Rosen & Barkin's 5-Minute Emergency Medicine Consult (606 page)

Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
7.95Mb size Format: txt, pdf, ePub
ICD9
  • 592.0 Calculus of kidney
  • 592.1 Calculus of ureter
  • 788.0 Renal colic
ICD10
  • N20.0 Calculus of kidney
  • N20.2 Calculus of kidney with calculus of ureter
  • N23 Unspecified renal colic
RENAL FAILURE (ACUTE KIDNEY INJURY)
Michael D. Burg

Matthew N. Graber
BASICS
DESCRIPTION
  • The disorder is now known as acute kidney injury (AKI); the term renal failure is outdated.
  • Changes in glomerular filtration rate (GFR) and urine output (UO) encompassing a spectrum ranging from normal physiologic response to end-stage renal disease (ESRD) and measured by accumulation of nitrogenous by-products.
  • Defined by the RIFLE criteria:
    • 3 stages of renal injury:
      • R
        isk: Increased creatinine (Cr) ×1.5 or GFR decrease >25%, UO <0.5 mL/kg/h × >6 h
      • I
        njury: Increased Cr ×2 or GFR decrease >50%, UO <0.5 mL/kg/h × >12 h
      • F
        ailure: Increased Cr ×3 or GFR decrease >75% or Cr ≥4 mg/dL (acute rise of ≥0.5 mg/dL), UO <0.3 mL/kg/h × 24 h or anuria × 12 h
    • 2 stages of outcome:
      • L
        oss: Loss of renal function >4 wk
      • E
        SRD: Loss of renal function >3 mo
  • The most severe marker defines stage.
  • AKI based upon changes within last 48h; however, must often base on most recent data.
  • Higher RIFLE stages correlate with higher 1 and 6 mo mortality rates for hospitalized patients.
ETIOLOGY
  • Prerenal AKI:
    • Caused by renal hypoperfusion
    • Renal tissue remains normal unless severe/prolonged hypoperfusion.
  • Intrarenal AKI:
    • Caused by diseases of the renal parenchyma
  • Iatrogenic AKI causes include:
    • Aminoglycoside antibiotics
    • Radiocontrast material administration
    • NSAIDs
    • ACE inhibitors
    • Angiotensin receptor blockers
  • Postrenal AKI:
    • Due to urinary tract obstruction (e.g., prostatic hypertrophy, prostatitis)
DIAGNOSIS
SIGNS AND SYMPTOMS
Acute Kidney Injury
  • Often asymptomatic and commonly diagnosed with incidental lab findings
  • Oliguria (<400 mL/d urine production)
  • Fluid overload:
    • Dyspnea
    • Hypertension
    • Jugular venous distention
    • Pulmonary and peripheral edema
    • Ascites
    • Pericardial and pleural effusion
  • Nausea/vomiting
  • Pruritus/skin changes
  • Confusion/mental status changes
Prerenal AKI
  • Absolute or relative volume deficit
  • Dry mucous membranes
  • Hypotension
  • Tachycardia
  • Low cardiac output
  • Congestive heart failure
  • Systemic vasodilation (e.g., sepsis, anaphylaxis)
Intrinsic AKI
  • Allergic Interstitial Nephritis:
    • Fever
    • Rash
    • Recent myocardial infarction
  • Renal vein thrombosis:
    • Nephrotic syndrome
    • Can be associated with pulmonary embolus
    • Flank or abdominal pain
  • Glomerulonephritis, vasculitis
  • Hemolytic uremic syndrome (HUS)
  • Thrombotic thrombocytopenic purpura (TTP):
    • Mild elevation of BUN/Cr
    • Fever
    • Altered mental status
    • Anemia & thrombocytopenia
    • Neurologic: Coma, seizure, headache, altered mental status
  • Allergic interstitial nephritis fever:
    • Rash
    • Arthralgias
Postrenal AKI
  • Abdominal or flank pain
  • Distended bladder
  • Oliguria or anuria
Complications of AKI
  • Uremic syndrome:
    • Altered mental status
    • Asterixis
    • Reflex abnormalities
    • Focal neurologic abnormality
    • Seizures
    • Restless leg syndrome
    • Pericarditis
    • Pericardial effusion/cardiac tamponade
    • Ileus
    • Platelet dysfunction
    • Pruritus
  • Hematologic disorders:
    • Anemia
    • Increased bleeding time & platelet dysfunction
    • Leukocytosis
History
  • Prior history of AKI
  • Medication history including nephrotoxins
  • Weight change
Physical-Exam
  • Mental status changes/confusion
  • Eyes: Fundoscopy
  • CV exam: Jugular venous distention, S3
  • Lungs: Rales, crackles
  • Abdomen: Flank tenderness, palpable kidneys
  • Edema
  • Skin changes
Geriatric Considerations
  • Prone to prerenal AKI
  • Cr will vary by body mass index, so a “normal” range in elderly may represent an elevation.
  • Increased risk of contrast- and medication-induced AKI
Pediatric Considerations
  • Prerenal AKI a concern in neonates
  • Anatomic abnormalities
Pregnancy Considerations
  • Intrinsic renal azotemia
  • Pre-eclampsia/eclampsia
  • Ischemia: Postpartum hemorrhage, abruptio placentae, amniotic fluid embolus
  • Direct toxicity of illegal abortifacients
  • Postpartum TTP, HUS
ESSENTIAL WORKUP
  • Electrolytes including Ca, Mg, PO
    4
  • BUN/Cr
  • Urinalysis (UA):
    • Centrifuged specimen helps to distinguish different etiologies of AKI.
    • Exam for casts, blood, WBCs, and crystals
  • Fractional excretion (FE) of Na and/or urea
  • CBC: Anemia common with chronic disease
  • Postvoid residual volume (>100 mL suggests obstruction) OR
  • Ultrasound to rule out obstruction—especially in older men (e.g., prostatic hypertrophy, prostatitis)
  • ECG
DIAGNOSIS TESTS & NTERPRETATION
Lab

Prerenal

UA:

  • Specific gravity >1.018
  • Osmolality >500 mmol/kg
  • Sodium <10 mmol/L
  • Hyaline casts
  • BUN/Cr ratio >20
  • FE
    NA
    <1%
  • Rapid recovery of renal function when renal perfusion normalized

Intrarenal

  • BUN/Cr ratio <10–15
  • FE
    NA
    >2%
  • Glomerulonephritis, vasculitis:
    • UA with red cell or granular casts
    • Complement and autoimmune antibodies
  • HUS or TTP:
    • UA normal
    • Anemia
    • Thrombocytopenia
    • Schistocytes on blood smear
  • Nephrotoxic acute tubular necrosis (ATN):
    • UA:
      • Brown granular or epithelial cell casts
      • Specific gravity = 1.010
      • Urine osmolality <350 mmol/kg
      • Urine Na >20 mmol/L
  • Ethylene glycol ingestion:
    • UA: Calcium oxalate crystals
    • Anion gap metabolic acidosis
    • Osmolar gap
  • Rhabdomyolysis:
    • Elevated serum K
      +
      , PO
      4
      , myoglobin, creatine phosphokinase, uric acid
    • Decreased serum Ca
      2+
  • Tubulointerstitial disease
  • Allergic interstitial nephritis:
    • UA with WBC casts, WBCs, RBCs, and proteinuria
    • Peripheral eosinophilia

Postrenal

UA:

  • Usually normal
  • May have some hematuria but no casts or protein
  • FE
    NA
    often >4%
  • Urine osmolality usually <350 mmol/kg
Imaging
  • US:
    • 98% sensitive for excluding obstruction
  • Helical CT scan:
    • Without contrast sensitive for obstruction
    • May detect intrarenal changes
  • Duplex scan for:
    • Renal artery or vein thrombosis
  • Renal arteriogram:
    • Definitive diagnosis of renal artery thrombosis
  • Inferior vena cava and renal vessel venogram for renal vein thrombosis
  • IV pyelogram
Diagnostic Procedures/Surgery

ECG:

  • Hypertension secondary to volume overload may cause ischemia.
  • Sensitive for significant, acute electrolyte changes
TREATMENT
PRE HOSPITAL
  • Airway, breathing, and circulation (ABCs):
    • Supplemental oxygen for hypoxia
  • IV NS for volume depletion
INITIAL STABILIZATION/THERAPY
  • ABCs:
  • Supplemental oxygen for hypoxia
  • IV NS for volume depletion
  • Correct electrolyte disturbances
  • Indications for emergent dialysis:
    • Intractable hypertension
    • Intractable volume overload
    • Uremic encephalopathy, bleeding, or pericarditis
    • BUN >100 mg/dL
    • Intractable metabolic acidosis (pH <7.2)
  • Avoid nephrotoxic drugs.
  • Monitor UO.

Other books

Songs of Spring by Amy Myers
Rain Glade by Carroll, John H.
The Shining Ones by David Eddings
Eternity by Heather Terrell
Aim by Joyce Moyer Hostetter
Forbidden Love by Shirley Martin
AdamsObsession by Sabrina York