CRAM Flashcards
Dietary recommendations: Ca++ stones and high urinary Ca++
Limit Na+
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++Oxalate stones + high urinary oxalate
Limit oxalate
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++ stones + low urinary citrate
Limit non-dairy animal protein and increase fruits and veggies
Dietary recommendations: Uric acid or Ca++ stones and high urinary uric acid
Limit non-dairy animal protein
Dietary recommendations: Cystine stones
Limit Na+ and protein intake
Medical therapy:
Recurrent stones + high urinary Ca++
Thiazide diuretic
Medical therapy:
Recurrent Ca++ stones + low urinary citrate
Potassium citrate
Medical therapy:
Recurrent CaOx stones + hyperuricosuria + normal urinary Ca++
Offer urinary allopurinol
If uric acid stones, DON’T offer allopurinol as first-line therapy
Medical therapy:
Recurrent Ca++ stones without other lab abnormalities
Empiric thiazide diuretics and/or K-cit
Medical therapy:
Uric acid and cystine stones
K-cit to raise urinary pH (these stones form in acidic urine)
Medical therapy:
Cystine stones refractory to dietary changes (adequate hydration, limit salt to 2-3 g daily) and urinary alkalinization (pH >7) or large recurrent stone burdens
Offer cysteine-binding thiol drugs (alpha-mercaptopropionylglycine = Thiola = tiopropin), which is better tolerated than D-Penicillinamine
Medical therapy:
Residual/recurrent struvite stones after surgery exhausted
Offer acetohydroxamic acid (AHA = Lithostat; urease inhibitor)
q3month CBC to monitor for hemolytic anemia
This drug decreases stone growth rate, doesn’t change stone recurrence
Renacidin = citric acid glucono-delta-lactone magnesium carbonate
Used for dissolution treatment of residual struvite stones/fragments
Urease-producing organisms
Proteus, klebsiella, staph aureus, pseudomonas, providentia, ureaplasma
Enteric/acquired hyperoxaluria is a/w:
IBD and short-gut syndrome
Unabsorbed fat binds to Ca++ –> oxalate goes unbound until it is reabsorbed in the colon –> high oxalate in the blood and then urine –> treat with Ca++ supplementation to bind oxalate in the gut
Crohn’s stone formation
low urine volume (dehydration) + low urine pH and hypocitraturia (metabolic acidosis) + hyperoxaluria (over absorption of intestinal oxalate –> CaOx stones
Isolated hypomagnesemia
Suggests IBD –> refer to GI
PO Reloxaliase
Recombinant oxalate decarboxylase enzyme derived from B. subtilis and expressed in E. Coli
Degredes oxalate within GI tract –> decreased oxalate absorption and urinary excretion
Lumasiran = Oxlumo
siRNA
decreases glycolate oxidase, which decreases glyoxylate’s conversion to oxalate
Approved for Tx of type 1 primary hyperoxaluria
CF is a/w which urinary abnormalities?
Hyperoxaluria, hypocitraturia (prone to stones)
Prevent stones: Roux-En-Y
Dietary Ca++ at mealtime
Decrease high oxalate foods
Metabolic acidosis –>decreased urinary citrate –> K-Cit
Stones: Colon resection and end ileostomy
Fluid and bicarbonate loss
Concentrated urine with low pH
Increased risk of uric acid stone formation
Lesch-Nyhan Syndrome
Absence of HGPRT
Neuro dysfunction, behavioral disturbances, uric acid overproduction with hyperuricosuria and hyperuricemia
A/w uric acid stones
Patients can get xanthine oxidase stones while on allopurinol –> decrease (don’t stop) allopurinol and start K-cit
Pregnancy and stones
Placental production of VitD –> increases calcium absorption and decreases serum PTH –> physiologic hypercalciuria
BUT
Urine citrate and GAG also increased so stone formation risk is unchanged
Ammonium acid urate stones
Rare, a/w chronic diarrhea and heavy laxative use/abuse, decreased urinary Na+ excretion,
pH >6.3, and ileal or large volume colon resection
Radiolucent stones, can be mistaken for uric acid stones
AAU stones no NOT dissolve with alkalinization
Idiopathic (endemic) bladder stones are also AAU (kids with cereal based diets)
Keto(genic) diet affect on stones
Excess meat (purine) consumption
Hyperuricosuria, increased urinary sulfate + urea nitrogen
Hypercalciuria
Hypocitraturia
Decreased urine pH
Uric acid + calcium nephrolithiasis
Treat with dietary changes +/- allopurinol
Topiramate and stones
Topiramate creates a chronic intracellular acidosis
Urinary milieu similar to distal RTA with hyperchloremic acidosis, HIGH urine pH, SEVERE hypocitraturia and hypercalciuria
Treat with cessation of topiramate or K-cit
Vitamin C effect on urine
10-20% is metabolized into oxalic acid and excreted into urine
Most common risk factor for Ca++ stones
Hypercalciuria
Absorptive hypercalciuria pathophysiology
Increased GI Ca++ absorption
Normal or increased serum Ca++
Decreased serum PTH and decreased vitamin D
Absorptive hypercalciuria management options
Avoid excess dietary Calcium
Decrease salt and animal protein in diet
Thiazides +/- K-Cit
Renal calcium leak hypercalciuria pathophysiology and management
Increased calcium loss into urine
Normal or decreased serum Calcium
Increased serum PTH
Management: Thiazides +/- K-Cit
Renal phosphate leak hypercalciuria pathophys and management
Increased phosphate loss in urine, decreased serum phos
Increases vitamin D, which increased GI calcium absorption
treat with PO orthophosphates
Resorptive hypercalciuria pathophys and management
HyperPTH leads to increased Ca++ resorption from bone + increased GI Ca++ absorption –> increased serum Ca++
Tx with parathyroidectomy
Drug-induced renal calculi: TIME
Triamterene: K sparing diuretic for edema and HTN
Indinavir: protease inhibitor for HIV (non-dense stone on CT)
Magnesium trisilicate: antacid for GERD
Ephedrine +/- guaifenesin: stimulant/expectorant
Stones form due to metabolic effect of the drug
Furosemide: increases urinae Ca++ excretion, causes stones in low birth weight infants
Acetazolamide and other carbonic anhydrase inhibitors
Topiramate: severe hypocitraturia and high urinary pH –> 2% of chronic users get CaPhos stones
Zonisamide: sulfonamide anticonvulsant –> 4% of long term users get CaPhos stones
Laxative abuse: ammonium acid urate stones
Vitamin C supplements - metabolized into oxalate
Vitamin D supplements: increase Ca++ absorption
Type 1 RTA
Distal tubule can’t excrete H+ (in the form of ammonium)
Leads to systemic acidosis (decreased serum CO2) and alkaline urine (pH >5.5)
Increased urinary calcium
Decreased urinary citrate
3/4 of these patients get CaPhos stones
Treat with K-Cit + bicarb to address systemic acidosis
- Type I RTA can be drug-induced (ifosfamide for NSGCT pr penile cancer)
Anion gap is not elevated in RTA
Type 1 distal RTA is a/w nephrocalcinosis
Type II Proximal RTA
Proximal tubule can’t reabsorb HCO3
Increased urine calcium but stable citrate, so not increased stone formation risk
What is a thiazide challenge?
Give two weeks of a thiazide
Recheck serum Ca++, PTH, urine calcium
Used to differentiate renal hypercalciuria (thiazide corrects primary problem of renal calcium leak so urinary Ca++ goes to normal) and true hyperparathyroidism (thiazide blocks appropriate renal response of Ca++ excretion leading to worsening hypercalcemia –> tx with parathyroidectomy)
Medullary sponge kidney + hypercalciuria treatment
Thiazide to arrect stone development
They still need metabolic evaluation
Radiolucent Stones
Ammonium acid urate
Indinavir
Uric acid
Xanthine
Triamterene
Citrate mechanism
Binds Ca++ in urine and intestines
Raises urine pH
Decreases spontaneous nucleation of CaOX
Medical treatment of nonobstructing uric acid stones (HU 300-500) with acidic urine (pH <5.5)
Try to dissolve stones by raising pH with K-Cit
Uric acid or cysteine stone formers whose urine remains pH <6.5 despite K-Cit…
Can try adding acetazolamide (CAI) to further raise pH
Recurrent CaOx stone former sand high urinary oxalate refractory to diet changes
Treat with pyridoxine (vit B6)
Increases conversion of glyoxylate to glycine and decreases conversion to oxalate by LDH
What should Cr level be in an adequately collected 24 hr urine study?
About 1 gram
Improved dusting efficiency
Longer pulse width/duration
Lower peak power (lower energy and higher frequency)
Improved fragmentation efficiency
Shorter pulse width/duration
Higher peak power (low frequency, higer energy)
Physiologic changes with ureteral stent placement
Hyperplasia and inflammation of urothelium
Smooth muscle hypertrophy
Decreased ureteral contractility
Increased VUR
Increased intrapelvic pressure
Physiology of complete ureteral obstruction
Increased glomerular perfusion pressure via preglomerular vasodilation (BL and UL)
Efferent arteriolar constriction (BL only)
Pathophysiology of unilateral renal obstruction
Acute phase (1-2 hours):
Increased renal blood flow (decreased afferent arteriolar resistance)
Little change in GFR
- Mediated by increased NO and PGE2
Mid phase (2-5 hours):
Renal blood flow decreases (increased afferent arteriolar resistance)
GFR decreases (increased proximal tubular hydraulic pressure, increased afferent arteriolar resistance)
Late Phase (24 hours):
Renal blood flow decreased (increased afferent arteriolar resistance)
GFR still decreased (now decreased proximal tubular hydraulic pressure, increased afferent arteriolar resistance)
- Mediated by decreased NO
In solitary kidney, GFR immediately goes down. Late phase mediated by ANP.
Physiology: PCT
2/3 of glomerular ultrafiltrate is reabsorbed in PCT (all AAs and glucose) in isosmotic fashion coupled to Na+ active transport
PCT is responsible for ammoniagenesis (formation of ammonia from glutamine)
Physiology: Descending Thin Loop of Henle
Descending = downhill = ‘easy’ for water to exit through the wall of the loop –> filtrate becomes hypertonic
Physiology: Ascending Thick Loop of Henle
Thick LoH = ascending = water impermeable
Reabsorption of Na+ via 2Cl-K-Na triporter is blocked by loop diuretics here
The medullary thick ascending loop of Henle is most ischemia-sensitive part of kidney and may be damaged with prolonged ischemia during partial nephrectomy
Physiology: Distal Convoluted Tubule
Thiazides block Na-Cl cotransporter in early distal tubule
- Promotes net calcium reabsorption Directly in Distal tubule and indirectly by way of extracellular volume depletion in proximal tubule –> decreased urine Ca++
PTH and Vitamin D stimulate calcium reabsorption in distal tubule
Renin promoters: Decreased BP (JG cells in glomerular afferent arteriole), Decreased Na+ delivery (Macula densa in DCT – abuts JG cells), increased sympathetic tone (Beta1 receptors)
Physiology: Collecting Duct
Principal cells facilitate NaCl reabsorption and Intercalated cells facilitate acid secretion
ADH increases the water permeability of distal tubule and collecting duct
- Blocked in kidney by lithium and release blocked in brain by alcohol
DDAVP works in collecting duct to absorb water
Aldosterone increases open Na+ channels and regulates Na+-K+ exchange in the collecting duct
- Amiloride blocks epithelial sodium channels in DCT and collecting duct –> reduces Na+ reabsorption and K+ secretion (K-sparing)
Parathyroid hormone
Secreted by chief cells in parathyroid in response to hypocalcemia or ectopically by peripheral malignancies (SCC of lung)
Primary role is in kidney: decreases phos reabsorption in proximal tubule and increases calcium reabsorption in ALoH, DCT and collecting duct
PTH activates enzyme 1 hydroxylase in proximal tubule –> increases vitamin D metabolism –> Increases gut absorption of Calcium
Primary hyperparathyroidism
Most common type
Inappropriate PTH secretion by parathyroid gland
= absorptive hypercalcemia
Secondary hyperparathyroidism
Appropriate PTH secretion
Occurs in response to hypocalcemia
Most commonly due to vitamin D deficiency
Angiotensin II maintains GFR during hypovolemia by…
Causing vasoconstriction of the efferent arteriole
ATN effects on urine
Renal tubular cells can no longer resorb sodium or water or excrete urea
Urine will have increased Na, decreased urea, decreased Osm
Urinary concentration is primarily the result of…
…hypertonic medullary interstitial fluid
Cisplatin is nephrotoxic because of…
…a direct toxic effect on renal tubular cells
IgA nephropathy vs. post-strep glomerulonephritis
In IgA, will have URI with renal/UA abnormalities simultaneously –> get renal biopsy
In post-strep, the renal/UA changes will be a few weeks after URI.
Path from biopsy:
IgA = crescent shaped glomeruli + mesangial proliferation
Post-strep GN = cellular proliferation
Sensitivity, specificity, PPV, NPV
Spot Urine Na+ meaning
Prerenal failure: UNa+ is <25 mEq/L because the nephron can still reabsorb Na+ and does so to increase intravascular volume
Intrinsic renal failure: UNa+ is >40 mEq/L because the nephron is no longer reabsorbing Na+ effectively
Sacral neuromodulation is FDA approved for:
Non-obstructive retention
UUI
Urgency/frequency syndrome
Chronic fecal incontinence
Interstitial cystitis
Botox mechanism of action
Decreased acetylcholine release from postsynaptic efferent nerves at presynaptic junction at bladder (by cleaving SNARE proteins (SNAP25) that otherwise allow ACh to be released into the synapse
On clinical evaluation, a patient has global polyuria as defined as >40 ml/kg urine in 24 hours. Testing and ddx?
Overnight water deprivation test
If >800 mOsm/kg –> primary polydipsia, tx with behavioral modifications
If <800 mOsm/kg –> Diabetes Insipidus, do renal concentrating capacity test
NLUTD: Unknown Risk
- Stratification
- Further workup
- Goal
Lesion in suprasacral SC (SCI, MS, transverse myelitis, spinal dysraphism) or any lesion with any GU complications or change in LUTS
Further workup: upper tract imaging + renal fxn + UDS
- Don’t perform cystoscopy
Goal: Determine medium vs. high risk
NLUTD: Medium Risk
- Stratification
- Surveillance
Imaging and renal function are normal, BUT PVR is elevated and/or UDS demonstrated retention, BOO, or DO with incomplete emptying
Surveillance: Annual H+P, renal function, annual vs. biannual upper tract imaging
- Don’t perform surveillance cysto
UDS: Repeat PRN if new symptoms/abnormalities arise
NLUTD: High Risk
- Stratification
- Surveillance
Abnormal/unstable imaging (hydro, scarring, parenchymal loss, staghorn, large/increased stone) and/or renal function and/or UDS demonstrates poor compliance, increasing storage Pdet with DO, DSD, or VUR
Surveillance: Annual H+P, renal function, annual upper tract imaging
- Don’t perform surveillance cysto
UDS: Repeat when clinically indicated and PRN if new symptoms/abnormalities arise
How is normal micturition initiated?
Relaxation of the striated (external) sphincter
Onuf’s nucleus (anterior horn S2-S4) contains the pudendal motor neurons that innervate the EUS
Onuf is the gatekeeper of micturition and needs to be inhibited in order to allow for micturition to proceed
(Sympa-gastrics, Para-pelvic, Soma-dendal)
Detrusor Leak Point Pressure Numbers
Note: This metric is only used for patients with neurogenic lower urinary tract dysfunction
DLPP is most reliable predictor of upper tract deterioration in NLUTD
DLPP >40 is predictive of future upper tract deterioration
DLPP >15 indicates impaired compliance
DLPP and VLPP are determined by the resistance of EUS to fluid leak
Interventions that don’t affect the resistance of EUS will not affect either LPP
Open bladder neck at rest without prior prostatectomy
Multiple System Atrophy
Progressive degeneration of neurons in multiple areas of the brain
Incomplete emptying, ED, “hot crossed buns sign” on MRI
Primary Bladder Neck Obstruction
Level of obstruction on VUDS is clearly the bladder neck itself
Reduce bladder neck with TUIP vs. TURP
Uroflow curve without pressure data: flattened bell
A/w adequate detrusor function with fixed obstruction
Uroflow curve without pressure data: saw tooth
A/w DU or DESD
“Poor compliance” on UDS
<10-15 cc/cm H2O is a reasonable rough definition
Practically, absolute storage pressure > 40 cm H2O is more relevant as this has been a/w deterioration of upper tracts
Spina Bifida and NGLUTD
Highly a/w NGB in children and highly a/w upper tract damage (especially with DESD on initial UDS) if not managed appropriately
Unlike SCI, in lumbosacral SB, neural function and UDS findings cannot be predicted by the level of the lesion
If SB patient develops new hydro, perform UDS
If findings concerning, get spinal MRI to rule out tethered cord or other changes prior to bladder augmentation
Higher chance of paternity with SB at which lesion level?
L5 or sacral level
Spinal shock
Bladder acontractility, areflexia, synergic internal and external sphincters, absent guarding reflex, absent somatic control of the external sphincter
Resolution: return of bulbocavernosus reflex or return of DTRs below the SCI
Guarding reflex
Ability of the striated sphincter (EUS) to contract during bladder filling
- External sphincter activity at the time of DO is part of the normal guarding reflex
Lesions above the pons (brainstem still functioning, CVA or Parkinson’s): bladder/ sphincter
Detrusor Overactivity: Yes (Parkinson’s with impaired contractility)
DESD: No
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult Pons to T6-8: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Yes
DISD: Yes
Autonomic Dysreflexia: Yes
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult T6-8 to S2: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Yes
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: No
Detrusor Areflexia: No
Neurologic Insult Injury below S2: bladder/sphincter
Detrusor Overactivity: No
DESD: No (may have fixed EUS tone at rest)
DISD: No (may have open or contracted IS)
Autonomic Dysreflexia: No
Intact Bladder Sensation: No
Detrusor Areflexia: Yes
Neurologic Insult MS: bladder/sphincter
Detrusor Overactivity: Yes
DESD: Maybe
DISD: No
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Neurologic Insult Multiple System Atrophy: bladder/sphincter
Detrusor Overactivity: Yes
DESD: No (may have EUS denervation)
DISD: No (may have open bladder neck at rest)
Autonomic Dysreflexia: No
Intact Bladder Sensation: Yes
Detrusor Areflexia: No
Lesions above the pons (brainstem still functioning like CVA or Parkinson’s)
DO with synergistic/coordinated activity of internal and external sphincters
The sphincters will relax appropriately during involuntary bladder contractions
Supra-pontine insults should NOT cause detrusor sphincter dyssynergia
Sphincter bradykinesia can occur with Parkinson’s –> slow relaxation of EUS at start of void
Lesions involving brain stem + cord above T6 (including C-spine)
After spinal shock:
Detrusor overactivity + detrusor external sphincter dyssynergia (DESD) + Smooth muscle sphincter dyssynergia (DISD) + autonomic dysreflexia
Autonomic dysreflexia
Afferent stimuli below T6 (bladder distention) in patient with injury above T6 –> massive reflex sympathetic discharge –> vasoconstriction, HTN, reflex bradycardia, flushing, HA, diaphoresis
Complete lesion between T6 and S2
After spinal shock:
Absent sensation + DO + DESD + smooth muscle sphincter synergy
DESD arises because the normal pathways for supraspinal centers to inhibit external sphincter contraction during voiding has been disrupted
Intact sacral nerve arcs (can be assessed by presence of bulbocavernosus reflex) are required for DESD
Detrusor External Sphincter Dyssynergia
Involuntary rise in EMG activity (EUS contraction) during an involuntary DO contraction, narrowing of the membranous urethra, which can lead to incomplete bladder emptying and risk to upper tracts
Further neurological evaluation is warranted (i.e. MS)
Sacral nerve arcs must be present to have DESD, intact bulbocavernosus reflex indicates the presence of sacral nerve arcs (only 70% of women have this reflex, 30% do not)
Sphincterotomy is a historical option for a patient with DESD (new hydro or on UDS) and inability/refusal to CIC.
Actual DESD is only possible in the setting of a spinal cord lesion; a patient may have pelvic floor dysfunction with symptoms that sound like DESD - the most likely UDS finding for such a patient is a low peak flow rate –> try PFPT or SNM
Cauda Equina (Horse’s Tail): L2-S5 spinal nerve bundle
STARTS at L1 vertebra, typically a/w spinal pathology (disc herniation) in the L4-S2 region injury
Typically presents with lumbar spinal pain a/w bladder and bowel incontinence
Nerve compression –> impairment of parasympathetic motor and sensory fibers to the bladder and pelvic floor (bulbocavernosus reflex absent) +/- impairment of pudendal nerve fibers innervating the external sphincter
- UDS shows detrusor areflexia, normal compliance +/- denervation potentials from external sphincter
- NSGY emergency to decompress nerve
Lesions at or distal to sacral cord
Detrusor areflexia and denervation potentials on EMG
Below S2: (after spinal shock) persistent detrusor areflexia +/- decreased compliance +/- open smooth sphincter +/- residual resting sphincter
The cremasteric artery is a branch of the…
…inferior epigastric artery (from external iliac)
The vasal artery is a branch of the…
…superior vesical artery (a branch of the anterior trunk of the internal iliac)
Inferior hypogastric plexus injury (after LAR or APR or TAH)
Denervation of bladder +/- sphincter mechanisms –> areflexia (pelvic nerve damage) + fixed external sphincter tone (pudendal nerve innervation of external sphincter is disrupted) –> increased outlet resistance –> areflexic poorly compliant bladder –> UDS shows decreased compliance, incompetent bladder neck, fixed EUS, detrusor underactivity
SCI in T11 - L2 may damage sympathetic supply to bladder and impair tonic outlet resistance…
Crede maneuver may allow patient to overcome remaining outlet resistance and void
Quinolones side effects
(ciprofloxacin, levofloxacin, etc)
Inhibit DNA gyrase
May cause false positive on opiate screen
Risk of tendon rupture
Affect metabolism of theophylline (tx asthma/COPD), caffeine
Painful necrotic penile ulcer + painful inguinal LAD
Gram-negative coccobacilli (haemophilus ducreyi)
Chancroid
Tx with Azithromycin (1g PO)
Gonorrhea treatment
Single dose IM ceftriaxone
Chlamydia treatment
10 days PO doxycycline
Non-gonoccocal urethritis
think chlamydia or ureaplasma
treat with two weeks PO doxycycline vs. single dose azithromycin
Alpha-blocker most likely to cause retrograde ejaculation?
Least likely?
Most = Silodosin
Least = Alfuzosin
Prostatitis is characterized into 4 syndromes
Category I: ABP, MC due to E. Coli
II: Chronic bacterial prostatitis - rUTI due to same organism, mc E. Coli, enterococcus or another gram -
III: Chronic prostatitis/pelvic pain syndrome. Type A = inflammatory with WBCs, Type B = non-inflammatory, no WBCs
IV: Asymptomatic inflammatory prostatitis - incidental Dx on TRUS Bx for elevated PSA
Male urethral blood supply
Internal iliac –> internal pudendal –> branches into (from ventral to dorsal) BCD
B = bulbourethral (artery of bulb of penis)
C = cavernosal (deep artery of penis)
D = dorsal penile arteries (also supplies most of blood flow to glans penis)
How is baseline flaccidity maintained?
Tonic contraction of penile vascular smooth muscle via norepinephrine release from postganglionic sympathetic nerves
How is an erection achieved?
Parasympathetic stimulation
Release of NO from non-adrenergic, non-cholinergic nerves
NOx binds guanylyl cyclase
Increases cGMP (cGMP is broken down by PDE5)
+ protein kinase
Opens K+ channels and closes Ca++ channels
Decreases intracellular Ca++
Ca++ dissociates from Calmodulin
Relaxation of penile arterial smooth muscle and increased arterial blood flow
PGE1 also increases conversion of ATP to cAMP by adenylate cyclase
Decreases intracellular Ca++
Ca++ dissociates from Calmodulin
Relaxation of penile arterial smooth muscle
Detumescence?
PDE5 breaks down cGMP so smooth muscle relaxation is reversed + PIP3 pathway
increased intracellular Ca++
cavernosal SM contraction
increased intracorporeal pressure
slow decrease in pressure as reopening of venous channels occurs with resumption of baseline arterial flow
Rapid decrease in intracorporal pressure
Flaccidity
After complete suprasacral SCI, reflexogenic (but not psychogenic) erections are generally preserved
Sacral SCI eliminates reflexogenic erections but may not eliminate psychogenic
Painless, slowly growing ulcers without lymphadenopathy
Granuloma inguinale (klebsiella granulomatosis)
Azithromycin 1g PO weekly for 3 weeks
Doxycycline for 3 weeks
Treat partners within 60 days
NLUTD: Low Risk
- Stratification
- Further workup
- Surveillance
Lesion is suprapontine (CVA, Parkinson’s, brain tumor, TBI, CP) or distal to cord (disk disease, s/p pelvic surgery, DM)
Spontaneously voiding with low PVR
No rUTIs
No bladder stones
Normal/stable renal function and upper tract imaging
Synergistic voiding on UDS
Further workup and surveillance not indicated
Reevaluate ID new problems arise (autonomic dysreflexia, UTIs, stones, upper urinary tract or renal function deterioration)
