Protect those nephrons! From AMR this week, a handy primer on CKD for your continuity clinic.
When do your patients have CKD? Decline in GFR for >3 months PLUS Evidence of Kidney Disease (evidenced by one of the following)
Albuminuria
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
Abnormalities detected by histology
Structural abnormalities detected by imaging
History of kidney transplantation
Figure out what caused it: 75% are HTN and/or Diabetes
Glomerular disease
Obstructive uropathy
Vascular diseases
Hepatorenal/cardiorenal syndromes
Congenital disease: PKD
Do the workup:
GET THE UA Active sediment/proteinuria vs a bland UA will be a major branch point in your evaluation, so you have to get a UA. Spot urine protein and creatinine are also useful.
US Looking for cystic kidneys, hydronephrosis, asymmetry, or even symmetric evidence of “medical renal disease” is useful.
Based on historical clues, you can also check: HIV, hepatitis serologies, SPEP/UPEP, ANA, ANCAs
Stage it: based on GFR. VGFR- MDRD and CKD-EPI are most commonly used formulas. Here’s a handy calculator that gives you both, plus the stage.
Stage
Description
GFR
1
Kidney damage with nl GFR
>90
2
Kidney damage with increased GFR
89-60
3a
Moderately decreased GFR
59-45
3b
44-30
4
Severely decreased GFR
29-15
5
Kidney failure
<14 or on dialysis
Call for Backup: Nephrology Referral
You don’t know why the patient has kidney disease
It is progressing quickly (loss of 50% of their GFR within one year)
Nephrosis: Lots of proteinuria (>3g/day)
Nephritis: active urine sediment with blood, protein, casts
Dialysis planning: sometime during stage3b is probably ideal, certainly by the time patient has GFR <30
Mortality benefit for patients that see nephrology earlier.
Well, I was publicly called out this week to do a post, so I better deliver. Thanks much for the suggestion, my goal is always to provide interesting, relevent content that helps you out in clinic. Remember that you can search the whole blog with the search box, tags, or use the big categories at the top of the page. Archives are there to help you!
Anyway… on to vertigo!
Vertigo is a sensation of movement without moving. If you’ve done this…
or this…or this…
then you know vertigo.
A big branch point in the differential diagnosis is Central vs Peripheral causes. Central causes are the “scarier” ones: brainstem or cerebellar stroke/TIA or MS. Peripheral causes are the ones we are more comfortable diagnosing and treating: BPPV, Meniere’s diease, vestibular neuritis, acoustic neuroma. Migrainous vertigo can walk the line between central and peripheral, and have features of both.
Most vertigo has some postural instability associated, and it often feels worse to move the head in the midst of an attack. Specific, predictable maneuvers (like rolling over in bed) that precipitate vertigo should make you think of BPPV. Most patients with peripheral causes of vertigo should be able to walk. When the postural instability is so severe that they can’t walk, that points toward a central cause.
Vertigo doesn’t last forever. Even with permanent damage to the vestibular system, the body compensates and the vertigo subsides. However, the time course can help you with the diagnosis: BPPVusually is short-lived– a minute or less, while migrainous vertigo can last minutes to hours. Vestibular neuritis, brainstem infarction and MS can produce vertigo that is severe and lasts for days.
Nystagmus is often found with vertigo. Central causes can have nystagmus in any direction, while peripheral causes will only have horizontal nystagmus. Nystagmus that reverse direction when the patient looks from right to left suggests a central cause.
Apart from the Romberg and nystagmus, an otherwise normal neurologic exam suggests a peripheral cause. If your patient has weakness, cerebellar signs, or abnormal reflexes, be worried about those central causes. Interestingly, hearing loss or tinnitus does suggest a peripheral cause, most commonly Meniere’s disease or acoustic neuroma.
Of course, there are some specific maneuvers that can help you out. The Dix Hallpike maneuver is most helpful if your patient is not symptomatic when you examine them. If you can elicit the vertigo and/or nystagmus with the maneuver, it is suggestive of BPPV. My favorite video demonstration of Dix-Hallpike is here.
There is also the Head Thrust Maneuver. This is useful for diagnosing vestibular neuritis as compared to a central vertigo. The concept is that the patient focuses on a distant object, and tries to maintain focus while the examiner abruptly turns the patient’s head about 15 degrees. A normal response is to keep the eyes fixed on the object. Patients with cerebellar lesions have a normal response. The abnormal response is for the eyes to deviate, toward the lesion, and then slowly return to the object. Peripheral causes of vertigo, like vestibular neuritis, tend to result in an abnormal head thrust response.
Up To Date has a great table to help differentiate the common and concerning causes of vertigo. It is so good, I’ve just reproduced it here for you. Another great resource for dizziness in general is this AAFP article (if you don’t have institutional access, Am Fam Physician. 2010 Aug 15;82(4):361-368).
Time course
Suggestive clinical setting
Characteristics of nystagmus•
Associated neurologic symptoms
Auditory symptoms
Other diagnostic features
Benign paroxysmal positional vertigo
Recurrent, brief (seconds)
Predictable head movements or positions precipitate symptoms
Falls toward side of lesion, no brainstem symptoms
Usually none
Head thrust test usually abnormal
Meniere disease
Recurrent episodes, last minutes to several hours
Spontaneous onset
Peripheral characteristics
None
Episodes may be preceded by ear fullness/pain, accompanied by vertigo, unilateral hearing loss, tinnitus
Audiometry shows unilateral low frequency sensorineural hearing loss
Migrainous vertigo
Recurrent episodes, last several minutes to hours
History of migraine
Central or peripheral characteristics may be present
Migraine headache and/or other migrainous symptoms accompanying or following vertigo
Usually none
Between episodes, tests are usually normal
Vertebrobasilar TIA
Single or recurrent episodes lasting several minutes to hours
Older patient, vascular risk factors, and or cervical trauma
Central characteristics
Usually other brainstem symptoms
Usually none
MRI w/DWI may demonstrate vascular lesion
Brainstem infarction
Sudden onset, persistent symptoms over days to weeks
As above
Central characteristics
Usually other brainstem symptoms, especially lateral medullary signs
Usually none; an exception is anterior inferior cerebellar artery syndrome
MRI will demonstrate lesion
Cerebellar infarction or hemorrhage
Sudden onset, persistent symptoms over days to weeks
Older patient, vascular risk factors, especially hypertension
Central characteristics
Gait impairment is prominent. Headache, limb dysmetria, dysphagia may occur.
None
Urgent MRI, CT will demonstrate lesion
* Other diagnoses described in text “Pathophysiology and differential diagnosis of vertigo”.
• Peripheral characteristics of nystagmus: horizontal or horizontal-torsional; suppresses with visual fixation, does not change direction with gaze. Central characteristics of nystagmus: may be horizontal, torsional, or vertical, does not suppress with visual fixation, may change direction with gaze.