The Clots That Traveled Far and Distal

Today we discussed a case of an elderly gentleman who presented for AKI 5 weeks after a FEVAR with bilateral renal artery stent placement for a 6.5cm juxtarenal AAA.

We first reviewed the major risk factors for AAA:

  • elderly age, male
  • smokers
  • connective tissue disease

We then reviewed the USPSTF recommendation for AAA screening, which is one-time screening of all male patients 65-75 with any smoking history

We discussed indications for AAA repair

  • Ruptured -> emergent repair (endovascular management is a possibility)
    • Severe pain, hypotension and pulsatile abdominal mass in 50% of patients
    • Often misdiagnosed as renal colic, diverticulitis, GI hemorrhage, ischemic bowel
  • Symptomatic of any size or configuration who do not have a prohibitive surgical risk for repair should be urgent AAA repair
    • Abdominal pain, flank pain, limb ischemia, systemic manifestations such as fever or malaise
  • Asymptomatic infrarenal AAA <5.5cm = conservative
  • Asymptomatic AAA >5.5cm OR rapid expansion OR co-existing PAD OR female gender = elective repair
  • Asymptomatic AAA > 5.5cm with life expectancy <2 years, no repair

We then started reviewing the case, and quickly found out that this patient’s prior hospitalization was notable for livedo reticularis, blue toe syndrome and ischemic colitis. His discharge Cr was roughly stable and it was only 3 weeks later that he started having a significant rise in the Cr. His urine revealed no RBCs, a single eosinophil and no casts. A CT abdomen/pelvis without contrast revealed no stent migration or kinks and a renal duplex US revealed patent flow.

Nephrology reviewed all the data and were confident in their diagnosis: renal atheroemboli. Here’s what you need to know:

  • Vast majority will be iatrogenic, so look for a precipitating event such as angiography, lytic therapy or cardiovascular surgery
  • Look for subacute kidney injury (peaking 3-8 weeks after the event) and signs of extrarenal embolization (GI bleeding, focal neurologic deficits, blue toe syndrome, livedo reticularis
  • Eosinophilia, Eosinophiluria and Hypocomplementemia may all suggest atheroemboly
  • No proven effective medical therapy in patients with atheroembolic renal disease and management is supportive as well as considering how to prevent further embolization
  • Prognosis is generally poor, as many will have a stepwise decline in their renal function due to scarring as well as new embolic events and up to 1/3 may require renal replacement therapy

 

2nd Degree Heart Block Dissected

Today we went over the case of an elderly man with episodes of lightheadedness for one month who was found to have 2nd degree AV block on EKG in the ED (with old LBBB as well). Capture

EKG Criteria for AV blocks:

1st degree: PR prolongation (>200msec)

2nd degree Mobitz I: Wenckebach, progressively prolonging PR interval followed by a “dropped beat,” or nonconducted p wave

2nd degree Mobitz II: constantly prolonged PR followed by a “dropped beat,” or nonconducted p wave

3rd degree or complete: complete AV dissociation between p waves and QRS’s

As you move from 1st toward 3rd degree, the block is more clinically severe, more likely to need treatment, and more symptomatic. Anatomically as you move from first to third, the block becomes more distal in the conduction system.

2:1 Second Degree AV Block: Is it Mobitz 1 or Mobitz II?

In the above EKG, we see a 2:1 second degree AV block, which means that every other p wave is conducted. This does not allow us to see the progression of the PR interval. How are we to know if it is prolonging (Mobitz I) or constant (Mobitz II)? There are 4 ways to help answer this question:

  1. Look at the company it keeps. If you see periods of 3:2 in your patient’s telemetry, the 2:1 block you see on your EKG is likely the same type of block as the periods of 3:2.
  2. If the PR is >300msec or the QRS is narrow, your block is more likely to be Mobitz I (higher up the conduction system in origin).
  3. Give atropine! If the AV nodal conduction is enhanced (less frequent nonconducted p waves), your block is likely Mobitz I. If there is no response, your block is likely Mobitz II.
  4. Carotid sinus massage: This increases vagal tone, which will increase the blockade in Mobitz I, but improve conduction in Mobitz II by allowing more time for excitability to return to the bundle of His.

 

Epidural Abscess

On February 5th, we went over a fascinating case of a middle-aged man with foot osteomyelitis due to chronic diabetic foot ulcer who presented with back pain, fever, and leukocytosis, found to have epidural abscess.

Below is the illness script for epidural abscess:

Capture

THE Dermatologic Emergency: SJS/TEN

On January 29th, our very own PGY-2 Hong Le, presented a case of the most well-known dermatologic emergency for our review: an elderly gentleman recently started on antibiotics for a urinary tract infection presents with a full body painful rash.

SJS and TEN are a spectrum of disease, TEN being more severe and SJS less severe. TEN covers >30% of total body surface area and SJS covers <10%. If between 10 and 30 percent of TBSA is covered by the rash, it is termed SJS/TEN overlap syndrome. A good way to estimate body surface area is to use the area of your hand as an estimate of 1%. 

Capturesure SJS/TEN is provoked by exposure to an inciting drug. Complete lists of drugs with reported association with this condition can be found online, but the most notable categories include allopurinol, antiepileptics, antibacterial sulfas, nevirapine (NNRTI), and NSAIDs ending in “-oxicam.” Patients with HIV have a particularly increased risk of developing SJS/TEN. The typical exposure period before reaction is 4 days to 4 weeks, but risk continued for 8 weeks after treatment with a new drug. 

The classic description and progression of SJS/TEN on physical exam are as follows. First, a flu-like prodrome may occur (malaise, myalgias, arthralgias, and fever) 1-3 days before the onset of rash. When the rash begins, it is extremely painful, ill-defined, coalescing macules with purpuric centers on the face and thorax that spread diffusely and symmetrically. These lesions are typically termed “dusky.” It usually spares the scalp, palms, and soles. Soon vesicles and bullae form and within days, the skin sloughs. Mucosal surfaces are involved in >90% of patients, which may cause symptoms such as photophobia, conjunctival itching/burning, odynophagia, dysuria, and painful defecation. Nikolsky sign is positive in these patients (the skin sloughs when tangential pressure is applied). Other diseases with a positive Nikolsky sign include pemphigus vulgaris and staphylococcal scalded skin syndrome. The “wet newspaper sign” is also classic for SJS/TEN, the shiny and lighter tone of exposed skin after a layer of affected epidermis sloughs off. The SCORTEN score can be used to determine prognosis and severity of the condition. 

Treating SJS/TEN is mainly supportive, including removing the offending agent, IV fluids, wound care, nutrition, and electrolyte repletion, but a multidisciplinary approach is necessary. Consults to dermatology, burn surgery, ophthalmology, OBGYN for a vaginal exam if the patient is female, and possible urology consult for males should occur immediately. High suspicion for infection and low threshold to start antibiotics are also beneficial.

There are multiple adjunctive treatments your dermatology consultants may recommend, but additional research is needed on most of them. Cyclosporine, anti-TNF drugs, steroids, IVIG, and plasmapheresis are a few of them.

Bilateral Lower Extremity Weakness

On January 28th, our wonderful PGY-1 Rainy Zhang presented a very interesting case of a young woman with a history of cancer presented with bilateral lower extremity weakness and numbness with hyperreflexia of the lower extremities concerning for spinal cord compression. Fortunately, the patient’s MRI spine did not show any pathology and her symptoms resolved within hours, indicating a likely somatic symptom disorder.

Here is a useful tidbit from our discussion:

Capture

 

HRS Type 1 and when to use a FENa

On January 15th, our amazing PGY2 Simi Sharma presented a case of a middle-aged man with alcoholic cirrhosis presented with decreased urine output, worsening leg swelling, and shortness of breath for one day. His labs revealed acute renal failure with a Cr of 5.8, up from a baseline of 1.2 only weeks before. Urinalysis did not show pyuria and only had 4 RBCs after Foley catheter placement, 11-20 granular casts were noted.

For this patient, getting urine electrolytes (Urine Cr, sodium, +/- urea) can be a valuable next step in finding the etiology of his acute renal failure. However, FENa calculations tend to be overused to determine the cause of AKI in hospitalized patients.

In order to use FENa (fractional excretion of sodium) to determine the cause of AKI, your patient should be oliguric without underlying CKD and NOT be on diuretics.

If your patient is not oliguric, FENa is not reliable to differentiate between prerenal AKI and ATN. In adults, oliguria is defined as a urine output of <0.5mL/kg/h or <300mL of urine per 24 hours.

If your patient has CKD, their sodium excretion may be enhanced or impaired to an unpredictable degree. Therefore, FENa may not be accurate.

If your patient is on diuretics, their sodium excretion will be increased regardless of the etiology of their kidney injury. FEUrea is a better way to distinguish between prerenal AKI and ATN in these patients. However, urine sodium should still be measured as an indication of hydration (if the urine sodium is low despite diuretics, they are likely very volume down).

The FENa should only be used to differentiate between prerenal AKI and ATN. It cannot exclude other causes of intrinsic kidney disease (glomerulonephritides etc) or postrenal kidney disease. Many causes of intrinsic AKI may have a FENa that looks prerenal. 

Hepatorenal Syndrome:

Hepatorenal syndrome is acute renal failure without other etiology in a patient with advanced cirrhosis and portal hypertension. It is essentially a diagnosis of exclusion. Their urinalysis should be bland, they should not be in shock or have an infection such as SBP, and they should not be on nephrotoxic drugs. Prerenal AKI should be excluded by volume expansion via albumin infusion 1g/kg body weight per day. If Cr rises despite this and other etiologies are excluded, HRS can be diagnosed.

HRS is classified in two different types. Type 1 HRS is rapidly progressive and defined by at least a twofold increase in serum Cr to a level of >2.5 during a period of less than 2 weeks. Type 2 HRS is any lesser degree of renal impairment.

Treatment of HRS type 1 includes ICU admission, octreotide infusion, and vasopressor support (usually norepinephrine in type 1 HRS) with continued albumin infusion of 25-50g/d until octreotide and pressors are discontinued. Treatment is continued for a total of 2 weeks. If there is some, but not total improvement in renal function, treatment duration may be extended, but if no improvement is noted, treatment is likely futile and prognosis is very poor. Hemodialysis can sometimes be used as a bridge to liver transplant or when there is a possibility of improvement in liver function, and therefore renal function, such as in potentially reversible causes of renal failure like Tylenol overdose.

However, if there is no possibility of listing a patient for liver transplant, HRS type 1 carries an 84% mortality at 6 months. For all patients with HRS type 1, palliative care and end of life discussions should be strongly considered. 

Tumor Lysis Syndrome

Today, Dr. Adrian Garcia presented an interesting case of tumor lysis syndrome in a patient with uncontrolled CML

Tumor lysis syndrome is a constellation of lab abnormalities caused my massive tumor cell lysis and is considered an oncologic emergency.  Classically, it presents soon after the initiation of cytotoxic therapy, but spontaneous TLS can also occur (usually in hematologic malignancies including leukemia and lymphoma).

It’s symptoms are nonspecific, but can include constitutional symptoms (anorexia, lethargy, nausea), symptoms of nephrolithiasis (hematuria, flank pain), and consequences of electrolyte abnormalities (heart failure, arrhythmias, seizures, muscle cramps, tetany, syncope, and sudden death). Lab findings include the following:

  • Byproducts of cell-lysis:
    • Hyperphosphatemia
    • Hyperkalemia
    • Hyperuricemia (nucleic acids are broken down into uric acid)
  • Secondary hypocalcemia caused by hyperphosphatemia
  • Acute kidney injury due to nephrolithiasis from uric acid and calcium phosphate stones

The treatment of tumor lysis syndrome includes:

  • High-volume normal saline with a loop diuretic to wash out renal crystals
  • Electrolyte correction:
    • Rasburicase for hyperuricemia
    • Phosphate binders for hyperphosphatemia
    • Hyperkalemia treatment: Kayexalate, insulin/D50, bicarb, albuterol, calcium gluconate if EKG changes
    • Do not treat hypocalcemia unless symptomatic due to increased risk of calcium phosphate precipitation in the renal tubules
  • Indications for hemodialysis:
    • severe oliguria or anuria
    • intractable fluid overload
    • persistent hyperkalemia
    • hyperphosphatemia-induced symptomatic hypocalcemia
    • calcium-phosphate product >= 70

Thanks so much for following along with our interesting cases.