out why…
Case 6 86yo F presents to ED c/o high BP. Says she takes her BP at home regularly and today it was 195/115. She’s been told this is “too high”. You go in to take a quick hx…nothing exciting. Nurse has not checked pt in yet. O/e: NAD. Lungs nil acute. CV nil acute. Abdo nil acute. Skin—note made of Cimino-Brescia fistula in L arm with thrill present You ask for a set of vitals and disappear to see your next pt…
Cont’d You come back a while later and find the BP cuff cycling q1min measuring her BP…last one 158/90. It’s cycling on her L arm…any problem? You check her fistula site and notice there is no longer a thrill, but still feel a strong palpable pulse. Concerned?
Thrombosis of access Avoid manipulating access site, as may cause venous embolization Call Vascular Occasionally they may use thrombolytic agents to open thrombosed access but usually surgical revision required Bottom line: don’t put tourniquet, check BP, or circumferential bandages on arm with fistula!!
Case 7 43yo M presents to ED c/o generalized abdo pain, malaise. He has a peritoneal dialysis line in place. Last seen by Nephro about 3wks ago, everything going well. Very conscientious about his peritoneal catheter and keeping it sterile! ROS: small amount of foul urine produced, diarrhea x1 yest, sore throat ~1wk ago
Cont’d O/e: T 38.2, HR 92, BP 142/78, sats 98% Lungs clear, HS normal, H+N small cervical lymphadenopathy, abdo sl distended, catheter site appears clean, mild abdo tenderness, no guarding, no rebound Investigations?
Results WBC 12 Lytes N, Cr 327, lipase N U/A--+RBC, +leuks, +WBC and granular casts Dialysate—cloudy, 105 WBC, 60% neuts, Gm stain pending
Peritonitis 70% of cases caused by staph aureus or staph epidermidis If polymicrobial infection, then suggests direct contamination from GI tract and should search for perf or fistula! Usually can be easily treated as oupt and does not require removal or replacement of catheter
Mgmt Intraperitoneal abx x10-14d: –Vanco 30mg/kg IP q5-7d –Ceftazidine 1gm IP q1d –Gentamicin 2mg/kg IP then 20mg/L q1d Don’t forget to think about other intra-abdo causes of peritonitis!!