NEPHROLITHIASIS (quick review)

10 Feb

submitted by Christina Brown, M.D. 

Kidney stones:anatomy_kidneystones

  • Most common cause of renal colic
  • Stone composition:
    • 80%: Calcium stones (calcium oxalate > calcium phosphate)
    • 5% uric acid
    • Others: Magnesium ammonium phosphate (struvite), cystine
  • Associated with infections caused by urea-splitting organisms (eg, Pseudomonas, Proteus, Klebsiella) along with an alkalotic urine
  • 90% of urinary calculi are radiopaque.


Epidemiology and Etiology

  • 1% of the population
  • Twice as common in men as women
  • Theories on stone formation:
    • Urinary supersaturation of solute followed by crystal precipitation
    • Decrease in the normal urinary proteins inhibiting crystal growth
    • Urinary stasis from a physical anomaly, catheter placement, neurogenic bladder, or the presence of a foreign body


Pediatric Considerations

  • Rare in children
  • When present, indication of an overt metabolic or genetic disorder
  • Painless hematuria common presentation (up to 30%)


Causes of stone formation:

  • Metabolic abnormalities (50%)
  • Urologic abnormalities (20%)
  • Infection (15%)



  • Sudden onset of severe pain in the costovertebral angle, flank, and/or lateral abdomen
  • Colicky or constant pain: Patient cannot find a comfortable position
  • Hematuria: Gross hematuria in 1/3 of patients
  • Nausea/vomiting



  • Urinalysis
  • Microscopic hematuria present in >80%
  • Gross hematuria
  • Absent urinary blood in 10–30%
  • No correlation between the amount of hematuria and the degree of urinary obstruction
  • WBC/bacteria suggests infection


Imaging – CT:

  • Helical CT has replaced IV pyelogram (IVP) as test of choice.
  • Detects calculi as small as 1 mm in diameter
  • Advantages over IVP:
    • Performed rapidly
    • Does not require IV contrast media
    • Detects other non-urologic causes of symptoms, such as abdominal aortic aneurysms (AAAs)
  • Indications:
    • 1st-time diagnosis
    • Persistent pain
    • Clinical confusion with pyelonephritis


Renal Ultrasound:

  • unilateral hydronephrosis suggests possible obstructive stone
  • no radiation involved, but does not eval for non-urologic causes of symptoms



  • Hydration:
    • Initiate IV crystalloid infusion with 1 L of normal saline infused over 30–60 min followed by 200–500 mL/hr.
    • Bolus volume compromised patients with 500-mL increments until urine output adequate
  • Analgesics (morphine, ketorolac):
    • Combination of IV NSAIDS and opioids decrease ED stay.
  • Antiemetics (prochlorperazine, ondansetron, droperidol, hydroxyzine)
  • α-Blockers (tamsulosin) or calcium-channel blockers (nifedipine) have been shown to decrease time to spontaneous stone passage:
    • Most efficacious for stones <5 mm in diameter
    • Tamsulosin and nifedipine equally effective
    • prescribe on discharge.



Admission Criteria

  • Obstruction in the presence of infection mandates immediate urologic intervention.
  • Intractable pain with refractory nausea and vomiting
  • Severe volume depletion
  • Urinary extravasation
  • Hypercalcemic crisis
  • Solitary kidney and complete obstruction
  • Relative admission indications (discuss with urologist):
    • High-grade obstruction
    • Renal insufficiency
    • Intrinsic renal disease
    • Stones of size <5 mm usually pass spontaneously; those >8 mm rarely do.

Discharge Criteria

  • Normal vital signs
  • No evidence of concomitant urinary tract infection
  • Adequate analgesia
  • Able to tolerate PO fluids to maintain hydration status



  • Do not miss a vascular catastrophe mimicking as renal colic.
  • Aggressive pain management and hydration promote passage of stones
  • The absence of hematuria does not exclude the diagnosis of acute renal colic.


1. Bartosh S M.: Medical management of pediatric stone disease. Urol Clin North Am. 2004; 31:575–587. [PMID: 15313066]
2. Hollingsworth J M, Rogers M A, and Kaufman S R et al.: Medical therapy to facilitate stone passage: A meta-analysis. Lancet. 2006; 368:1171–1179.
3. Marx J A, Hockberger R S, and Walls R M: eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th ed.St. Louis, MO:Mosby;2009.

4. picture


2 Feb

Submitted by Amit Kumar, M.D.


Alpha 1: In vascular walls; causes: vasoconstriction

Beta 1: In heart; causes: increased inotropy & chronotropy

Dopamine: In renal, splanchnic, cerebral, coronary vascular beds; causes: vasodilation

Vasopressin: V1 receptors in vessels; causes: vasoconstriction, V2 receptors in kidney; maintains osmolality via ADH



VASOPRESSORS (A-1 adrenergic):

Norepinephrine (Levophed):

  • Works on A1 and B1 receptors
  • Causes: Potent vasoconstriction (+reflex bradycardia) and modest increase in CO; latter negated by reflex tachycardia
  • 1st line treatment for septic shock
  • 0.5-10mcg/min, titrate up

Phenylephrine (Neo-Synephrine):

  • Works on A1
  • Causes: Potent vasoconstriction
  • 100-180mcg/min. Once BP stable, titrate down to 40-60mcg/min

Epinephrine (Adrenalin)

  • Works primarily on B1, some on A1 and B2. Increase A1 activity in higher doses
  • Causes: Increased CO. At higher doses causes vasoconstriction as well.
  • 1st line for anaphylactic shock, 2nd line for septic shock
  • 0.1-4mcg/kg/min

Dopamine (Intropin)

  • Doses 2-5mcg/kg/min: dopaminergic (vasodilation);
  • 5-10mcg/kg/min: B1 (increased CO);
  • >10mcg/kg/min: A1 (increased vasoconstriction)

INOTROPE (B-1 adrenergic):

Dobutamine (Dobutrex)

  • Works on B1
  • Causes: Increased CO (+ reflex vasodilation)
  • 2.5-20mcg/kg/min

INOTROPE (PDE-inhibitor):

Milrinone (Primacor)

  • Optional loading dose: 50mcg/kg over 10 mins, followed by 0.125-0.75mcg/kg/min


Vasopressin (Pitressin)

  • 0.03-0.04U/min
  • Causes: vasoconstriction


-Avoid reflex hypotension by titrating pressors down

-Gold standard: use central lines. For extravasation, use phentolamine 5-10mg SC including through the infiltrated line.

-Hypovolemia should be corrected first to achieve maximal vasopressor efficacy

-Do not use low-dose dopamine solely for “renal protection”/to increase UOP


-Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:580.?

-Hollenberg SM. Vasoactive drugs in circulatory shock. Am J Respir Crit Care Med 2011; 183:847.?

-Picture: Tintinalli’s

ovarian cysts (quick review)

23 Jan

submitted by Christina Brown, M.D.

Follicular cysts:

  • Most common
  • Occur from fetal life to menopause
  • Unilocular; diameter 3–8 cm
  • Thin wall predisposes to rupture, which usually causes minimal or no bleeding.
  • Rupture during ovulation at midcycle is known as mittelschmerz.

Corpus luteal cysts:

  • Most significant
  • Diameter 3 cm, but usually <10 cm
  • Rapid bleeding from intracystic hemorrhage causes rupture.
  • Rupture is most common just before menses begins.
  • Can cause severe intraperitoneal bleeding
  • Gradual bleeding into cyst or ovary distends capsule and may cause pain without rupture.



  • Follicular cysts result from non-rupture of mature follicle or failure of atresia of immature follicle.
  • Corpus luteal cysts result from unrestrained growth in early pregnancy or from normal intracystic hemorrhage days after ovulation.
  • Other cysts:
    • Theca lutein
    • Cystic teratoma
    • Endometrioma (chocolate cyst)


  • Abdominal pain
    • Sharp, unilateral
    • Intermittent vs. constant
    • Migration
    • Previous episodes
    • May occur with exercise, intercourse, trauma, or pelvic exam
  • Fever is rare.
  • Irregular menses (may suggest polycystic ovary syndrome).


Physical Exam

  • Abdominal tenderness (mild to severe with peritonitis)
  • Adnexal tenderness
  • Pelvic mass
  • Hemorrhagic shock possible:
    • Usually from corpus luteal cyst rupture
    • Orthostasis, hypotension, tachycardia

Lab work:

  • Urine or serum human chorionic gonadotropin determination
  • CBC
  • Urinalysis
  • If significant hemorrhage, type and cross packed RBCs
  • Cervical cultures to rule out PID

Transvaginal US:

  • Adnexal cysts and masses:
    • Cystic masses <5 cm in premenopausal women generally benign
    • Should be reevaluated at end of menstruation
  • Pelvic free fluid


  • May demonstrate cysts or evidence of torsion or suggest alternative diagnosis
  • May provide enough information to proceed to laparoscopy if abnormal ovary and no other cause of pain identified
  • Uterus may be shifted to side of torsed adnexa.
  • Ascites may be present.

Disposition – If hemorrhagic conversion due to ruptured ovarian cyst, admit to Gynecology.
FOLLOW-UP RECOMMENDATIONS:  If pain is resolved and cyst is <4–5 cm, close follow-up is recommend with gynecology for further studies.


Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Ovarian Cyst/Torsion. Rosen’s 5-minute EM Consult.
Bottomley C and Bourne T.: Diagnosis and management of ovarian cyst accidents. Best Pract Res Clin Obstet Gynaecol. 2009; 23:711–724.
McWilliams GDE, Hill M J, and Dietrich C S.: Gynecologic emergencies. Surg Clin North Am. 2008; 88:265–283.


modified valsalva maneuver (quick reference)

12 Jan

for a more in-depth look, check out last May’s ACEP Now article.

brief highlights:

  • 428 patient study
  • modified valsalva maneuver
    • forced strain (e.g. blow into 10 cc syringe)
    • lie patient flat
    • elevate legs to 45 degrees x 15 seconds
  • return to sinus rhythm at 1 minute:
    • 43% with modified valsalva
    • 17% standard valsalva (strain x 15 sec, no position change)
    • NNT = 4


quick visual aid (start at the 1:17 mark if short on time):


There you go.  Add it to the toolbox.

References: ACEP Now article; video

Subarachnoid Hemorrhage (SAH) – quick review

19 Dec

submitted by Christina Brown, M.D.

Definition – Bleeding into the subarachnoid 300px-subarachnoidpspace and CSF:

  • Spontaneous – Most often results from cerebral aneurysm rupture.
  • Traumatic – Represents severe head injury.


Epidemiology – Although rare, SAH is a leading cause of pediatric stroke.



  • Headache is often occipital or nuchal, but may be unilateral.
  • Distinct from prior headaches.
  • Usually develops within seconds and peaks within minutes
  • Maximal at onset.
  • Can be associated w/ seizures, transient loss of consciousness, or altered level of consciousness occur in more than 50% of patients.
  • Vomiting occurs in 70%.
  • High risk features – Syncope, diplopia, and seizure.


Physical Exam

  • 33% – Focal neurologic deficits occur at the same time as the headache
  • 10-15% – Third cranial nerve (CN III) palsy (“down and out”)
  • 25%–70% – Nuchal rigidity.
  • Isolated CN VI palsy or papillary dilation may also occur.
  • Retinal hemorrhage may be only clue in comatose patient.


Work Up:

  • Emergent noncontrast head CT scan:
    • Diagnoses 93%–98% of SAH if performed within 12 hrs of onset.
    • CT is less sensitive after 24 hr or if hemoglobin <10 g/L.
  • Lumbar puncture (LP) and CSF analysis must be performed if CT negative and history suggests possibility of SAH.

Diagnostic Procedures

  • Lumbar puncture:
    • Presence of erythrocytes in CSF indicates SAH or traumatic tap:
      • If traumatic tap suspected, LP should be performed one inter-space higher.
      • Xanthochromia is diagnostic of SAH if performed 12 hours after onset.
    • An elevated opening pressure may indicate SAH, cerebral venous sinus thrombosis, or pseudotumor cerebri.


  • Manage airway, resuscitate as indicated:
    • Rapid sequence intubation


  • Manage intracranial pressure (ICP):
    • Elevate head of bed to 30 degrees.
    • Consider pretreatment with lidocaine and defasciculating dose of nondepolarizing paralytic to blunt increase in intracranial pressure (ICP) during intubation.
    • Prevent increases in ICP from vomiting and defecation with antiemetics and stool softeners.
  • Blood pressure (BP) control:
    • Balance HTN-induced rebleeding vs cerebral hypoperfusion
    • Goal systolic BP <160, mean goal between 100-120.
      • Nicardipine, Labetalol
    • Correct hypovolemia:
      • Treat hypotension with volume expansion.
  • Seizure prophylaxis
  • Transfer to facility with neurosurgical capabilities.



  • All patients with SAH should be admitted to an ICU.
  • Patients with negative CT findings and equivocal LP findings should be admitted.



  1. Edlow J A, Malek A M, and Ogilvy C S.: Aneurysmal subarachnoid hemorrhage: Update for emergency physicians. J Emerg Med.2008; 34(3):237–251.
  2. Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Subarachnoid Hemorrhage. Rosen and Barkin’s 5 minute Emergency Medicine Consult.
  3. Armin S S, Colohan A R, and Zhang J H.: Traumatic subarachnoid hemorrhage: Our current understanding and its evolution over the past half century. Neurol Res.2006; 28(4):445–452.
  4. Bederson J B and ConnollyES Jr. et al.: Guidelines for the management of aneurysmal subarachnoid hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. 2009; 40:994–1025.
  5. picture

Epidural Hematoma (quick review)

2 Dec

submitted by Christina Brown, M.D.


Definition – Inward bending of cavarum causes bleeding when dura separates from skull:

  • Middle meningeal artery is involved in bleed >50% of time.
  • Meningeal vein is involved in 1/3.



  • Mortality is 12% and is related to preoperative condition.  
  • Skull fracture is associated in 75% of cases, less commonly in children. 


Pediatric Considerations

  • Head injury is the most common cause of death and acquired disability in childhood.  
  • Bleeding is more likely to be venous.
  • Good outcome in 95% of children <5 yr



  • LOC: 85% will have at some point in course:
  • Only 11–30% will have a lucid interval.


MORE Pediatric Considerations

  • Many times the only clinical sign is drop in hematocrit (Hct) of 40% in infants.
  • Bulging fontanel with vomiting, seizures, or lethargy also suggest EDH in infants.
  • Less than 50% of children have LOC at time of injury.
  • Posterior fossa lesions are seen more commonly in children.


Physical Exam

  • Pupillary dilation:  Usually on same side as lesion (90%)
  • Hemiparesis >1/3:  Usually on opposite side from lesion (80%)


Imaging (CT Head)

  • Lenticular, biconvex hematoma with smooth borders may be seen.
  • Mixed density lesion may indicate active bleeding.
  • Most commonly seen in temporal parietal region




Initial Stabilization/Therapy

  • Head-injured patients have 25% improved mortality when triaged to regional trauma centers
  • Prevent hypoxia and hypotension:
    • Rapid-sequence intubation for signs of deterioration or increased intracranial pressure (ICP)
  • Perform rapid neurologic assessment


ED Management

Early surgical intervention (<4 hr) in comatose patients with EDH.  Nonsurgical intervention in asymptomatic patients is associated with high rate of deterioration; >30% require surgical intervention.

Control ICP

  • Prevent pain, posturing, and increased respiratory effort
  • Elevate head of bed 15–20% after adequate fluid resuscitation.
  • Controlled ventilation to PCO2 of 35–40 mm Hg (Avoid hyperventilation unless signs of brain herniation are present).

Continuous end tidal CO2 monitoring

Arterial line placement for close monitoring of MAP, PO2, PCO2

Treat HTN:  Nicardipine, Labetalol

Treat hyperglycemia if present: Associated with increased lactic acidosis and mortality in patients with TBI

Treat and prevent seizures: diazepam, levitiracetam, etc.

and once again, Early (neuro)surgical intervention


  1. Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Epidural Hematoma, Rosen & Barkin’s 5-Minute Emergency Medicine Consult.
  2. Bullock M R et al.: Surgical management of traumatic brain injury. Neurosurgery.2006; 58(3 Suppl):S16–S24.
  3. Marion D M.: Epidural hematoma.  In: Bradley W G: ed. Neurology in Clinical Practice,5th ed.Elsevier;2008: 54 A,B:1083–1114.
  4. Vincent J L and Berre J.: Primer on medical management of severe brain injury. Crit Care Med.2005; 33(6):1392–1399.
  5. Huh J W and Raghupathi R.: New concepts of treatment in pediatric traumatic brain injury. Anesth Clin.2009: 27(2):213–240.
  6. picture



Pyelonephritis (quick hits)

8 Nov

submitted by Christina Brown, M.D.

Definition – Ascension of bacteria from lower urinary tract infection (UTI) into the upper pyelourinary tract. Primarily a clinical diagnosis.

Epidemiology of Male/female ratio:
• 1:10 in 1st years of life
• 1:5 in children
• 1:50 in reproductive years
• 1:1 in fifth decade and later

Bacteriology: Escherichia coli 80–95% predominates.

Risk Factors – Recent instrumentation, urinary obstruction, urinary retention, recent pyelonephritis (within 1 yr), anatomic variation, neurogenic bladder, DM, immunosuppression, pregnancy.

Signs & Symptoms
– Dysuria, urgency, frequency
– Back, flank, or abdominal pain
– Fever, chills, N/V, Malaise
– CVA Tenderness or suprapubic TTP


Pediatric Considerations
– Renal scarring: More common sequelae in young children than in adults.
– Group B streptococci

Geriatrics – AMS, nausea/vomiting, diarrhea, fever may predominate.

Urine Culture: >100,000 colony-forming units (CFU)/mL is (+).

CT Imaging:

Consistent or concerning findings:
• Stranding or inflammation and edema of parenchyma
• Perinephric fluid
• Calculi, obstruction
• Renal/perinephric abscess
• Intraparenchymal gas formation (consistent with emphysematous pyelonephritis)

ED Treatment – 14 days duration
– Oral Antibiotics – Ciprofloxacin, Cefdinir
– PEDS – Amoxicillin, Keflex
– IV Antibiotics – Ceftriaxone, Ciprofloxacin
– PEDS 0-3 months – Amp + Gent, Cefotaxime. 3+ months – Ceftriaxone may be used in place of Cefotaxime.

Additional Pediatric Considerations
All children with 1st episode of pyelonephritis should have urinary tract imaging performed later with pediatrician.

Renal US:
• Within 48 hr if no clinical improvement
• Within 3–6 wk if clinical improvement
Girls 4–10 yr old: Voiding cystogram for UVR w/ pediatrician
Boys 4–10 yr old: Voiding cystourethrogram after urine is sterile and bladder spasm has subsided


– Admit septic, unable to tolerate PO intake, immunocompromised.

– If clinically stable, discharge home w/ pediatrician f/u within next 48 hrs with appropriate antibiotic regimen.



1. Bitner M, Schaider, J., lfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Pyelonephritis. Rosen & Barkin’s Five Minute Emergency Medicine consult.

2. Piccoli B G, Cresto E, and Ragni F et al.: The clinical spectrum of acute uncomplicated pyelonephritis from an emergency medicine perspective. Int J Antimicrob Agents. 2008; 31(suppl S):S46-S53.

3.  Stunnell H, Buckley O, and Feeney J et al.: Imaging of acute pyelonephritis in the adult. Eur Radiol. 2007; 17:1820-1828.