Renal Ultrasound for Elevated Serum Creatinine

A sagittal ultrasound image of the right kidney shows a normal-sized kidney with normal parenchymal echogenicity in a patient with acute renal failure. 

What clinicians want to know is whether elevated serum creatinine "acute or chronic" 

• This information is important to narrow differential diagnosis, urgency of investigation and treatment. 
• Chronicity of renal dysfunction can be determined with 1) a search for previous measures of renal function (i.e., old labs), 2) clinical history (i.e., recent onset of acute illness, oliguria that would suggest acute renal failure), 3) daily deterioration of renal function (suggestive of acute renal failure - ARF), 4) ultrasound
• ARF can be prerenal, renal or postrenal

Why Ultrasound?

• Ultrasound can help determining the kidney size. Small renal size (less than 8 cm in adults) is suggestive of CRF
• Demonstrate hydronephrosis, suggesting a postrenal cause. Note that to produce ARF, both kidneys must be affected (i.e., bilateral ureteric obstruction or bladder outlet obstruction, or hydronephrosis of a single functioning kidney)
• To exclude obstruction, US should be done as early as possible. But US is not necessary if there are "clear reversible causes on initial assessment + Rx instituted + clear evidence of prompt response with return to normal renal function within a few days"
• Increased echogenicity of renal cortex is not a sensitive measure of renal function. When present, it is more commonly seen in tubulointerstitial disease rather than glomerular disease

Limitations of Ultrasound

• No hydronephrosis is not equal to no obstruction. False negative study can occur 1) in the first few days of obstruction because the collecting system is relatively noncompliant, 2) if ureters and collecting systems are encased by tumor or fibrosis
• Detection of hydronephrosis can be difficult in patients with cystic kidney disease

Reference:

Baxter GM, Sidhu PS. Ultrasound of the urogenital system, 2006.

Gallbladder Cholesterolosis

Longitudinal US image of the gallbladder demonstrates multiple tiny echogenic spots within the wall with comet-tail artifacts. No evidence of gallbladder wall thickening. 

Facts:

• Other names: cholesteatosis, strawberry gallbladder
• Common, degenerative, proliferative changes of gallbladder
• Usually in females during their 4th and 5th decades
• Usually asymptomatic
• Not associated with increased risk of malignancy, cholelithiasis or cholecystitis

Differentiation from Adenomyomatosis:

• May be difficult at times because they may coexist and are believed to be a continuum of same pathology
• In cholesterolosis, the gallbladder has normal size, shape, lumen and often normal wall thickness

Reference:

Schmidt G. Differential diagnosis in  ultrasound imaging: A teaching file, 2006

Early Signs of Ischemic Brain Injury on Noncontrast CT

Axial noncontrast CT images of the brain of two different patients presenting with acute stroke within 3 hours of symptom onset. The top row is images in a "brain" window, while the bottom row shows images in an "acute stroke" window. Early ischemic changes (cortical ribbon sign) of the right posterior inferior cerebral artery (left images) and right middle cerebral artery (right images) are much better appreciated on the acute stroke window.  

Loss of gray-white differentiation

• Lenticular obscuration: loss of distinction among basal ganglia nuclei
• Insular ribbon sign: blending of densities of cortex and white matter of insula
• Cortical ribbon sign:  blending of densities of cortex and white matter of other lobes

Swelling of gyri producing sulcal effacement

Detectability

• Seen on less than 1/3 of patients imaged within 3 hours of symptom onset
• Detection influenced by infarct size, severity and time between symptom onset and imaging
• Large interobserver variability, which may be improved by the use of a structured scoring system such as Alberta Stroke Program Early CT Score (ASPECTS) or the CT Summit Criteria, as well as the use of better CT windowing and leveling (use of "acute stroke" window)

Implications of these signs to management

• More rapid these signs become evident, the more profound the degree of ischemia
• Presence, clarity and extent of these signs on noncontrast CT correlates with higher risk of hemorrhagic transformation after Rx with fibrinolytic agents
• Involvement of greater than 1/3 of MCA territory increases risk of intracranial hemorrhage, shown in a European trial in patients of less than 6-hour symptom onset. This criterion has been used as an exclusion from entry in several trials evaluating the benefit of IV fibrinolytic therapy in the 3- to 4.5-hour window

Reference:
Jauch EC, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013 (January)

Updated Nomenclature of Vasculitides

A sagittal-curved-reformatted CT image of the aorta of a 31-year-old man demonstrate extensively calcified intima and focal narrowing of the mid/distal thoracic aorta, consistent with Takayasu arteritis.

Very recently, the international consensus conference addressed the revision of the nomenclature of systemic vasculitides as follows:

• LARGE-vessel vasculitis: Takayasu arteritis and giant cell arteritis
• MEDIUM-vessel vasculitis: polyarteritis nodosa, Kawasaki disease
• SMALL-vessel vasculitis: ANCA-associated vasculitis (microscopic polyangiitis, Wegener, Churg-Strauss), immune complex vasculitis 
• VARIABLE-vessel vasculitis: Behcet disease, Cogan syndrome
• SINGLE-ORGAN vascuiltis: cutaneous leukocytoclastic angiitis, primary CNS vasculitis, and others
• Vasculitis associated with systemic diseases such as lupus, rheumatoid arthritis and sarcoid
• Vasculitis associated with probable etiology (e.g., associated with viral hepatitis, drugs) 

Categorization by vessel size reflects the arteries those are predominantly affected. Vasculitis in each category can affect any size artery. 

Reference:

Jennette JC, et al. 2012 revised international chapel hill consensus conference nomenclature of vasculitides. Arthritis Rheum 2013;65:1-11.

Endovascular Treatment Not Superior to Intravenous TPA for Acute Stroke

A study published in the New England Journal of Medicine (6 Feb 2013) did not find different outcomes of acute stroke patients treated with endovascular therapy vs intravenous TPA

Background

• IV recombinant tissue plasminogen activator (t-PA) is the standard treatment for acute ischemic stroke
• Endovascular (intraarterial) treatment has higher recanalization rates but whether this translates into more favorable clinical outcome is unknown
• Prior trials of endovascular treatment showed promising results but there were problems with 1) limited generalizability, 2) lack of comparison between endovascular Rx and IV t-PA, 3) endovascular Rx was not assessed as a multimodality procedure

Study Methods and Results

• Multicenter, open-treatment clinical trial with a blinded end point
• Questions: whether outcomes were better with endovascular Rx than with IV t-PA
• Included patients are between 18-80 years, with a clearly defined time of stroke onset that was less than 4.5 hours (for IV t-PA) or 6 hours (for endovascular Rx)
• 362 patients with acute ischemic stroke were randomized to either endovascular Rx (IA thrombolysis with rt-PA, mechanical clot disruption or retrieval, or a combination of these) or to IV rt-PA
• Primary outcome = disability-free survival at 90 days, secondary outcome = proportion of patients with mild neurologic deficit or none and several safety measures
• Disability-free survival at 90 days = 30% in endovascular group, 35% in IV group. This did not change after adjustment for age, sex, stroke severity or presence of atrial fibrillation

Reference:
Ciccone A et al. Endovascular treatment for acute ischemic stroke. N Eng J Med 2013 Feb 6.
Read the full study HERE