Episode 65 – Contrast-Induced Nephropathy and Genitourinary Trauma

iTunes or Listen Here

We cover Free Open Access Medical Education (FOAM) on Contrast-Induced Nephropathy (CIN).  A large retrospective study by Hinson and colleagues in Annals of Emergency Medicine, reignited enthusiasm in the FOAM world about the questionable entity (and clinical significance) of CIN. The data on CIN is somewhat difficult to parse out as the data consists entirely of retrospective cohort and case-control studies. The highest risk of CIN seems to come from large volume contrast procedures such as percutaneous coronary angiography. Studies looking at the risk of CIN after contrast-enhanced CT scan have been less conclusive.

The American College of Radiology (ACR) Manual on Contrast Induced Nephropathy

CIN

This Emergency Medicine Literature of Note post covers the AMACING  trial, which looks at intravenous fluid administration (0.9% NaCl) versus usual care in patients “at risk” for CIN undergoing contrast-enhanced CT scan.   The study found a difference of -0.1% (95% CI -2.25 to 2.06), which was below the non-inferiority margin. Prior literature shows similar results, with no clear-cut efficacy from prevention strategies for CIN.

This post by Dr. Joel Topf (nephrologist @kidneyboy) on the Precious Bodily Fluids blog discusses a nephrologist’s take on CIN.

EM topics post on fluids in CIN.

Core Content

We then delve into core content on genitourinary trauma using Rosen’s Chapter 47 and Tintinalli’s Chapter265 as a guide.

Screen Shot 2017-02-28 at 1.43.40 PM Screen Shot 2017-02-28 at 1.44.33 PM

 Rosh Review Emergency Board Review Questions

An 18-year-old man involved in a motor vehicle collision is transferred from a rural facility after being diagnosed with a pelvic fracture. After your initial assessment and stabilization, a secondary survey is performed. On examination, he is noted to have blood at his urethral meatus as well as a scrotal hematoma. Which of the following is the most appropriate next step?

A. Retrograde cystogram

B. Retrograde urethrogram

C. Suprapubic catheter placement

D. Transurethral urinary catheter placement

[accordion]
[toggle title=”Answer” state=”closed”]

B. The patient should undergo a retrograde urethrogram to rule out an underlying urethral injury. In patients with a pelvic fracture and signs of urethral injury, a retrograde urethrogram should be performed in the supine position prior to urethral instrumentation. If a partial disruption is identified, one attempt to place a 12- or 14-French Foley or coude catheter can be made. If unsuccessful or a complete tear is diagnosed, then a suprapubic catheter will need to be placed. Pelvic fractures with displacement of the pubic symphysis can cause laceration or avulsion of the prostatic urethra. The three classic findings of urethral injury include blood at the urethral meatus, a high-riding prostate and a scrotal or perineal hematoma. Failure to recognize a urethral injury can lead to urethral stricture formation and urinary incontinence.

Urethral manipulation can convert a partial urethral tear to a complete tear, therefore transurethral urinary catheter placement (D) should be avoided until urethral integrity is known. Suprapubic catheter placement (C) may ultimately be necessary if complete urethral injury is diagnosed, however in this case a retrograde urethrogram should be performed prior to proceeding with suprapubic placement. The patient may also have a bladder injury and may require a retrograde cystogram (A), however urethral integrity must be evaluated by a retrograde urethrogram prior to performing a cystogram

[/accordion]

A 29-year-old man presents to the ED after a MVC. A pelvic fracture is identified on radiography. His vital signs are stable. The decision is made to place a Foley catheter, but blood is noted at the urethral meatus. Which of the following is an appropriate next step?

A. Consult a urologist

B. Obtain a CT scan to evaluate for urethral injury

C. Perform a retrograde urethrogram

D. Place a condom catheter

[accordion]
[toggle title=”Answer” state=”closed”]

C. Perform a retrograde urethrogram. In general, a Foley catheter should not be placed in the setting of suspected urethral injury. In such cases, it is recommended that further testing be performed to evaluate for urethral injury. A retrograde urethrogram should be performed. If there is no contrast extravasation, then a Foley catheter can safely be inserted.  A urologist should be consulted (A) if a urethral injury is confirmed by the retrograde urethrogram. A CT scan (B) is a poor study to identify urethral injuries. A condom catheter (D) does not allow for accurate urine output measurements and may delay identification of a urethral injury.

[/accordion]

References:

  1. Hinson JS, Ehmann MR, Fine DM, et al. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann Emerg Med. 2017
  2. ACR Manual on Contrast Media.  v10.2. 2016. p33-40
  3. “Genitourinary System.”  Rosen’s Emergency Medicine, 8th ed. Chapter 47, 479-499.e1
  4. “Genitourinary Trauma.” Tintinalli’s Emergency Medicine: A Comprehensive Review.  8th ed.  Chapter 265

Episode 57 – Lithium Toxicity & Rhabdomyolysis

The Free Open Access Medical Education (FOAM) 

Listen Here or iTunes

We cover a post from Dr. Josh Farkas on PULMcrit on lithium toxicity. The key message from the post is: a single serum lithium level doesn’t necessitate dialysis, despite a recommendation from the EXTRIP working group  to initiate dialysis in patients with a lithium level > 5 mEq/L [1].  Dr. Farkas advocates for aggressive management in asymptomatic patients with chronic lithium toxicity and patients without impaired renal function.

Lithium neurotoxicity does not correlate with serum lithium levels; it depends on the concentration in the CNS.

  • The argument is that the neurologic effects, among the most worrisome sequelae of lithium toxicity, results from lithium crossing the blood-brain-barrier (BBB) into the central nervous system (CNS). Thus, in an acute ingestion, patients may have a higher serum lithium level, but given the acuity, the lithium may not cross into the CNS.  Conversely, a patient with chronic toxicity may have a mildly elevated serum lithium level but the lithium has had time to cross the BBB into the CNS so more neurotoxicity can result from lower serum lithium concentrations.

Differentiating between acute, chronic, and acute on chronic toxicity is important in management.

  • Acute – expect the levels will rise rapidly as the bolus of lithium is absorbed.
  • Chronic – expect the levels will not rise rapidly given a lack of lithium bolus.
  • Acute on chronic – again, expect levels to rise rapidly and may see more neurotoxicity as some lithium may have passed through the BBB into the CNS.

screen-shot-2016-09-30-at-6-19-25-pm

screen-shot-2016-09-30-at-6-02-28-pm

Core Content

We review rhabdomyolysis using Rosen’s Emergency Medicine (8e)  Chapter 160 and Tintinalli’s Emergency Medicine (8e), Chapter 181.

screen-shot-2016-10-01-at-12-05-27-pm

Generously Donated Rosh Review Questions

A 17-year-old man presents to the ED from a correctional facility complaining of general malaise with nausea and vomiting one day after a weightlifting competition. Vital signs are T 37.2°C, BP 100/65 mm Hg, HR 125, and RR 22. Physical exam reveals an uncomfortable, fatigued male who has diffuse muscle soreness. Urinalysis shows 3+ blood without red blood cells. What is the most important next test to direct the acute management of this patient?

A. Creatine kinase assay

B. Electrocardiogram

C. Electrolyte panel with blood urea nitrogen and creatinine

D.Microscopic urinalysis

[accordion]
[toggle title=”Answer” state=”closed”]

B. Electrocardiogram. The patient presents with exercised-induced rhabdomyolysis. Although the causes of rhabdomyolysis are manifold, potential complications are independent of etiology. Of all the complications, hyperkalemia is the most concerning and, undiagnosed, can lead to sudden cardiac death. ECG changes indicative of hyperkalemia are thus critical to identify early in the course of management. Hyperkalemia results from impaired calcium transport with increased intracellular calcium accumulation, cellular necrosis, and expulsion of intracellular contents (including potassium) into the bloodstream. Rhabdomyolysis can also lead to acute tubular necrosis and kidney failure, which will exacerbate developing hyperkalemia by decreasing renal potassium clearance. Hyperkalemia is an immediate life-threatening condition that develops shortly after muscle injury. Absent point-of-care electrolyte analyzers, the most rapid way to screen for hyperkalemia is through an electrocardiogram.

Rhabdomyolysis is not defined by a specific creatine kinase (A) level. But, in general, a serum CK >5 times the upper limit of normal (a threshold that may differ by lab) is considered indicative of rhabdomyolysis. Although kidney injury can occur at any level, higher CKs correlate with an increased likelihood for the development of acute renal failure. In the absence of cerebral or myocardial infarction, a CK >5 times is diagnostic for serious muscle injury. Urinalysis (D) typically shows brownish discoloration with “large” blood on dipstick but few, if any, red blood cells on microscopic evaluation. This occurs because most dipstick tests cannot distinguish myoglobinuria from hematuria or hemoglobinuria. Protein, brown casts, and renal tubular epithelial cells may also be present. Measures of renal function and an electrolyte panel (C) should be obtained in all patients with suspected rhabdomyolysis. But, as mentioned, waiting for results may lead to a delay in the identification of life-threatening complications. In addition to hyperkalemia, hyperphosphatemia and hypocalcemia may also be seen. Additional (though less worrisome) laboratory abnormalities include elevated uric acid and low albumin.

[/toggle]
[/accordion]

One Step Further Question: What is the late complication of rhabdomyolysis associated with thrombocytopenia, hypofibrinogenemia, and an elevated D-dimer?

[accordion]
[toggle title=”Answer” state=”closed”]

Disseminated intravascular coagulopathy may occur and is a result of muscle necrosis with liberation of activating substances from injured cells.

[/toggle]
[/accordion]

 

  • References:
  • 1. Decker BS, Goldfarb DS, Dargan PI et al. Extracorporeal Treatment for Lithium Poisoning: Systematic Review and Recommendations from the EXTRIP Workgroup. Clinical Journal of the American Society of Nephrology. 10(5):875-887. 2015.
  • 2. “Chapter 160. Lithium.”  Rosen’s Emergency Medicine.  8th edition.
  • 3. “Chapter 181. Lithium.” Tintinalli’s Emergency Medicine: A Comprehensive Review. 8th edition.
  • 4. Grellar H. “Chapter 72. Lithium.” Goldfrank’s Toxicology. 10th edition.
  • 5.  “Chapter 127. Rhabdomyolysis. Rosen’s Emergency Medicine.  8th edition.
  • 6. “Chapter 89. Rhabdomyolysis.” Tintinalli’s Emergency Medicine: A Comprehensive Review. 8th edition.

Episode 21 – Acute Kidney Injury

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

Dr. Josh Farkas of the PulmCrit blog has produced a couple of blog posts on the importance of renal protection in sepsis, Renoresuscitation: Sepsis resuscitation designed to avoid long-term complications and Renal microvascular hemodynamics in sepsis: a new paradigm.  Much of this is theoretical and certainly not something that is standard practice, rathery a theory extrapolated from subgroups of several trials.

Suggested renoresuscitation measures:

(1) Avoid renal failure – avoid nephrotoxins (many antibiotics, NSAIDs, ace-inhibitors), avoid hyperchloremic metabolic acidosis.

(2) Avoid volume overload – treating decreased urine output by flooding a patient with fluids is not necessarily the best move.

(3) Protect the glycocalyx of the endothelium – this suggestion proffers more questions than answers. Steroids? Albumin? Certain vasopressors?  Stay tuned, as we’re not really certain what this entails.

The Bread and Butter

We summarize some key topics from Rosenalli, that’s Tintinalli (7e) Chapter 91; Rosen’s (8e) Chapter 97.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Acute Kidney Injury – typically a creatinine 1.5-2x the patient’s baseline is classified as acute kidney injury.  Urine output can be increased initially but determine whether a patient is making urine and how much, as urine output <0.5 mL/kg/h qualifies as AKI.

RIFLE criteria
RIFLE criteria

Importance – AKI is associated with worse outcomes, although it’s unclear as to whether this is merely a marker of

  • Found in 35-65% of admissions to the intensive care unit, in 5-20% of hospital admissions.  Furthermore, AKI is associated with higher mortality.
  • Renal failure can also cause significant problems for the patient such as electrolyte abnormalities (hyperkalemia the most worriesome, but also hyperphosphatemia) and pulmonary edema.

Etiology – many causes of AKI are reversible or amenable to treatment.

Prerenal – this is one of the most common causes of acute kidney injury and basically is caused by decreased blood flow to the kidney.  Associated with a high BUN/creatinine ratio, increased urine osmolality, a urine sodium concentration less than 20 mEq/L, and FENa less than 1% (this is why getting urine sodium and a concurrent chemistry panel is key).

  • Hypovolemia – volume depleted, hemorrhage, intravascular volume depletion from congestive heart failure or cirrhosis.
  • Hypotension – poor cardiac output (heart failure, valvular problems), shock
  • Decreased flow through the renal artery disease – Nonsteroidal anti-inflammatories: inhibit prostaglandins in the afferent arteriole.  ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II, which when absent decreases the GFR because of dilatation of the efferent arteriole.

Post Renal (Obstructive) – Check out Episode 2 on urologic emergencies.

  • Benign prostatic hypertrophy (BPH) is the most common cause but medications such as anticholinergics and pseudoephedrine. Trauma, stones, strictures, and malignancy can also cause obstruction.

Intrinsic acute renal failure– divided into: tubular disease (most common), glomerular disease, vascular disease and interstitial disease.

  • Least common form of AKI in the ED, more common in inpatients.
  • Acute Tubular Necrosis (ATN) most common cause – via nephrotoxins such as aminoglycosides and contrast.
  • Granular “muddy brown” casts – think of necrosis from the “N” in ATN and necrosis tends to be dark.

Indications for emergent dialysis – AEIOU

A- Acidosis

E- Electrolyte emergencies (hyperkalemia!)

I-  Intoxication with dialyzable toxins (ethylene glycol)

O- Overloaded with volume

U- Uremia

 Generously Donated Rosh Review Questions 

Question 1. A 72-year-old man is brought to the ED from a nursing home for evaluation of oliguria. He is found to have an acutely elevated BUN and plasma creatinine from baseline. A Foley catheter is placed; his urine sodium (UNa) is measured below 20 mEq/L and fractional excretion of sodium (FENa) below 1%. [polldaddy poll=8545511]

Question 2.  A 54-year-old man presents to the ED in acute renal failure (ARF). [polldaddy poll=8545512]

Answer 1.  D. This patient’s oliguria with acutely elevated BUN and plasma creatinine suggest that he is in acute renal failure (ARF). His UNa <20 mEq/L and FENa <1% indicate that he has intact reabsorptive function and is able to conserve sodium. This is consistent with prerenal azotemia as the cause for his ARF.

Acute tubular necrosis (ATN) (A), loop diuretics (e.g., furosemide) (B), and osmotic diuresis (e.g., mannitol) (C)all lead to UNa >20 mEq/L and FENa >1% because there is impairment in the ability to concentrate the urine. In such cases, a high-sodium load is excreted.

Answer 2. A.   Acute tubular necrosis (ATN) is a severe form of impairment of tubular epithelial cells caused by ischemia or toxic injury. It is a leading cause of ARF. One of its hallmarks is the presence of brown granular casts on urinalysis. These contain cellular debris rich in cytochrome pigments. In contrast, hyaline casts (B) are usually nonspecific but present after exercise; red cell casts (C) are indicative of glomerular hematuria (e.g., glomerulonephritis); and white cell casts (D) imply renal parenchymal inflammation (e.g., acute interstitial nephritis, pyelonephritis).