FINAL Flashcards
3 WAYS TO CALCULATE HR FROM EKG
1) number of QRS complexes in 6 second strip x 10
2) 300 / 150 / 100 / 75 / 60 / 50
3) 1500 / number of small squares between R waves
WHAT ARE THE LIMB LEADS
WHAT ARE THE PRECORDIAL LEADS
LIMB LEADS = I II III AVR AVL AVF
PRECORDIAL LEADS = V1 V2 V3 V4 V5 V6
WHAT IS THE J POINT ON EKG
Transition from S wave to T wave
- changes from vertical to horizontal
LIMB LEAD PLACEMENTS
AVR = right arm
AVL = left arm
AVF = left leg
I = AVR (-) to AVL (+)
II = AVR (-) to AVF (+)
III = AVL (-) to AVF (+)
SEPTAL LEADS
ANTERIOR LEADS
INFERIOR LEADS
LATERAL LEADS
SEPTAL LEADS = V1 V2
ANTERIOR LEADS = V3 V4
INFERIOR LEADS = II III AVF
LATERAL LEADS = I AVL V5 V6
NORMAL DURATIONS OF EACH EKG SECTION
P WAVES
PR INTERVAL
QRS COMPLEX
QT INTERVAL
P WAVES < 0.12 (3 boxes)
PR INTERVAL = 0.12 - 0.20 (3-5 boxes)
QRS COMPLEX = 0.04 - 0.12 (1-3 boxes)
QT INTERVAL = 0.36 - 0.44 (9 - 11 boxes)
WHAT DOES THE P WAVE INDICATE?
WHAT DOES THE Q WAVE INDICATE?
WHAT DOES THE QRS COMPLEX INDICATE?
WHAT DOES THE T WAVE INDICATE?
P WAVE = atrial depolarization
Q WAVE = interventricular septum depolarization
QRS COMPLEX = ventricular depolarization (atrial repolarization is hidden in there)
T WAVE = ventricular repolarization
RBBB CRITERIA
o QRS > 0.12
o rsR in leads V1 - V3 - “bunny ears”
LBBB CRITERIA
o QRS > 0.12
o deep S wave in V1/V2
o broad R waves in I, AVL, V5, V6
o absent Q wave in I, V5, V6; may have a slight or narrow one in AVL
o inverted T waves (or going opposite direction of QRS)
if Q wave is >/= 1/3 the height of R wave = indicative of
transmural MI
U WAVE
can be normal or pathologic
prominent U waves = hypokalemia
repolarization of purkinje fibers
RATES FOR
- SINUS RHYTHM
- BRADYCARDIA
- TACHYCARDIA
- SVT
sinus rhythm = 60-100
bradycardia < 60
tachycardia > 100
SVT = 150-200
significance of a prolonged PR interval
caused by a blocking of the conduction from the SA node to the AV node
1st degree AV block
prolonged PR interval (> 0.20)
PR interval should be 0.12 - 0.20 (3-5 boxes)
2nd degree AV blocks (2 of them)
o Type I (Wenckebach) = longer longer longer drop = PR interval progressively gets longer, until QRS complexes drops (doesn’t show up)
o Type II (Mobitz II) = PR interval is fixed, but some QRS complexes don’t show up (if some p’s don’t get through)
IVCD vs RBBB/LBBB
Intraventricular Conduction Delay = QRS complex > 0.12, but other criteria for bundle branch blocks not met
AXIS = look at leads ________
axis should never both be _________
If I is positive and AVF is positive =
If I is positive and AVF is negative =
If I is negative and AVF is positive =
I / II / AVF (supposed to look at I & AVF, but can compare I to II also)
should never both be negative = indeterminate
If both leads are positive (upwards) = normal
If I is positive and AVF is positive = normal
If I is positive and AVF is negative = LAD (left axis deviation)
If I is negative and AVF is positive = RAD (right axis deviation)
P WAVE MORPHOLOGY
BIPHASIC vs P PULMONALE vs P MITRALE
mostly look at lead II for R/L atrial enlargement
Evaluate leads II, III, AVF and V1 for atrial deformities
may be biphasic P waves in V1 = normal
normal = < 2.5mm in limb leads & < 1.5mm in precordial leads
mostly look at lead II to find this
P PULMONALE = Right atrial enlargement = right atrial depolarization lasts longer than left = will see a tall P wave in lead II and a biphasic wave with increased height of the initial positive p wave deflection (>1.5mm)
P MITRALE = Left atrial enlargement = lasts longer (not taller, but wider), > 0.12s. Notch in lead II, and increased depth of second negative p wave deflection in V1
RVH (right ventricular hypertrophy)
look at the precordial leads (V1 - V6)
tall R waves in V1 / V2 (get smaller as it goes to V5/V6)
deep S waves in V5 / V6 (start smaller in V1/V2)
***RVH should accompany RAD (right axis deviation)
LVH (left ventricular hypertrophy)
look at precordial leads (V1 - V6)
deep S waves in V1 / V2
tall R waves in V5 / V6
Amplitude of S wave in V1 + R wave in V5 = > 35mm
may also have inverted / asymmetrical / depressed T waves in lateral leads
Hypokalemia on EKG
Hyperkalemia on EKG
Hypokalemia = U waves
Hyperkalemia = peaked T waves (> 5mm in II/III) (> 10mm in V3/V4); can also have flattened P waves
Hypocalcemia on EKG
Hypercalcemia on EKG
Hypocalcemia = prolonged QT interval (can also seen with hypomagnesemia & hypokalemia & hypothermia)
Hypercalcemia = shortened QT interval; may see J wave
Hypothermia on EKG
J waves
prolonged PR, QRS, and QT
PE on EKG
S1Q3T3
***Most common finding = Sinus Tachycardia
S wave in lead I
Q wave in lead III
inverted T waves in lead III
transient RBBB`
ventricular strain
- associated with ventricular hypertrophy
- strain results in depression of the ST segment
RV strain = V1
LV strain = V5, V6
THERE ARE MANY MARKERS OF ISCHEMIA
- Pathologic Q waves
- Poor R wave progression
- ST segment elevation or depression (make sure when looking at ST segment to look at where T wave is starting to tell if ST is elevated or depressed)
- T wave abnormalities (flattening, peaking, inverted)
Q waves
small Q waves = insignificant
can signify hypokalemia
pathologic Q waves = indicate necrosis or scarring
Criteria for abnormal/pathologic Q waves
> 1 mm wide OR
> 1/3 the height of QRS complex
Q waves = seen in STEMI, not NSTEMI
R wave progression
QRS complex should start out negative in V1 and end positive in V6
R wave should be tallest in V3/V4 = where the transition should occur
if the transition occurs in V1/V2 (early) = can be indicate of a previous posterior wall MI
Causes of poor R wave progression
- anterior MI (old if no other signs of ischemia, new if other signs of ischemia)
- lead misplacement (frequently in obese women)
- LBBB or Left anterior fascicular block
- LVH
- WPW
- Dextrocardia
- Tension pneumothorax with mediastinal shift
- CHD
EKG CRITERIA FOR STEMI
ST elevation at J point in 2 contiguous leads of >/= 1mm
ST elevation of >/= 2mm in men in leads V2 / V3
ST elevation of >/= 1.5mm in women in leads V2 / V3
ischemia = ST depression, peaked T waves, T wave inversion
Infarction = ST elevation & appearance of Q waves
Fibrosis = ST & T waves return to normal, Q waves may persist
NSTEMI EKG
ST depression & T wave inversion = infarction or ischemia
After injury = ST returns to normal, but inverted T wave persists
NSTEMI = could see ST depression or T wave inversion or both
infarction vs ischemia
Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia.
ischemia –> infarction –> fibrosis
Hypomagnesemia EKG
prolonged QT
Torsades de pointes (give magnesium sulfate; reversed with calcium gluconate)
cranial nerves for eye muscles
CN IV = superior oblique
CN VI = lateral rectus
CN III = superior rectus, inferior rectus, medial rectus and inferior oblique
SMALL BOWEL OBSTRUCTION
MC cause = post-surgical adhesions
- other causes = incarcerated hernias, malignancy, IBD, Intussusception, volvulus
SIGNS/SYMPTOMS (cavo)
- cramping / abdominal pain
- abdominal distention
- vomiting
- obstipation (lack of stool / flatus)
PHYSICAL EXAM
- abdominal distention
- high pitched tinkling sounds (hyperactive bs with early obstruction)
- hypoactive bs with late obstruction
- may have tachycardia, peritoneal signs (guarding, etc)
- perform DRE to check for masses / blood
DIAGNOSTICS
- can do labs (BUN / CR elevated due to dehydration), serum LDH (due to lack of perfusion/oxygen to tissues –> breakdown)
IMAGING
- abdominal XRAY (flat & standing to check for perforation) - see dilated bowel loops & air-fluid line = initial test
- can do CT for better view of site / severity
TREATMENT
- IV fluids (NS)
- antiemetics (Zofran / Phenergan)
- analgesic (morphine)
- stool softeners (Colace)
- bowel decompression via NG tube
- may need abx / surgery
cranial nerves for eye muscles
CN IV = superior oblique
CN VI = lateral rectus
CN III = superior rectus, inferior rectus, medial rectus and inferior oblique
AMBLYOPIA
“lazy eye”
DECREASED VISION in one or both eyes due to abnormal development of vision in infancy or childhood.
Vision loss occurs because nerve pathways between the brain and the eye aren’t properly stimulated.
May not have obvious problem with the eye.
Brain favors one eye.
Brain is trained to ignore one eye (worse vision) and focus on the vision of the better eye - loses nerve connection with that other eye
STRABISMUS
Eye misalignment caused by an imbalance in the muscles holding the eyeball, or neuro involvement.
esotropia (in), exotropia (out), hypotropia (down), and hypertropia (up)
Can cause Amblyopia
DIAGNOSIS
- Hirschberg corneal light reflex testing
- cover-uncover test to determine the angle of strabismus, cover test, convergence testing
MANAGEMENT
- Patch therapy* - normal eye covered to stimulate & strengthen the affected eye
- corrective surgery if severe or unresponsive to conservative therapy
**If not treated before 2 years old, amblyopia may occur = where have decreased visual acuity that is not correctable by refractive means
TERMS
ANISOMETROPIA
APHAKIA
ASTHENOPIA
CONVERGENCE
DIPLOPIA
ACCOMMODATION
ANISOMETROPIA = one eye has much poorer vision than the other (aniso - uneven or unequal)
APHAKIA = no lens in the eye (congenital or due to trauma/ infection)
ASTHENOPIA = eye strain
CONVERGENCE = eye turned inwards so that they are aimed towards a near object
DIPLOPIA = blurry vision
ACCOMMODATION = ability to switch from near to far or far to near vision
EXOPHTHALMOS
COMMONLY SEEN WITH
bulging of the eye out
commonly seen in Grave’s disease
CYCLOPLEGIA
Paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation (inability to switch from near to far or far to near objects) or a consistently dilated pupil
HEMIANOPSIA
a blindness or reduction in vision in one half of the visual field due to damage of the optic pathways in the brain.
decreased vision or blindness in half the visual field. can occur in one eye or both eyes
homonymous hemianopsia = both right sides or both left sides of visual fields are decreased/blind
(due to damage of optic tract on one side); if damage on the optic tract on the left side = goes to the left side of both eyes = then lose vision on right side of both eyes
if damage to optic tract on the right side = goes to the right side of both eyes = then lose vision in the left side of both eyes
if damage at the optic chiasm (where cross-over occurs) = goes to the inner vision of both eyes = then lose vision on lateral sides of both eyes = bitemporal hemianopsia
if damage at the optic nerve = supplies both the inner and outer vision of the same eye –> monocular blindness
HYPHEMA
blood in the anterior chamber
usually from trauma. Can sometimes fill up the anterior chamber so much that it impedes vision
HYPOPYON
Presence of leukocytes in the anterior chamber (white crescent instead of red crescent from hyphema - blood)
PAPILLEDEMA
Swelling of the optic disc caused by increased Intracranial Pressure
ECTROPION
EYELID & LASHES TURN OUTWARD
- due to relaxation of the orbicularis oculi muscle
- MC seen in elderly (tends to be bilateral) but can be congenital, scar tissue, infectious, or with CN 7 palsy
SIGNS/SYMPTOMS
- irritation
- ocular dryness
- tearing
- sagging of the eyelid
- increased sensitivity
TREATMENT
- surgical correction if needed
- lubricating eyedrops for symptom relief (artificial tears)
ENTROPION
EYELID & LASHES TURNED INWARD
- may be caused by spasms of the orbicularis oculi muscle
- MC seen in the elderly
SIGNS/SYMPTOMS
- eyelashes may cause corneal abrasion / ulcerations
- erythema
- tearing
- increased sensitivity
TREATMENT
- surgical correction if needed
- lubricating eye drops for symptom relief
DACROCYSTITIS
INFECTION OF THE LACRIMAL SAC
MC Etiology = STAPH AUREUS
others: GABHS, Staph epidermidis, H. flu, strep pneumo
SIGNS / SYMPTOMS
- **Tearing
- tenderness
- edema
- **Redness to medial canthal of lower lid (+/- purulent)
TREATMENT o Acute = Antibiotics, warm compresses - Clindamycin - Augmentin - Vancomycin + Ceftriaxone
o Chronic = Dacryocystorhinostomy
- can get infected –> cellulitis, cause sinusitis or brain infection…send to ophthalmologist if not getting better
BLEPHARITIS
INFLAMMATION OF THE LID MARGINS
- common in patients with down syndrome & eczema
ETIOLOGY
o Anterior = less common; involves the skin and base of eyelashes
- 1) infectious (STAPH AUREUS or staph epidermidis)
- 2) SEBORRHEIC
o Posterior = more common; Meibomian gland dysfunction
- associated with rosacea & allergic dermatitis
SIGNS/SYMPTOMS
- eye irritation / itching
- ***crusting, scaling, red rimming of the eyelid & eyelash flaking
- burning, erythema
- may or may not also have entropion or ectropion (especially with posterior blepharitis)
inflammation involving the lid margin
characterized by: erythema, crusting, & scaling
Often associated with systemic conditions such as rosacea & seborrheic dermatitis
RISK FACTORS = people who have a tendency towards oily skin, dandruff, and dry eyes
CLINICAL PRESENTATION = burning, watering, crusting of lashes and medial canthus, scaling, erythematous eyelids. Usually a chronic course with intermittent exacerbations
PHYSICAL EXAM = eyelids show erythema & crusting of lashes & lid margins. May be some injection of conjunctiva
TREATMENT = systematic/long term commitment to eyelid margin hygiene! = application of HEAT (warm compresses) - promotes evacuation/cleansing of secretory passages. Mechanical WASHING of eyelid margin - baby shampoo with warm water/gentle washing of eyelid margins, NOT just the skin of the lids.
ANTIBIOTIC SOLUTION OR OINTMENT applied to eyelid margin (azithro solution, erythromycin ointment) during exacerbations. In some stubborn cases = can be used nightly for prophylaxis
for posterior blepharitis = eyelid hygiene, regular massage / expression of Meibomian gland
- can give systemic abx in severe/unresponsive cases = Tetracyclines or Azithromycin
Patients should be educated/understand that this is a chronic condition with intermittent exacerbations
HORDEOLUM (stye)
PAINFUL
- local abscess of eyelid MARGIN***
- MC = STAPH AUREUS
o External = infection of eyelash follicle or external sebaceous glands near the LID MARGIN***
o Internal = inflammation / infection of Meibomian gland
SIGNS / SYMPTOMS
- painful, warm, swollen red lump on eyelid-near margin
TREATMENT
- **warm compresses = mainstay of treatment (most eventually point & drain spontaneously)
- can give antibiotic topical (erythromycin or bacitracin)
CHALAZION
NOT PAINFUL
- painless granuloma of the internal Meibomian sebaceous gland –> focal eyelid swelling
- often larger, firmer, slower growing and less painful than hordeolum
SIGNS / SYMPTOMS
- non tender eyelid swelling
- rubbery nodule
TREATMENT
- eyelid hygiene*
- warm compresses
- antibiotics usually not necessary; injection of steroid or I&D may be necessary in larger ones affecting vision
PTERYGIUM
elevated, superficial, FLESHY TRIANGULAR SHAPED FIBROVASCULAR MASS
- GROWS!
- starts on conjunctiva, can move onto the cornea and impede vision; vast majority = asymptomatic
MC location = inner corner/nasal side of eye - grows laterally
***Associated with UV EXPOSURE in sunny climates, as well as SAND, WIND, DUST exposure
TREATMENT
- observation for most + artificial tears
- removal only if growth affects vision
PINGUECULA
- yellow, elevated nodule on nasal side of sclera (fat / protein)
- does NOT grow! (unlike pterygium)
TREATMENT = observation in most cases
- may be excised for cosmetic reasons or if it becomes inflamed
GLOBE RUPTURE
- the outer membranes of the eye are disrupted due to BLUNT OR PENETRATING TRAUMA
OPHTHO EMERGENCY**
SIGNS/SYMPTOMS
- diplopia
- ocular pain (may be painless)
PHYSICAL EXAM
- misshapen eye
- markedly reduced visual acuity
- enophthalmos*** - recession of globe within orbit
- foreign bodies may be present
- severe conjunctival hemorrhage***
EXAM
- Seidel’s test = fluorescein dye - orange, but turns green under blue lamp; indicates leakage of aqueous humor from anterior chamber
- see fluorescein streaming
- have obscured red reflex
- teardrop or irregularly shaped pupil
- hyphema
TREATMENT
- **Rigid eye shield - protect eye from applied pressure
- leave impaled object if present
- immediate ophtho consult
- IV antibiotics
- avoid topical eye solutions
- if hyphema present = keep at 45 degrees to keep RBCs from staining the cornea
ORBITAL FLOOR “BLOWOUT” FRACTURE
- fractures to orbital floor as a result of trauma
- may lead to trapping of eye structures (eye muscles get trapped, can’t move eyes in certain directions)
SIGNS/SYMPTOMS
- decreased visual acuity (trapped orbital tissue)
- diplopia, especially with upward gaze*** - if inferior rectus muscle entrapment
- orbital emphysema*** (eyelid swelling after blowing nose - due to air from maxillary sinus)
- epistaxis
- hyperalgesia or anesthesia to anteromedial cheek due to stretching of infraorbital nerve
***may have paresthesias/numbness in gums, upper lips, cheeks
DIAGNOSIS
- CT scan = test of choice
- may show “teardrop” sign
TREATMENT
1) nasal decongestants = decreases pain
- avoid BLOWing nose (swelling from maxillary sinus)
- steroids to reduce edema
- antibiotics (unasyn or Clindamycin)
2) surgical repair = in severe cases; patients with enophthalmos or for persistent diplopia
MACULAR DEGENERATION
Risk factors: > 50** Caucasians, females, smokers
*MC CAUSE OF PERMANENT LEGAL BLINDNESS & VISUAL LOSS IN THE ELDERLY (> 75)
- **LOSS OF CENTRAL VISION & loss of detail / color
- macula = responsible for central vision / detail / color
2 types of MD
1) DRY (ATROPHIC) = much more common
- gradual breakdown of macula –> gradual blurring of central vision
- Drusen*** = small, round, yellow-white spots on outer retina (scattered, diffuse) = due to accumulation of waste products from retinal pigment epithelium
2) WET (NEOVASCULAR / EXUDATIVE) = New, abnormal vessels grow under central retina, which leak & bleed –> retinal scarring
- rarer than dry MD, but progresses more rapidly
SIGNS/SYMPTOMS
- bilateral blurred or loss of central vision (including detail & color vision)
- scotomas = blind spots, shadows
- metamorphopsia*** (straight lines appear bent) - amsler
- micropsia (object seen by affected eye looks smaller than in unaffected eye)
DIAGNOSIS
- fluorescein angiography***
- test = Amsler grid
TREATMENT
o Dry MD = Amsler grid at home to monitor stability (zinc, vitamin A/C/E may slow progression, but no proof)
o Wet MD = BEVACIZUMAB (Intravitreal anti-angiogenics) - inhibits VEGF (vascular endothelial growth factor) –> reduces neovascularization
- laser photocoagulation
- optical tomography to monitor treatment response
- think of Mac from veronica mars; wet & dry; wet mac = beaver: bevacizumab
DIABETIC RETINOPATHY
MC CAUSE OF NEW, PERMANENT VISION LOSS/BLINDNESS IN 25-74y/o
Diabetic retinopathy = due to advanced glycosylation end products - excess sugar attaches to the collagen of the blood vessels –> capillary wall breakdown - retinal blood vessel damage –> retinal ischemia / edema
o NONPROLIFERATIVE DIABETIC RETINOPATHY = micro-aneurysms –> hemorrhages
- flame shaped hemorrhages
- cotton wool spots
- hard exudates
- Not associated with vision loss**
- treatment = pan-laser treatment, strict glucose control
o PROLIFERATIVE DIABETIC RETINOPATHY = neovascularization - new abnormal blood vessel growth, vitreous hemorrhages
- treatment = VEGF inhibitors = Bevacizumab
laser photocoagulation, strict glucose control
TREATMENT FOR DIABETIC RETINOPATHY
- laser photocoagulation
- strict glucose control
- proliferative = VEGF inhibitors = Bevacizumab
HYPERTENSIVE RETINOPATHY
damage to retinal blood vessels from longstanding HTN
- copper wiring*
- AV nicking (grade I)
- flame shaped hemorrhages (grade II)
- cotton wool spots (grade III)
- papilledema (malignant HTN) (grade IV)
management = control HTN!
RETINAL DETACHMENT
PAINLESS
retinal tear - retinal layer detaches from choroid plexus
MC risk factors = Myopia (nearsightedness) & cataracts
SIGNS/SYMPTOMS
- flashing lights with detachment (photopsia)
- floaters
- progressive unilateral vision loss
- shadow: “curtain coming down” - starts peripherally, then moves centrally - moves diagonally
(unlike MD = starts centrally)
DIAGNOSIS
- fundoscopy: see retinal tear - detached tissue flapping in the vitreous humor
- also see SHAFER’S SIGN = clumping of brown-colored pigment cells in anterior vitreous humor = “tobacco dust” - see darkened spot
SHAFER’S SIGN = retinal detachment
TREATMENT
- OPHTHO EMERGENCY*** - keep patient supine while awaiting consult
- ***don’t use miotic drops
- laser, cryotherapy, ocular surgery
ddx = amaurosis fugax = temporary “curtain” that “lifts up” usually within 1 hour; whereas this does not go away
FOREIGN BODY
- foreign body sensation
- tearing
- red
- painful
1ST CHECK VISUAL ACUITY
symptoms = eye pain & inability to open eye due to foreign body sensation. Excessive tearing may occur, conjunctival injection and eyelid swelling may be present. Inspect the eye thoroughly to identify & use fluorescein staining if necessary
- may leave a rust ring
FOREIGN BODY REMOVAL = try irrigation first. if irrigation doesn’t work, try swab moistened with proparacaine. If swab doesn’t work, refer. Treat with topical antibiotic ointment (erythromycin) and no patches!
- do NOT send patients home with topical anesthetics
TREATMENT APART FROM REMOVAL
- Abx = topical erythromycin, sulfacetamide
CORNEAL ABRASION
- foreign body sensation
- tearing
- red
- painful
1ST CHECK VISUAL ACUITY
DIAGNOSIS
- fundoscopic exam
- fluorescein staining
- do upper eyelid search to look for foreign body
TREATMENT
- patching not indicated for small abrasions; may patch large abrasions, but don’t do > 24 hours
- DO NOT PATCH for contact lens wearers / concerned for pseudomonas = give Ciprofloxacin eye drops
- other abx = erythromycin, sulfacetamide ointment
VIRAL CONJUNCTIVITIS
inflammation of the conjunctiva
- majority of conjunctivitis = viral (adults & kids)
MC ETIOLOGY = ADENOVIRUS
MC source = swimming pool
MC in kids - highly contagious = “pink eye”
SIGNS/SYMPTOMS
- foreign body sensation
- erythema
- itching
- normal vision
- may have accompanying viral symptoms
PHYSICAL EXAM
- Preauricular lymphadenopathy
- copious watery discharge
- may have punctate staining on slit lamp exam
TREATMENT
- supportive - cool compresses, artificial tears
- can give antihistamines for itching/redness (olopatadine) - H1 blocker topical antihistamine
ALLERGIC CONJUNCTIVITIS
inflammation of the conjunctiva
- red eyes
- may have other allergic symptoms (rhinorrhea, etc)
PHYSICAL EXAM
- cobblestone mucosa
- itching
- tearing
- redness
- stringy / ropey discharge
- chemosis - conjunctival swelling
TREATMENT
- topical antihistamines: H1 blockers = Olopatadine (Patanol), Pheniramine/Naphazoline (Naphcon A)
- can give topical NSAID - ketorolac
- topical steroids
- (se of long term steroid use on eyes = glaucoma, cataracts, and HSV keratitis)
BACTERIAL CONJUNCTIVITIS
inflammation of the conjunctiva
- less common than viral conjunctivitis (more in kids)
MC ETIOLOGIES
- Staph Aureus**
- Strep pneumo**
- H. flu
transmitted via direct contact / autoinoculation
SIGNS/SYMPTOMS
- purulent discharge - continuous throughout the day, not just in the morning (all conjunctivitis) - green / yellow / white discharge
- lid crusting
- no visual changes
- mild pain
TREATMENT
- topical antibiotics = Erythromycin, Fluoroquinolones (moxifloxacin), sulfonamides, aminoglycosides (can be toxic to cornea)
- if contact lens wearer = Cipro (pseudomonas) or aminoglycoside
STAPH & STREP; purulent discharge / crusting
ORBITAL CELLULITIS
- usually secondary to sinus infections (ethmoid = 90% of the time)***
staph, strep pneumo, GABHS, H. flu
may be caused by dental / facial infections or bacteremia; MC occurs in children
SIGNS/SYMPTOMS
- decreased vision*******
- pain with ocular movement*****
- proptosis (bulging eye)*******
- eyelid erythema & edema
DIAGNOSIS
- high resolution CT scan**** = see infection of the fat & ocular muscles
TREATMENT
- IV abx: Vancomycin, Clindamycin, Cefotaxime, Ampicillin/sulbactam (unasyn)
**difference between orbital cellulitis and preseptal or periorbital cellulitis = there is no pain with eye movement and no visual changes
bitemporal hemianopsia = caused by damage to the
can also be caused by what tumor
optic chiasm
pituitary adenoma
KERATITIS
corneal ulcer / inflammation
MC CAUSE = BACTERIAL
- could also be inflammation, pseudomonas or acanthamoeba, fungal
SIGNS/SYMPTOMS
- pain
- photophobia
- reduced vision
- tearing
- conjunctival erythema
PHYSICAL EXAM
- conjunctival injection / erythema
- CILIARY INJECTION (LIMBIC FLUSH)***
- see corneal ulceration/defect on slit lamp
- purulent or watery discharge
Bacterial Keratitis = hazy cornea. Treat with fluoroquinolone drops (moxifloxacin) - do NOT patch!
HSV Keratitis = DENDRITIC LESIONS - branching seen with fluorescein staining
- treat with topical antivirals = trifluridine, vidarabine, ganciclovir ointment, PO acyclovir
UVEITIS (IRITIS)
o Anterior = inflammation of iris (iritis) or ciliary body (cyclitis)
o Posterior = choroid inflammation
ETIOLOGIES = systemic inflammatory diseases (spondyloarthropathies, sarcoid, Behcets), or Infectious (CMV, syphilis, TB, toxoplasmosis), trauma, etc.
SIGNS/SYMPTOMS
o Anterior = Unilateral ocular pain, redness, photophobia, excessive tearing
- Anterior usually occurs after blunt trauma
o Posterior = blurred / decreased vision
- floaters, absent symptoms of anterior involvement
- no pain
so anterior uveitis = pain
posterior uveitis = blurry/decreased vision, no pain
PHYSICAL EXAM
- CILIARY INJECTION (LIMBIC FLUSH)
- Consensual photophobia
- visual changes (if posterior)
- Inflammatory cells (WBC) & flare (protein) within aqueous humor
TREATMENT
- steroids
Anterior = topical steroids, Scopolamine, topical cycloplegics
Posterior = systemic steroids
CATARACTS
LENS OPACIFICATION (THICKENING)
usually bilateral
RISK FACTORS = aging (MC > 60), SMOKING**, Steroids, DM, UV light, malnutrition, trauma
- could be congenital: ToRCH = Toxoplasmosis, Rubella, CMV, HSV
SIGNS/SYMPTOMS
- blurred / loss of vision over months/years
PHYSICAL EXAM
- absent red reflex
- opaque lens
MANAGEMENT
- surgical
ddx = Retinoblastoma = also have absent red reflex
PAPILLEDEMA
OPTIC NERVE (DISC) SWELLING due to increased ICP
CAUSES
- idiopathic intracranial HTN (pseudotumor cerebri)
- space occupying lesion - tumor / abscess
- increased CSF production
- cerebral edema - severe malignant HTN
SIGNS/SYMPTOMS
- headache
- nausea / vomiting
- vision = usually well preserved but may have changes
DIAGNOSIS
- fundoscopy = swollen optic disc with blurred margins
- need MRI or CT first to r/o mass effect, then get LP to test for increased CSF pressure
TREATMENT
- diuretics: Acetazolamide - decreases aqueous humor production & CSF
OPTIC NEURITIS
Acute inflammatory demyelination of optic nerve
MC in young patients: 20-40
ETIOLOGIES
- **MC = MS (multiple sclerosis)
- medications: ETHAMBUTAL, chloramphenicol
- autoimmune
SIGNS/SYMPTOMS
- loss of color vision**
- visual field defects (central scotoma/blind spot)
- loss of vision over a few days
- ocular pain that is worse with movement****
PHYSICAL EXAM
- Marcus Gunn Pupil*** (affected eye dilates with light and constricts when other eye has light)
- Fundoscopy = optic disc swelling
TREATMENT
- IV methylprednisolone followed by oral steroids
- vision usually returns with treatment
MARCUS GUNN PUPIL = Relative Afferent Pupillary Defect
during swinging flashlight test: when light is shone into unaffected eye, the affected eye will also constrict
when light shone into affected eye = dilates, or only slightly constricts
RAPD = ray (light) in affected pupil = dilates
ARGYLL-ROBERTSON PUPIL
pupil constricts with accommodation (switching from near to far) but DOES NOT react to bright light
MC CAUSE = NEUROSYPHILIS***
CRVO
Central retinal vein thrombus –> fluid backup in retina
Also have acute, sudden monocular vision loss
Painless
Risk factors = HTN, DM, glaucoma, hypercoagulable states
DIAGNOSIS
- extensive retinal hemorrhages****
“blood & thunder” appearance
TREATMENT
- no known effective treatment
- anti-inflammatories, steroids, laser photocoagulation
- may resolve spontaneously or progress to permanent vision loss
CRVO
Central retinal vein thrombus –> fluid backup in retina
Also have acute, sudden monocular vision loss
Painless
Risk factors = HTN, DM, glaucoma, hypercoagulable states
DIAGNOSIS
- extensive retinal hemorrhages****
“blood & thunder” appearance
TREATMENT
- no known effective treatment
- anti-inflammatories, steroids, laser photocoagulation
- may resolve spontaneously or progress to permanent vision loss
TESTICULAR TORSION
- twisting of the spermatic cord that suspends the testis
- 2 age peaks
⦁ perinatal & prepubertal
⦁ presents between ages 10-25
incidence decreases with age. 65% occur in teenagers (10-20)
- This is a UROLOGICAL / SURGICAL EMERGENCY**
viability of the testes is at risk; cuts off blood supply → necrotic testicle
Appearance = high-riding testicle, edematous, inflamed
- as torsion continues = will continue to elevate testicle
- HUSKY BLUE DOT hue due to lack of blood supply
TESTICULAR TORSION
- twisting of the spermatic cord that suspends the testis
- 2 age peaks
⦁ perinatal & prepubertal
⦁ presents between ages 10-25
incidence decreases with age. 65% occur in teenagers (10-20)
- This is a UROLOGICAL / SURGICAL EMERGENCY**
viability of the testes is at risk; cuts off blood supply → necrotic testicle
Appearance = high-riding testicle, edematous, inflamed
- as torsion continues = will continue to elevate testicle
- HUSKY BLUE DOT hue due to lack of blood supply
- the testes rotates on the long axis of the tunica vaginalis, rotates about the distal spermatic cord
- cuts off blood supply to the testes
- rarely seen after age 30
- early recognition & early treatment = essential!
Due to coiling, epididymis becomes more horizontal than vertical, and testicle is elevated
SYMPTOMS
- patient presents with SEVERE DISTRESS WITHIN HOURS of onset
- often accompanied with NAUSEA & VOMITING
- large, firm and tender testes
- pain radiates to inguinal area
- testicle is often high in the scrotum and in an abnormal orientation
- CREMASTERIC REFLEX = FREQUENTLY ABSENT
- degree of swelling & redness depends on the duration of symptoms
IMAGING
Color Doppler Ultrasound - must be done right away
⦁ see decreased blood flow, or avascular testicle
- refer to urology! have a 4-6 hour window; the sooner the better
MANAGEMENT
- can attempt manual detorsion - using pain relief as the guide for successful detorsion
- similar to “opening a book” - always twist outward / laterally because most torsions twist inwards and towards mid-line
- manual detorsion often doesn’t work, but should try; often won’t be able to do in clinic, especially due to pain; if caught early and hasn’t spun much, may able to succeed manually
o Surgery
⦁ surgical detorsion & Orchiopexy (fixation of testicle); usually prophylactic fixation of opposite testicle is performed
⦁ Orchiectomy = done when testis is deemed nonviable after surgical detorsion; salvage rates are directly related to duration of torsion; usually prophylactic fixation of opposite testicle is performed
HISTORY
- sudden onset of severe pain
- possible inciting event (trauma) or may occur spontaneously
SYMPTOMS
- lower abdominal pain, inguinal canal pain, or testicular pain
⦁ pain is not positional
⦁ can be constant or intermittent pain
⦁ pain is sudden in onset - may awaken in the middle of the night from pain
⦁ may have associated N/V
PHYSICAL EXAM
- high-riding (elevated) testis on affected side
- early on = may have significant swelling
- epididymis may be displaced and not found in its normal posterolateral position
- testicle is firm
- exquisite tenderness
- cremasteric reflex is usually absent
DIAGNOSIS
⦁ Color Doppler US - can determine if there is intratesticular flow, but if unsure of the diagnosis, don’t wait to call the urologist!
more horizontal laying of testes than vertical due to torsion
TREATMENT OF TESTICULAR TORSION
- emergent urologic consultation & surgery
- potential for manual detorsion - painful! - twist laterally like opening a book. May need to twist up to 720 degrees. If successful = can give immediate relief of pain…but still need to have surgical exploration to have orchiopexy (attachment of testes to scrotum, usually do other side)
EPIDIDYMITIS
- 2 major types
⦁ STIs
⦁ non-STI infections
STIs - associated with urethritis - associated with young men ⦁ gonorrhea ⦁ chlamydia
PRIMARY NON-SEXUALLY TRANSMITTED INFECTIONS - Associated with UTIs and Prostatitis - associated with men > 35 ⦁ E. coli ⦁ Pseudomonas ⦁ Gram-positive Cocci
- could also occur post-vasectomy
- or due to trauma
*most cases of epididymitis = caused by bacterial pathogens (infection)
epididymitis = inflammation of the epididymis, doesn’t necessarily mean infection; but most of the time, it is
⦁ STD (gonorrhea or chlamydia) > urethritis > sets up shop in epididymis→ inflammation
⦁ non-STI = UTIs/prostatitis (E-coli, pseudomonas, some gram positives)
SIGNS/SYMPTOMS OF EPIDIDYMITIS
- unilateral pain & swelling in the epididymis over a period of days
- erythema & edema of overlying scrotal skin - can become extremely large (reactive hydrocele)
- tenderness over the groin or in the lower abdomen
- fever
- dysuria
- could have urethral discharge if gonococcal
can cause inflammation to the testicle as well
LABS ⦁ CBC (WBCs - left shift) ⦁ UA & culture ⦁ urethral culture (or urine NAAT) ⦁ gram stain
TREATMENT
⦁ Scrotal elevation and support (Phren’s sign = pain relief with scrotal elevation)
⦁ Antibiotics appropriate to age, physical findings, urinalysis, cultures or gram’s stain, sexual history
⦁ Oral analgesics and antipyretics
⦁ Sexual activity or physical strain should be avoided until symptoms resolve
- can be acute or chronic
o ACUTE
⦁ < 6 weeks
⦁ swelling of epididymis with exquisite tenderness
⦁ +/- inguinal lymphadenopathy
⦁ may have systemic symptoms of fever, chills, irritative voiding symptoms
⦁ may be seen in combination with acute prostatitis
o CHRONIC ⦁ > 6 weeks ⦁ subtle epididymal induration and tenderness ⦁ no irritative voiding symptoms ⦁ +/- inguinal lymphadenopathy
Acute = much more painful, and may have systemic symptoms and irritative voiding symptoms
PHYSICAL EXAM
- tenderness posterior and lateral to testis
- DRE to eval for prostatic involvement if history suggests
- in acute cases = may have swelling with a reactive hydrocele (epididymo-orchitis)
- May have Phren’s sign = pain relief when lifting affected testicle
WORK UP
- CBC
- UA & urine culture
- test for GC & Chlamydia (urine)
- urethral swab if discharge present
- rule out other causes of scrotal pain (get an US to rule out torsion if acute in onset)
TREATMENT
- in younger men < 35 = consider GC & Chlamydia = give Ceftriaxone 250mg IM + Doxy 100mg BID x 10 days (if septic = hospitalize for IV hydration & IV antibiotics)
- in older men or hx of BPH, urethral stricture, or chronic UTI = consider enteric gram negative bacteria = Levaquin 500mg qday x 10 days: outpatient management
SYMPTOMATIC TREATMENT
⦁ NSAIDS
⦁ Scrotal elevation
⦁ Ice
lot of symptomatic relief while waiting for ABX to work
INFLAMMATORY EPIDIDYMITIS o Risk Factors ⦁ medication rxn ⦁ prolonged sitting ⦁ vigorous exercise ⦁ trauma ⦁ autoimmune dz
- may also be secondary to reflux of urine within the ejaculatory ducts
- Presentation = progressive, gradual onset of pain
- Treatment = scrotal elevation, warm baths, NSAIDS (not related to infection, so no abx)
TESTICULAR TORSION
- twisting of the spermatic cord that suspends the testis
- 2 age peaks
⦁ perinatal & prepubertal
⦁ presents between ages 10-25
incidence decreases with age. 65% occur in teenagers (10-20)
- This is a UROLOGICAL / SURGICAL EMERGENCY**
viability of the testes is at risk; cuts off blood supply → necrotic testicle
Appearance = high-riding testicle, edematous, inflamed
- as torsion continues = will continue to elevate testicle
- the testes rotates on the long axis of the tunica vaginalis, rotates about the distal spermatic cord
- cuts off blood supply to the testes
- rarely seen after age 30
- early recognition & early treatment = essential!
Due to coiling, epididymis becomes more horizontal than vertical, and testicle is elevated
SYMPTOMS
- patient presents with SEVERE DISTRESS WITHIN HOURS of onset
- often accompanied with NAUSEA & VOMITING
- large, firm and tender testes
- pain radiates to inguinal area
- testicle is often high in the scrotum and in an abnormal orientation
- CREMASTERIC REFLEX = FREQUENTLY ABSENT
- degree of swelling & redness depends on the duration of symptoms
IMAGING
Color Doppler Ultrasound - must be done right away
⦁ see decreased blood flow, or avascular testicle
- refer to urology! have a 4-6 hour window; the sooner the better
MANAGEMENT
- can attempt manual detorsion - using pain relief as the guide for successful detorsion
- similar to “opening a book” - always twist outward / laterally because most torsions twist inwards and towards mid-line
- manual detorsion often doesn’t work, but should try; often won’t be able to do in clinic, especially due to pain; if caught early and hasn’t spun much, may able to succeed manually
o Surgery
⦁ surgical detorsion & Orchiopexy (fixation of testicle); usually prophylactic fixation of opposite testicle is performed
⦁ Orchiectomy = done when testis is deemed nonviable after surgical detorsion; salvage rates are directly related to duration of torsion; usually prophylactic fixation of opposite testicle is performed
HISTORY
- sudden onset of severe pain
- possible inciting event (trauma) or may occur spontaneously
SYMPTOMS
- lower abdominal pain, inguinal canal pain, or testicular pain
⦁ pain is not positional
⦁ can be constant or intermittent pain
⦁ pain is sudden in onset - may awaken in the middle of the night from pain
⦁ may have associated N/V
PHYSICAL EXAM
- high-riding (elevated) testis on affected side
- early on = may have significant swelling
- epididymis may be displaced and not found in its normal posterolateral position
- testicle is firm
- exquisite tenderness
- cremasteric reflex is usually absent
DIAGNOSIS
⦁ Color Doppler US - can determine if there is intratesticular flow, but if unsure of the diagnosis, don’t wait to call the urologist!
more horizontal laying of testes than vertical due to torsion
TREATMENT OF TESTICULAR TORSION
- emergent urologic consultation & surgery
- potential for manual detorsion - painful! - twist laterally like opening a book. May need to twist up to 720 degrees. If successful = can give immediate relief of pain…but still need to have surgical exploration to have orchiopexy (attachment of testes to scrotum, usually do other side)
ORCHITIS
inflammation of the testicle
usually VIRAL
- usually MUMPS, coxsackie, rubella, echovirus, parvovirus
1/3 of post-pubertal men with mumps have concomitant orchitis
Mumps parotitis precedes the onset of orchitis by 3-10 days
Gradual onset of scrotal pain, erythema & swelling
may have associated fever, chills, and irritative voiding symptoms
symptoms may follow acute strain: sex, lifting, exercise
POSITIVE PHREN’S SIGN
normal cremasteric reflex
No diagnostic studies needed for mumps orchitis
TREATMENT
- symptomatic treatment = bed rest, scrotal elevation, cool compresses, analgesics (NSAIDS)
ORCHITIS
inflammation of the testicle
usually VIRAL
- usually MUMPS, coxsackie, rubella, echovirus, parvovirus
1/3 of post-pubertal men with mumps have concomitant orchitis
Mumps parotitis precedes the onset of orchitis by 3-10 days
Gradual onset of scrotal pain, erythema & swelling
may have associated fever, chills, and irritative voiding symptoms
symptoms may follow acute strain: sex, lifting, exercise
POSITIVE PHREN’S SIGN
normal cremasteric reflex
No diagnostic studies needed for mumps orchitis
TREATMENT
- symptomatic treatment = bed rest, scrotal elevation, cool compresses, analgesics (NSAIDS)
APPENDICEAL TORSION
- torsion of the appendix testis (small appendage of normal tissue usually located on upper portion of testis) - occurs when this appendage twists
Most cases = between age 7-14
SYMPTOMS
- gradual onset of pain…mild to severe
- reactive hydrocele - may trans-illuminate
- localized tenderness
- exam = classic “blue dot” sign - tender blue or black spot beneath the skin
DIAGNOSIS
- ULTRASOUND - shows torsed appendage as a lesion of low echogenicity with a central hypoechogenic area
TREATMENT o Conservative ⦁ Rest, Ice, NSAIDS ⦁ recovery = slow with discomfort ⦁ the infarcted tissue is usually reabsorbed
o Surgical
⦁ excision of appendix testis - not necessary, but is safe and quick, and is usually reserved for persistent pain
⦁ patients can usually resume normal activity without pain in a few days
TESTIS RUPTURE
- rip or tear in tunica albuginea resulting in extrusion of testicular contents
- seen in blunt or penetrating trauma
- rare in sports
SYMPTOMS
⦁ scrotal swelling
⦁ severe pain
⦁ ecchymosis
DIAGNOSIS
⦁ SCROTAL ULTRASOUND
TREATMENT
- referral to urologist for scrotal exploration
- pain management
- IV access
- blunt or penetrating trauma
- rare in sports
EXAM
⦁ scrotal swelling
⦁ ecchymosis
IMAGING
- Scrotal Ultrasound
⦁ loss of tunic continuity ( tunica albuginea) - so all testicular contents are floating around in the scrotum
⦁ internal echos, heterogenicity
TREATMENT
- referral!
- pain management - IV access
PRIAPISM
- painful, prolonged erection > 4 hours (has nothing to do with arousal)
ISCHEMIC = MOST COMMON, painful
NON-ISCHEMIC = rare, painful, usually from development of a traumatic A/V fistula between cavernosal artery and corpus cavernosum
Most common cause in adults = iatrogenic (intracavernous injections)*
PRIAPISM
- painful, prolonged erection > 4 hours (has nothing to do with arousal)
ISCHEMIC = MOST COMMON, painful
NON-ISCHEMIC = rare, painful, usually from development of a traumatic A/V fistula between cavernosal artery and corpus cavernosum
Most common cause in adults = iatrogenic (intracavernous injections)*
DIAGNOSIS
- primarily based on hx & pe
- may perform ABGs
- cavernosal blood gas: low flow = hypoxemia, hypercarbia and acidemia
- doppler US = normal or high flow with non-ischemic, low flow or absent flow with ischemic
TREATMENT FOR LOW FLOW (ISCHEMIC PRIAPISM)
1st line = PHENYLEPHRINE = alpha agonist intracavernous injection - causes contraction of smooth muscle - will increase venous outflow
TERBUTALINE = PO or SQ - constricts cavernosal artery - decreases arterial inflow; may be used if < 4 hrs
Needle Aspiration of corpora to remove blood; especially if > 4 hours duration - can also give phenylephrine in addition to aspiration
surgery if not responsive to medication / aspiration
TREATMENT FOR HIGH FLOW (NON-ISCHEMIC)
- observation
- can do arterial embolization or surgical ligation if refractory
PRIAPISM
- painful, prolonged erection > 4 hours (has nothing to do with arousal)
ISCHEMIC = MOST COMMON, painful
NON-ISCHEMIC = rare, painful, usually from development of a traumatic A/V fistula between cavernosal artery and corpus cavernosum
Most common cause in adults = iatrogenic (intracavernous injections)*
DIAGNOSIS
⦁ CBC - rarely the CBC will identify undiagnosed leukemia as cause of priapism; Patient’s with sickle cell disease should have a CBC and a reticulocyte count
⦁ Color Doppler Ultrasound = to distinguish ischemic (normal or high-flow) from non-ischemic priapism (low flow or absent flow)
⦁ Evaluate aspirated blood from corpus cavernosum
- darkly colored = unoxygenated = ischemic
- bright rid = oxygenated = non-ischemic
- can do ABGs on aspirated blood (low flow/ischemic = hypoxemia, hypercarbia, acidemia)
TREATMENT FOR LOW FLOW (ISCHEMIC PRIAPISM)
1st line = PHENYLEPHRINE = alpha agonist intracavernous injection - causes contraction of smooth muscle - will increase venous outflow
TERBUTALINE = PO or SQ - constricts cavernosal artery - decreases arterial inflow; may be used if < 4 hrs
Needle Aspiration of corpora to remove blood; especially if > 4 hours duration - can also give phenylephrine in addition to aspiration
surgery if not responsive to medication / aspiration
TREATMENT FOR HIGH FLOW (NON-ISCHEMIC)
- observation
- can do arterial embolization or surgical ligation if refractory
PENILE FRACTURE
- rupture of one or both of the tunica albuginea that covers the corpora cavernosa
CAUSE
- rapid blunt force to an erect penis
⦁ vaginal intercourse
⦁ aggressive masturbation
SIGNS / SYMPTOMS
⦁ popping or cracking sound
⦁ severe pain
⦁ immediate loss of erection
DIAGNOSIS
⦁ RUG (retrograde urethrogram) if suspected urethral injury
TREATMENT
⦁ surgical correction
COMPLICATIONS
⦁ ED
⦁ Penile curvature
⦁ Pain
PARAPHIMOSIS
- foreskin in uncircumcised or partially circumcised male is retracted behind the glans penis, develops venous and lymphatic congestion and cannot be returned to its normal position
UROLOGIC EMERGENCY
HISTORY
- swelling of penis & penile pain
- cause of irritability in preverbal infant
- recent penile exam, foley insertion, cystoscopy
PHYSICAL FINDINGS
- ensure that there are no constricting foreign bodies (ex: hair is wrapped around)
- edema & tenderness of glans
- painful swollen retracted foreskin
- penile shaft is unaffected
- with ischemia, the color of the glans will change from normal pink to blue or black, and will be firm rather than soft
Need to R/O angioedema or constricting band
- if constricting band, such as hair = must be cut and removed
- pain control for the patient
NONINVASIVE TECHNIQUES FOR REDUCTION
- Ice
- lidocaine gel
- compression bandages
- osmotic agents (sugar: 50% dextrose or mannitol)
- manual compression & reduction (procedural sedation & possibly a dorsal penile block)
- traction with forceps (sedation likely required)
o INVASIVE TECHNIQUES FOR PARAPHIMOSIS REDUCTION
⦁ puncture technique - puncture of glans with small needle to allow for lymph fluid to escape
⦁ glans penis aspiration
⦁ dorsal slit procedure = if all above has failed - refer to urology for this
URINARY RETENTION
- the inability to voluntarily pass urine
- almost always secondary to BPH
- uncommon in women
3 factors causing retention
⦁ outflow obstruction (prostate- BPH, could be a stone, etc)
⦁ neurologic impairment
⦁ inefficient detrusor muscle (can’t contract properly to expel urine)
HISTORY PHYSICAL EXAM - lower abdomen - rectal - pelvic exam (female) - neurologic exam
DIAGNOSTICS
- bladder ultrasound - see how much urine is retained in the bladder (can see cc’s)
- catheter insertion (therapeutic & diagnostic - helps pt and may see a LOT of urine)
- UA / Culture (to check for an infectious process involved)
- Creatinine level (if elevated = consider renal ultrasound)
TREATMENT ⦁ Catheter (14 - 16 french) ⦁ Self cath for patient ⦁ Suprapubic cath ⦁ Alpha blocker meds - Tamsulosin (Flomax), Doxazosin (Cardura)
COMPLICATIONS WITH CATHETERIZATION
⦁ hematuria
⦁ post-obstructive diuresis - with removing all the fluid at once - can end up getting hypotensive - lose a lot of fluids & electrolytes (sometimes remove some fluid but not all…) as the body sometimes continues to diurese past homeostasis of volume
LABS
- UA
⦁ pyuria can be seen with UTI (rare in men), chlamydia/gonococcal urethritis
⦁ hematuria + pyuria rules out STI
⦁ hematuria alone without symptoms & signs of urolithiasis may be due to cancer - patient should have further follow up….particularly men!!!
Urine culture recommended with pyelonephritis in men, or complicated UTI in women
PYELONEPHRITIS
UTI - often goes along with cystitis; MC cause = E.coli. MC cause in sexually active women = staph saprophyticus
- will have pyuria
PRESENTATION ⦁ flank pain, abdominal pain, pelvic pain ⦁ N/V ⦁ fever > 99.8F ⦁ may have CVA tenderness ⦁ +/- symptoms of cystitis
LABS
- UA may show white cell casts; send urine for culture and sensitivities
- CBC
- Pregnancy test in females
TREATMENT o Mild to Moderate ⦁ rehydrate patient & give parenteral dose of antibiotics in ER - observe 8-12 hrs ⦁ IV ABX = Ceftriaxone ⦁ Discharge pt on fluoroquinolone x 7d
o Severe Illness - requiring hospitalization
⦁ high fever, pain, marked debility
⦁ inabililty to maintain oral hydration or take oral meds
⦁ pregnant
⦁ concerns about patient compliance
NEPHROLITHIASIS
men affected more often than women
initial presentation = 30s - 50s
prevalence increases with age
5 major stone types ⦁ calcium oxalate = most common*** ⦁ calcium phosphate ⦁ struvite (form staghorn calculi) ⦁ urice acid ⦁ cystine (genetic)
MOST COMMON STONE TYPE = CALCIUM OXALATE
85% of patients with kidney stones form CALCIUM STONES (either phosphate or oxalate)
- uric acid stones also often have a calcium component
only CALCIUM & STRUVITE stones appear on KUB - are radiopaque
- stone formation thought to be from supersaturation of calcium
- stones form in interstitium; get extruded at renal papilla
Same pt may have more than one stone type at the same time
RISK FACTORS FOR STONES ⦁ Areas of high humidity ⦁ Elevated temperatures ⦁ Incidence greater in the summer months ⦁ Sedentary lifestyle ⦁ High protein and salt intake ⦁ Genetic factors –particularly with calcium stones
**but most common risk factor for kidney stones = decreased fluid intake
Citrate lowers calcium levels. so for calcium stones = have hypercalcuria, hyperoxaluria, and hypocitraturia
- UA with culture = may have microscopic or gross hematuria (Most pts experience hematuria); but could still be a stone with no hematuria present
- Urine pH (normal = 5.8-5.9)
⦁ pH < 5.5 = uric acid or cystine stone
⦁ pH 5.5-6.8 = calcium oxalate stone
⦁ pH > 7.2 = struvite or calcium phosphate stone - Pregnancy test
- CBC
- BMP (chem 8)
METABOLIC EVALUATION OF STONES
- strain urine to catch stones for analysis
- complete metabolic evaluation required for recurrent stone formers (or family hx)
⦁ serum PTH, calcium, uric acid, electrolytes, creatinine, BUN
⦁ 24 hour urine collection = volume, pH, calcium, uric acid, oxalate, phosphate, sodium, citrate
DIAGNOSIS OF KIDNEY STONES
- CT scan / Ultrasound = both can detect presence of stone, obstruction, and hydronephrosis
- KUB can only detect large radiopaque stones (calcium & struvite stones), will miss radiolucent stones, and does not detect obstruction
- MRI = rarely used
- IV pyelography = determines extent of obstruction & severity (used to be gold standard)
so…Gold standard = CT - noncontrast abdomen/pelvic CT ordered; but initial = US
most painful part of kidney stone passage = ureter
TREATMENT FOR KIDNEY STONES - ACUTE THERAPY- ⦁ IV hydration ⦁ Pain Meds = Ketorolac/Toradol, or Morphine IV ⦁ Antiemetic = Metoclopramide/Reglan IV
- can give alpha-1 blocker (Tamsulosin/Flomax - alpha 1 blocker - causes dilation) to help pass stone
- if the pain is under control, stable, and there are no signs of infection, the patient can be discharged and followed-up as an outpatient**
WHEN KIDNEY STONES BECOME A MEDICAL EMERGENCY
= any obstructing stone with an associated infection***
WHEN TO ADMIT THE PATIENT WITH KIDNEY STONES
⦁ intractable nausea/vomiting or pain
⦁ obstructing stone with signs of infection (emergency!)
REASONS FOR UROLOGICAL CONSULT FOR KIDNEY STONES
⦁ evidence of urinary obstruction*
⦁ urinary stone with associated flank pain*
⦁ anatomic abnormalities or solitary kidney**
⦁ concomitant pyelonephritis or recurrent infection
THERAPEUTIC INTERVENTION IS NEEDED WHEN:
⦁ failure to pass stone in 4 weeks
⦁ fever, intolerable pain, persistent nausea or vomiting
SURGICAL TREATMENT
⦁ Ureteroscopy with stent placement
⦁ ESWL = extracorporeal shock wave lithotripsy
⦁ Percutaneous Nephrolithotomy (PNL)
PREVENTION OF KIDNEY STONE FORMATION
⦁ increase fluid intake** (most important)
⦁ avoid sodium
⦁ reduce animal protein consumption
⦁ limit foods high in oxalate (beer, tea, coffee)
allopurinol = reduces amount of uric acid produced by body (helps with gout and when chemo increases uric acid levels)
GENITOURINARY TRAUMA
10% of trauma patients have injuries to GU tract
80% of GU traumas = BLUNT TRAUMA**
⦁ MVA
⦁ falls from heights
⦁ direct blows to torso or external genitalia
⦁ injuries to female genitalia = often associated with pelvic fractures, or can be a result of physical or sexual assault
85% of testicular injuries = a result of blunt trauma
GU TRAUMA INITIAL MANAGEMENT
- focus on rapid identification & stabilization of life-threatening injuries
- GU traumas = rarely life-threatening, however, a shattered kidney or major renal vascular laceration can pose a threat to kidney or life itself
- once patient is stabilized = evaluate for GU injury
GU TRAUMA ASSESSMENT = SECONDARY SURVEY (once stable from life-threatening injuries)
- inspect perineum & external genitalia
- look for blood in underwear
- look in folds of buttocks for perineal lacerations - may indicate a pelvic fracture
- rectal exam (sphincter tone, presence of blood, position of prostate - riding high or boggy = disruption of membranous urethra too)
MOST COMMON SITE OF URETHRAL INJURY = BULBOMEMBRANOUS JUNCTION
- Avulsion of puboprostatic ligament => stretching of membranous urethra - can result in partial or complete disruption of urethra at its weakest point = bulbomembranous junction
MALES
- examine scrotum for bruising or testicular rupture
- look for blood at penile meatus
FEMALES
- check vaginal introitus for lacerations or hematoma
- any suspicion of pelvic trauma/ hematoma / bruising = do bimanual exam to evaluate for vaginal blood
- any sign of vaginal blood = need speculum exam to rule out vaginal laceration
WHEN TO SUSPECT URETHRAL INJURY
⦁ blood at urethral meatus
⦁ gross hematuria
⦁ inability to void
⦁ absent or abnormally positioned prostate
⦁ ecchymosis or hematoma of penis, scrotum, perineum
⦁ plain films reveal a pelvic fracture
If you suspect a urethral injury = need a RUG prior to inserting foley catheter to evaluate the integrity of the urethra
- RUG is deferred only if pelvic angiography is being done to control pelvic hemorrhage
In the presence of gross hematuria without other signs of urethral injury = foley catheter may be inserted. Any resistance = abort cath attempt! do RUG
If foley catheter has been placed and there is gross hematuria or a pelvic fracture with microscopic hematuria = evaluate for bladder rupture with retrograde cystography or retrograde CT cystography
BLADDER INJURIES
o Contusions = partial thickness injuries to bladder wall without rupture
o Intraperitoneal rupture
⦁ occurs from blunt force injury to lower abdomen with a full bladder
⦁ results in rupture of the bladder dome followed by extravasation of urine into the peritoneal cavity
o Extraperitoneal rupture
⦁ occurs in association with pelvic fractures
⦁ injury force causes rupture of the anterior or anterior - lateral wall
⦁ sometimes bony fragments impale the bladder
All patients with a pelvic fracture or gross hematuria = should have a CYSTOGRAM to rule out bladder rupture
- pic = extraperitoneal bladder rupture - see leaking of contrast out
SUSPECT RENAL INJURIES WHEN: ⦁ bruising, pain or tenderness of the flank or abdomen ⦁ posterior rib or spine fractures ⦁ hematuria (gross or microscopic) ⦁ shock ⦁ fever ⦁ flank mass (urinoma)
WORK-UP FOR RENAL INJURIES
- UA
- Renal imaging (CT scan) is indicated in patients with
⦁ penetrating trauma
⦁ lower rib fracture
⦁ gross hematuria
⦁ blunt trauma with microscopic hematuria + shock
⦁ all clinical signs indicating abdominal organ injury or significant deceleration injury
CYSTITIS
colonization of vaginal introitus from fecal flora –> ascends to bladder via urethra (cystitis) –> ascends to kidneys causing pyelonephritis
- this route is much more difficult in males due to much longer urethra
MOST COMMON ORGANISM OF UTIs
⦁ E. coli
- other organisms = Proteus & Klebsiella
UTIs = much less common in men
Men with UTIs = get much bigger work up because they aren’t as common in men
UTI PRESENTATION ⦁ dysuria ⦁ frequency ⦁ urgency ⦁ suprapubic pain ⦁ hematuria
PYELONEPHRITIS
- symptoms of cystitis may or may not be present with pyelonephritis
- chills
- flank pain with costovertebral angle tenderness
- Nausea & Vomiting
DIAGNOSTIC TESTS
CYSTITIS
- UA is a MUST! - look for positive leukocytes and/or positive nitrites
- if uncertain about diagnosis or resistance is possible = do urine culture
- ALL MALES with cystitis = need a culture
FOR PYELONEPHRITIS
- UA
- urine culture & sensitivity
TREATMENT FOR WOMEN WITH CYSTITIS
⦁ Nitrofurantoin
⦁ Bactrim
⦁ can give phenozopyridine (pyridium) - analgesic agent - turns urine dark orange
-reserve fluoroquinolones for other uses in case resistance is built
TREATMENT FOR MEN WITH CYSTITIS
- ddx = prostatitis, urethritis secondary to STI, Urinary tract abnormality, nephrolithiasis
⦁ Bactrim
⦁ Fluoroquinolone
- want to cover possible prostatitis (also treat with either bactrim or cipro for acute or chronic)
- men = usually have longer lengths of abx
TREATMENT FOR PYELONEPHRITIS
- outpatient (mild to moderate illness / can keep meds down) = Fluoroquinolone (cipro or levaquin) if resistance is low. Others = bactrim or augmentin
- inpatient treatment = fluoroquinolone + aminoglycoside
BLACK WIDOW BITES
black widows release a neurotoxin called Alpha-Latrotoxin - released by all Latrodectus genus
- mostly found outside
- found predominantly in warmer climates; live in piles of firewood, old lumber, rock piles, bales of hay, etc
- not aggressive; timid - bite ONLY when bothered or protecting egg sac
- may have immediate sharp pain with bite, but may also be painless and go unnoticed
- 2 fang marks visible in approximately 80% of cases
Mild black widow reactions resolve in less than 12 hours with no residual symptoms
- a systemic reaction (Latrodectism) has 3 phases
⦁ Exacerbation Phase
- up to 24 hours after the bite
- muscle spasms near the bite, but can occur anywhere in the body, especially the abdomen & lower extremities
- autonomic stimulation = may include sweating, N/V, tachycardia, tachypnea, restlessness, HTN, HA
- coma & death can ensue, but rare and usually in a child
⦁ Dissipation Phase
- 1-3 days following the bite
- symptoms decline in most cases without specific treatment
⦁ Residual Phase
- weeks to months following the bite
- muscle spasms, tingling, nervousness and weakness may occur
- blanched circular patch with surrounding red perimeter & central punctum
- appears like a “target” lesion in 50% of cases
- primarily based on symptoms & signs with hx
- no specific lab studies
⦁ leukocytosis
⦁ elevated creatinine
⦁ elevated LFTs - In adults with cardiac risk factors = consider
⦁ EKG
⦁ Cardiac enzymes
TREATMENT
o Mild envenomation
⦁ gently clean bite with mild soap & water
⦁ Oral analgesic (acetaminophen, ibuprofen, oxycodone or hydrocodone)
⦁ oral muscle relaxer (benzo - valium, Methocarbamol - Robaxin)
⦁ Tetanus prophylaxis if indicated
o Mod / Severe Treatment
⦁ local wound care - clean with soap / water
⦁ tetanus prophylaxis if indicated
⦁ parenteral opioids (morphine)
⦁ parenteral benzos (lorazepam) to reduce frequency & severity of muscle spasms
⦁ antiemetic therapy (sublingual or IV ondansetron)
⦁ consider antivenom administration - consult with medical toxicologist - small risk of anaphylactic reactions
BROWN RECLUSE SPIDER BITES
- looks like a violin in the center
- in north & south America
- notorious for becoming necrotic
- Systemic reaction = Loxoscelism - can result in syndrome associated with hemolysis - may result in death, but very rare
- Loxosceles genus
- brown
- releases Sphingomyelinase D - unique to Loxosceles genus - causes necrosis
- systemic reaction is mild - nonspecific signs & symptoms
- symptoms usually develop 2-8 hrs after a bite
- usually initially painless, some have minor burning like a bee sting
- after about 4 hours = severe pain at bite site
SYSTEMIC SYMPTOMS ⦁ malaise ⦁ Nausea / vomiting ⦁ fever ⦁ myalgias
- initially, bite = mildly red, may reveal fang marks
- blistering = common
- necrosis of skin & subcutaneous fat (less common)
- severe destructive necrotic lesions with deep wide borders (rare)
DIAGNOSIS
- based on hx & clinical presentation
- Definitive diagnosis = a spider was seen biting the pt & spider was collected & properly identified by expert entomologist
If both conditions are not met, then other conditions must also be excluded
TREATMENT
- clean local wound with mild soap & water, apply cold packs and maintain affected part in elevated or neutral position
- Dapsonece
- Pain management
⦁ NSAIDS or opioids if necessary - Tetanus prophylaxis if necessary
- no antivenom available in the US
SCORPTION STING
- The most dangerous scorpions are located outside the US
- within the US = only 1 scorpion considered to be dangerous = BARK SCORPION
- Bark Scorpion = found mostly in Arizona, New Mexico, Southeastern Cali, Texas & Mexico
- scorpions use venom only for defense; they rarely sting their prey
PRESENTATION
- neurotoxin can cause prolonged & excessive depolarization
- systemic symptoms are not common, but can be severe, especially in children
⦁ pain & paresthesias in stung extremity - may become paralyzed
⦁ abnormal EOMs, blurred vision, pharyngeal muscle incoordination and drooling
⦁ excessive motor activity may appear seizure-like
⦁ may have N/V, tachycardia and severe agitation
⦁ without antivenom, symptoms can last 24-48 hours
⦁ deaths are rare
TREATMENT - SCORPIONS
⦁ initial treatment = supporitve with analgesics
⦁ antivenom = only available in AZ, and production has been stopped - should therefore be reserved for cases of severe systemic toxicity
BEE STING
- generally honeybees & bumblebees are docile and only sting when provoked
- males don’t have stingers
- when females sting, they eventually die
- Africanized honeybees = “killer bees” = very aggressive, but no more toxic than non-aggressive honey bees
⦁ can respond to a perceived threat with > 10x the number of bees ; massive stinging can result in multisystem damage and death from venom toxicity
⦁ has no natural predators
⦁ while worried about venom toxicity with Africanized bees, the greatest worry is still an anaphylactic reaction
LYME DISEASE
- symptoms may not be obvious for days or weeks after the tick bite
- deer tick: Borrelia burgdorferi (gram negative spirochete)
- MC = Ixodes scapularis tick, MC sources = White-tailed deer and White-footed mice
- MC in spring and summer
- MC in Northeast, Midwest + Mid-Atlantic regions of US
highest likelihood of transmission = tick is engorged and/or has been attached for at least 72 hours
SYMPTOMS
- early localized = ERYTHEMA MIGRANS = the characteristic rash of lyme disease = expanding, warm, annular, erythematous rash - salmon color and expands over a few days or weeks. Center of rash = lighter color - “bull’s eye” appearance - central clearing. Lesion usually expands slowly over days to weeks; may be accompanied by viral-like syndrome: headaches, fever, malaise or lymphadenopathy
- 80-90% of ppl with lyme dz will develop erythema migrans rash
- early disseminated symptoms (1-12 weeks) = RHEUMATOLOGIC = arthritis (especially in large joints). NEUROLOGIC = headache, meningitis, weakness, CN palsies (ex: CN VII/facial nerve palsy). CARDIAC = AV Block, pericarditis
- may have multiple erythema migrans lesions
- late disease = persistent synovitis, persistent neurological symptoms, subacute encephalitis. Acrodermatitis chronica atrophicans = bluish discoloration of extremities (seen in Europe)
DIAGNOSIS = clinical: especially in early Lyme disease = based on presence of EM rash, hx of tick bite and arthritis; patients with EM rash are often seronegative in early stage
- Serologic testing = ELISA. if positive = Western blot
TREATMENT = Doxycycline 100mg BID x 10-21 days.
- if Kid < 8 or Pregnant = Amoxicillin x 14-21 days
- if Doxy CI and PCN allergy = Azithromycin or Erythromycin
Late/severe disease = IV Ceftriaxone if patient is experiencing 2nd/3rd degree AV heart block, syncope, dyspnea, chest pain, CNS disease (meningitis)
NEED FOR PREVENTATIVE TREATMENT?
- IDSA recommends preventive treatment with abx only in people who meet ALL of the following criteria:
⦁ the attached tick is identified as an adult or nymphal deer tick
⦁ the tick is estimated to have been attached for > 36 hours - Antibiotic treatment can begin within 72 hours of tick removal; the patient can take doxycycline if not pregnant, not breastfeeding and not < 8 years old (given amoxicillin); if allergic to PCN and doxy is CI = give azithromycin or erythromycin
- if the patient meets all of the above criteria = single dose of 200mg for adults, and 4mg/kg in children > 8
- if allergic to doxy = no prophylaxis is given
KOPLIK SPOTS
MEASLES
FEVER THAT GOES AWAY, THEN DEVELOP RASH
ROSEOLA
HEMOPHILIA A
- factor 8 deficiency (intrinsic pathway) –> failure to form hematomas
- MC type of hemophilia; fairly common
- X-linked recessive = occurs almost only in MALES
Blood does not clot normally; does not bleed more profusely or bleed faster than others, but just bleeds for a longer time
- external wounds usually not serious; more concerned with internal bleeding
- hemorrhages are usually in joints (hemarthrosis - especially knees/ankles/elbows) and into tissues and muscles
SIGNS/SYMPTOMS OF HEMOPHILIA A
- petechiae & ecchymosis ABSENT - normal platelet function (present with vWD)
- bleeding into joints (hemarthrosis) - knees / ankles / elbows
- bleeding into muscles
- GI bleeding
- mild disease = bleed after major trauma or surgery
- mod/severe disease = bleed with mild trauma or surgery
- severe disease = bleed spontaneously
Hemarthrosis = medical emergency
- recurring bouts may lead to destruction of a joint and painful deformities later in life
DIAGNOSIS (LABS) ⦁ low factor 8 ⦁ prolonged PTT ⦁ normal PT ⦁ normal platelets
TREATMENT
- avoid aspirin!!!
- factor 8 replacement = recombinate factor 8 concentrate (dose depends on severity of bleeding)
- cryoprecipitate
- for mild hemophilia = can use DDAVP (desmopressin - ADH) = increases factor 8 & vWF (as these are the only factors excreted through the kidneys)
⦁ can use EACA (Amicar) along with DDAVP = synthetic antifibrinolytic
HEMOPHILIA B
- also called Christmas disease
- X-linked bleeding disorder
- factor 9 deficiency
- less common than hemophilia A
- also almost exclusively in males
- clinical features = almost identical to hemophilia A
- factor 9 = intrinsic pathway, so have prolonged PTT, normal PT, and decreased factor 9 levels
- deep tissue bleeding but same symptoms
TREATMENT
- avoid aspirin!
- factor 9 concentrates
- giving factor 8 concentrates are INEFFFECTIVE, and DDAVP = INEFFECTIVE too (DDAVP only used in hemophilia A and vWD)
VON WILLEBRAND DISEASE
- common inherited bleeding disorder
- autosomal dominant pattern; affects both sexes equally (unlike hemophilia = more males)
- vWD = disorder of platelet function & coagulation pathway
- deficiency of von Willebrand Factor - which is required for platelet adhesion (doesn’t affect platelet aggregation, just adhesion)
- MC in women
- MC hereditary bleeding disorder***
- vWF = necessary for initial platelet adhesion and also prevents factor 8 degradation. vWF = carrier molecule for factor 8 in plasma. With vWF deficiency, factor 8 is rapidly degraded
- factor 8 & vWF are NOT produced in the liver - so are still present with liver disease
CLINICAL PRESENTATION
-vWD = relatively common, but only small amount are diagnosed with it and ever seek medical attention due to bleeding symptoms
- manifests as a hemostasis problem
⦁ easy bruising
⦁ skin bleeding
⦁ prolonged bleeding from mucosal surfaces (oropharyngeal, GI, uterine)
⦁ petechiae (rare in hemophilias, as hemophilia = normal platelet function)
***Mucocutaneous bleeding = easy bruising, epistaxis, gums, GI, menorrhagia
SIGNS/SYMPTOMS ⦁ excessive menstrual & postpartum bleeding ⦁ GI bleeding ⦁ epistaxis ⦁ gingival bleeding ⦁ easy bruising ⦁ UNCOMMON for joints to be involved
LAB FINDINGS
- decreased vWF
- may have decreased factor 8
- prolonged PTT (normal PT)
- bleeding time & PTT prolongation worse with aspirin
stress, surgery, pregnancy and OCP may increase vWF levels
BLEEDING TIME = measure of interaction of platelets with blood vessel wall - is prolonged in patients with moderate & severe VWD, but is often normal with mild VWD
- keep in mind that in patients with mild vWD, the ingestion of aspirin or other antiplatelet meds, such as NSAIDS, can precipitate bleeding that may not have occurred otherwise*
- some patients remain asymptomatic - are only diagnosed because of screening done after family member diagnosed with severe vWD
TREATMENT
- avoid ASA & NSAIDS if mild
- for more severe vWD
⦁ DDAVP (causes release of vWF from endothelial cells, increases factor 8 levels) - give IV, SQ, or intranasally
⦁ Factor 8 concentrates (humate-P = Armour)
⦁ EACA = E-amincaproic acid - good with dental procedures
⦁ vWF containing products
- “intermediate purity” factor 8 concentrate = contains vWF too
- highly purified vWF concentrates
- recombinant vWF products (still in development)
- cryoprecipitate (not recommended)
VITAMIN K DEFICIENCY
- Source of vitamin K = green vegetables; synthesized by intestinal flora
- Vitamin K = required for synthesis of factors 2, 7, 9, 10, and protein C & S
- Causes of Vitamin K deficiency = malnutrition, biliary obstruction, malabsorption, antibiotic therapy (particularly cephalosporins)
- Treatment = Vitamin K, FFP
2, 7 and 10 = major clotting factors for the extrinsic pathway; depend on a healthy liver & adequate dietary intake of vitamin K
- some vitamin K derives from bacterial production by gut flora
Vitamin K deficiency leads to reduced hepatic synthesis of factors 2/7/9/10
VITAMIN K DEFICIENCY = COMMON SEEN IN ⦁ alcoholics ⦁ chronic liver disease ⦁ biliary obstruction ⦁ intestinal malabsorption ⦁ poor dietary intake ⦁ long term use of antibiotics (particularly cephalosporins)
LAB FINDINGS
⦁ PT prolonged (more so than PTT)
⦁ PTT prolonged
TREATMENT = vitamin K supplementation (but this doesn’t work with liver disease…still won’t be able to produce coagulation factors)
ITP (IDIOPATHIC THROMBOCYTOPENIC PURPURA)
- acquired, abnormal isolated thrombocytopenia (low platelet count) of idiopathic cause
- primary ITP = idiopathic
- secondary ITP
⦁ immune mediated - associated with underlying disorder (SLE, HIV, HCV, etc)
⦁ medication induced: Sulfonamides, Thiazides, Cimetidine, Heparin
ACUTE ITP = MC in children after a viral infection** (often self-limited) - commonly occurs in childhood after viral infection
CHRONIC ITP = MC in adults - often recurrent. Women < 40, Males > 70; Females > Males
Often results from: Blood transfusions, IVDU, Graves disease, or can be chronic
PATHOPHYSIOLOGY = autoimmune antibody reaction against platelets –> splenic platelet destruction often following an acute infection (ex: viral)
- Antibody against GPIIbIIIa receptor found on platelets
- pathologic antibodies bind to platelets. Splenic macrophages bind to antibody coated platelets and destroy them
CLINICAL MANIFESTATIONS
- often asymptomatic
- increased mucocutaneous bleeding (like with vWD) - purpura, easy bruising, petechiae, bullae, epistaxis, menorrhagia, melena, bleeding of tooth & gums, wet purpura (blood blisters in mouth), retinal hemorrhages
- spontaneous hemorrhage rarely occurs
- NO SPLENOMEGALY***
DIAGNOSIS
- diagnosis of exclusion;
- isolated thrombocytopenia; very low platelet counts
- normal coagulation tests (PT/PTT normal) - because this is a platelet disorder, not clotting d/o
- smear = may show megakaryocytes or large-sized platelets
TREATMENT
o Children = observation (80% resolve w/o treatment within 6 months) or IVIG
- in adults, specific therapy required if platelet count < 50,000 or if patient is bleeding
o Adults = STEROIDS*** (blunts immune response), IVIG, or Splenectomy if refractory
o platelet transfusion only if < 20,000 to prevent spontaneous intracranial hemorrhage
o if mild acute ITP (platelet count > 30,000 and no mucosal bleeding) = may not require treatment other than trauma protection (esp head) & avoid ASA
o for more severe ITP (platelet count < 30,000 & mucosal bleeding) = PREDNISONE 1-2mg/kg
⦁ steroids decrease the affinity for splenic macrophages for antibody-coated platelets
⦁ high steroid dose until platelet count is normal, then gradually taper
⦁ bleeding diminishes within days (often 1 day)
⦁ platelet count improves within 2 weeks
- for severe ITP or failure to respond to Prednisone = Splenectomy (most definitive treatment) or IVIG (reserved for bleeding emergencies -such as preparing severely thrombocytopenic patient for surgery)
**For patients who fail to respond to Prednisone AND splenectomy = Danazol - inhibits macrophages
TTP (THROMBOTIC THROMBOCYTOPENIC PURPURA)
- a process characterized by abnoral activation of platelets and endothelial cells, with fibrin deposition in microvasculature and peripheral destruction of platelets & RBCs
PENTAD
1) Thrombocytopenia (Petechiae, bruising, purpura, mucocutaneous bleeding - skin, oral, epistaxis, GI, GU - menorrhagia)
2) Microangiopathic hemolytic anemia - anemia, jaundice, fragmented RBCs/schistocytes on peripheral smear
3) Kidney failure / uremia (not as common) = hematuria, proteinuria, elevated BUN/creatinine
4) Neurologic symptoms (headache, CVA, AMS)
5) Fever (rare)
ETIOLOGIES
o Primary TTP = idiopathic (autoimmune) - antibodies against ADAMTS13 –> so have decreased ADAMTS13 levels
o Secondary TTP = secondary to malignancy, marrow transplantation, SLE, estrogen, pregnancy, HIV
- may be associated with an antibody against or a deficiency of the protease which cleaves the high molecular weight multimers of vWF (ADAMTS13) = primary TTP
- can also be induced by drugs (ticlopidine, quinine, cyclosporine, tacrolimus, rapamycin, mitomycin, bleomycin) = secondary TTP
- increased incidence of TTP with pregnancy or HIV = secondary TTP
Thought to be autoimmune - platelet CONSUMPTION, not platelet destruction; platelets are being used up, not tagged and destroyed (ITP)
Multiple Organ System Abnormalities
⦁ Microangiopathic hemolytic anemia - results when capillaries are partially occluded by fibrin - RBCs get destroyed when they run into the occluded vessels)
⦁ Thrombocytopenia - often with purpura, but not usually severe bleeding
⦁ Acute renal insufficiency - may be associated with anuria and may require acute dialysis
⦁ Neurologic abnormalities - usually fluctuating - headache, CVA, AMS
⦁ Fever
PATHOPHYSIOLOGY
- decreased ADAMTS13 (a vWF cleaving protease) –> large vWF multimers adhere to platelets and cause endothelial platelet adhesion –> small vessel thrombosis –> RBCs become sheared and damaged as they circulate in partially occluded small vessels –> hemolytic anemia
Seen primarily in young adults between 20-50
slight female predominance
occasionally precipitated by: Estrogen use, Pregnancy, Drugs, Infections
SIGNS/SYMPTOMS
- patient appears acutely ill, febrile, pallor, purpura, petechiae
- signs of neurological dysfunction (waxes & wanes) = HA, confusion, aphasia, AMS, sleepiness, stupor, stroke, coma, seizures
DIAGNOSIS ⦁ thrombocytopenia ⦁ normal coagulation factors (PT/PTT) - like HUS, but unlike DIC ⦁ reticulocytosis ⦁ hemolytic anemia - peripheral smear. increased reticulocytes (immature RBCs), schistocytes (bite/fragmented helmet cells), increased LDH, increased indirect bilirubin, decreased haptoglobin ⦁ hemoglobinuria, hemoglobinemia ⦁ negative Coombs test ⦁ SPLENOMEGALY
TREATMENT
- requires prompt recognition & emergent treatment (THIS IS AN EMERGENCY)
⦁ PLASMAPHARESIS - TOC - removes antibodies against ADAMTS13 and adds missing ADAMTS13 to serum. Done daily until platelets > 150,000 x 2 days. Monitor LDH / platelets / H&H / creatinine until normal x 2 days
⦁ Steroids, Cyclophosphamide etc.
⦁ do NOT give platelet transfusion - may cause thrombi formation - have been associated with CVA, death, lawsuits, etc.
⦁ can perform splenectomy if refractory to plasmapharesis and steroids. Can try vincristine or Rituximab too
TTP = not common (1/50,000); inherited or idiopathic. >90% fatal without therapy. 80-90% survive with therapy. 1/3 of patients will relapse within 10 years- most within 1 month of diagnosis
HUS (HEMOLYTIC UREMIC SYNDROME)
usually classified along with TTP as “TTP/HUS”
- has fewer neurologic sequelae, and more renal manifestations than TTP
- better prognosis than TTP
TRIAD
1) Thrombocytopenia (bruising, purpura, bleeding)
2) Microangiopathic Hemolytic Anemia (anemia, jaundice, fragmented RBCs/schistocytes)
3) Kidney failure (uremia) - more common with HUS than with TTP
HUS = associated MC with children - high incidence of renal failure
- lacks the fever & neurologic symptoms seen with TTP
- **DIFFERENTIATED FROM TTP by Renal Failure & lack of neurologic findings (HA/CVA/AMS)
- **DIFFERENTIATED FROM DIC by normal coags with HUS
HUS = difficult to distinguish from TTP because labs are all similar
Predominantly seen in CHILDREN - usually preceded by E.COLI, Shigella, or Salmonella gastroenteritis
- When HUS occurs in adults = seen with HIV, SLE, and antiphospholipid syndrome
- in adults = often precipitated by estrogen use or post-partum state (like TTP)
Suspect HUS if renal failure in a child who had a diarrhea prodrome
PATHOPHYSIOLOGY = Platelet activation by exotoxins (shigella toxin & shiga-like toxin in E.coli) - the toxins enter the blood and damage the vascular endothelium –> activates platelets –> microthrombi formation –> platelet depletion (thrombocytopenia)
- the toxins damage the kidney –> uremia & HTN
- the small vessel thrombosis cause RBC damage as they circulate through vessels –> hemolytic anemia
DIAGNOSIS = same as with TTP
⦁ Thrombocytopenia
⦁ Normal PT/PTT
⦁ Hemolytic anemia - smear = increased reticulocytes, schistocytes, increased LDH, increased indirect bilirubin (less severe hemolytic anemia than TTP)
⦁ increased BUN / Creatinine (kidney damage)**
⦁ Elevated fibrin degradation products (D-Dimer)
STRIKING RED BLOOD CELL FRAGMENTATION = the defining diagnostic finding***
TREATMENT
- children = observation in most kids (self-limiting); IV fluids to maintain renal perfusion
- Plasmapharesis (like with TTP)*** with FFP if severe, neurologic complications or nonrenal complications
- management of renal failure: many patients have chronic renal insufficiency
DIC (DISSEMINATED INTRAVASCULAR COAGULATION)
- Pathological activation of coagulation system - a process characterized by the abnormal activation of coagulation, generation of thrombin, consumption of clotting factors, destruction of platelets, and activation of fibrinolysis
- Release of tissue factor substances that activate the extrinsic pathway of coagulation
- Associated with massive injury to the endothelial lining of blood vessels; large scale aggregation of platelets and activation of coagulation cascade
-
CONSUMPTION OF CLOTTING FACTORS & PLATELETS*
1) widespread microthrombi which consumes coagulation proteins (V, VIII, fibrinogen) & platelets
2) severe thrombocytopenia –> diffuse bleeding from skin, respiratory tract, GI tract
ETIOLOGIES
⦁ Infections: MC = gram negative sepsis**, or endotoxins
⦁ Malignancies - AML, lung, GI, prostate, etc.
⦁ Obstetric: Preeclampsia, abruptio placentae, septic abortion, amniotic embolus
⦁ Massive tissue injury (burns, RMSF, liver disease, viral, aortic aneurysm, ARDS)
⦁ hemolysis, heat stroke, snake bites, etc.
something above causes widespread damage to vessels –> kicks of process to DIC
CLINICAL MANIFESTATIONS
- patients are acutely ill: Bleeding & thrombosis, but bleeding = more common. Spontaneous bleeding & oozing at venipuncture sites or wounds
- shock & widespread bleeding
1) widespread hemorrhage venipuncture sites*** - mouth, nose, extensive bruising
2) thrombosis - renal, hepatic, respiratory dysfunction, gangrene (clots block circulation) –> digital ischemia & gangrene, renal necrosis, CNS dysfunction (seizures, delirium, coma), respiratory failure - can lead to microangiopathic hemolytic anemia
- bleeding: Petechiae, ecchymosis are common along with blood oozing from wound sites, IV lines and catheters; blood in urine, stool, vomitus and sputum
- renal dysfunction, hepatic dysfunction, respiratory dysfunction, shock, thromboembolism, & CNS involvement
DIAGNOSIS
⦁ Thrombocytopenia (< 100,000 and rapidly declining)
⦁ Prolonged or increased PT/PTT
⦁ low levels of coagulation inhibitors (Antithrombin III, protein C)
⦁ low levels of coagulation factors (5, 8, 10, 13)
⦁ low fibrinogen levels
⦁ increased thrombin formation
⦁ peripheral smear = fragmented RBCs (schistocytes)
⦁ increased fibrinolysis - increased D-Dimer (fibrin degradation product - released when clots are broken up)
TREATMENT
- treat the underlying cause! = most important step
- for patients actively bleeding =
⦁ platelet transfusions (PLT < 50K)
⦁ if PT significantly elevated = give FFP
⦁ if fibrinogen < 50 = cryoprecipitate
⦁ Blood
SPINAL CORD COMPRESSION
- PRESENTS AS BACK PAIN for most patients
- inflammation & paresthesias
- then AUTONOMIC DYSFUNCTION FOLLOWS MOTOR/SENSORY SYMPTOMS
- usually occurs in diseases with vertebral body mets (not hematogenous dural mets)
- RAPID deterioration predicts a worse outcome than longer (weeks)
This is a common complication of cancer - especially breast, lung, MM and prostate cancer - most commonly cause spinal cord compression
Most common = thoracic spine - the thecal sac is what is actually being compressed. The tumor starts to invade the epidural space (back pain), then progresses
DIAGNOSIS = MRI of WHOLE spine -
- or CT
- with or without myelogram
TREATMENT
⦁ DECADRON (dexamethasone) = 4-6mg po or IV q4-6hrs; some suggest 100mg bolus, then 24mg q6hr
⦁ Neurosurgery in most circumstances -especially if no dx or vary rapid onset
⦁ XRT - radiation IF multiple levels
HYPERVISCOSITY
- relatively nonspecific symtoms: somnolence, headache, blurry vision, dizziness
- Hyperviscosity = mostly with WALDENSTROMS (less commonly with MM or Polycythemia vera, and rarely essential thrombocytosis)
- PE for hyperviscosity = look at eyes = have bulging vasculature
TREATMENT = hydrate the patient!
- Waldenstroms = B-cell lymphoma that produces excess IgM; have Hyperviscosity syndrome. Tx = plasmapharesis to treat hyperviscosity syndrome
- Plasmapharesis for IgM + Chemotherapy
- phlebotomy for Polycythemia vera - replace units with NS
- hydroxyurea & aspirin for essential thrombocytosis
LEUKOSTASIS
- mostly in AML with WBC > 100,000
- altered mental status, coma common, but other organs also involved; dizziness, lethargic, etc.
- hypoxia
- renal insufficiency
- may worsen during induction chemo for AML
TREATMENT
- hydrate the patient!!!
- Quinton access (renal) & Chemotherapy (oncology)
- gen an LP for cytology to rule in/out CNS leukemia
- steroids may help here too (like with decadron for cord compression)
CARDIAC TAMPONADE
- a pericardial effusion that causes significant pressure on the heart –> restricts cardiac ventricular filling –> decreases cardiac output
-
BECK’S TRIAD
1) distant / muffled heart sounds
2) increased JVP
3) systemic hypotension
PULSUS PARADOXUS = upon inspiration = > 10mmHg decrease in systolic BP = decreased pulses with inspiration - because increased filling of the right side of the heart during inspiration and decreased left sided ventricular filling –> pulsus paradoxus
- Dyspnea, fatigue, peripheral edema, shock, hypotension, reflex tachycardia, cool extremities
DIAGNOSIS = ECHO = see presence of effusion + diastolic collapse of cardiac chambers (due to pericardial fluid pressure pushing on relaxed chamber –> collapse)
TREATMENT = PERICARDIOCENTESIS (immediate)
- pericardial window if drainage is recurrent
Malignant pericardial effusions are common, just not commonly symptomatic; mortality probably from other aspects of the patient’s disease
- MC = lung cancer & breast cancer
- EKG = ELECTRICAL ALTERNANS
seen with cardiac tamponade and severe pericardial effusion
Presents with left or right sided failure, pulsus paradoxus, and big heart on CXR (bottle shaped heart = with pericardial effusion & cardiac tamponade)
TREATMENT
- need an Echo & Cytology for pericardiocentesis
- Pericardiocentesis = catheter drainage of pericardial fluid
- medical management
- onocology input: chemotherapy
- CT surgery input: subxiphoid pericardial window or balloon pericardiotomy - especially for recurrent effusions in patients with good performance status
SVC SYNDROME
- seen with Bronchogenic Carcinoma
- SVC syndrome = dilated neck veins, prominent chest veins, facial plethora
- SOB = MC symptom** (also have facial / arm swelling) & varicose veins across chest/neck
- MC with small cell carcinoma (oat cell)
usually from lung cancer
- could also be from lymphoma, breast cancer, mediastinal tumors
CLINICAL MANIFESTATIONS
- facial edema
- symmetric or asymmetric upper extremity edema also common
- SOB common, but not hypoxic
only a relative emergency, even with CNS symptoms
- mainly from Bronchogenic carcinoma, but can be from Pancoast tumor too
Supra-azygos SVC obstruction (obstruction above junction of SVC & azygos vein = causes arm/neck/chest vein distention & edema of face/arms) vs Infra-azygos SVC obstruction (more severe symptoms - obstruction in SVC)
DIAGNOSIS
- need pulse ox & CXR
- Chest CT to outline the mass that will need therapy
- oncology involved = chemo for small cell, lymphoma and germ cell
- radiation for almost all else
- heparin or steroids
- SVC stenting…new
TUMOR LYSIS SYNDROME
- occurs in tumors with high body burden & high chemosensitivity
⦁ usually high-grade lymphomas or leukemias
⦁ small cell or germ cell = less common - usually due to therapy, so you know the diagnosis already; may occur at onset of therapy or after a day or two, up to 5 days later
- few clinical symptoms other than being ill with obvious lab abnormalities due to
RENAL FAILURE**
tumors with high proliferative rate respond well to chemo, however, can lyse and spew toxins everywhere –> renal failure
⦁ HYPERURICEMIA (uric acid crystals can cause a lot of kidney damage)
⦁ HYPERKALEMIA
⦁ HYPERPHOSPHATEMIA
⦁ HYPOCALCEMIA
- due to rapid turnover of tumor cells (with or without anti-tumor therapy)
TREATMENT
- fix conditions that will make effects worse (dehydration, renal obstruction, IV contrast)
- get baseline labs (K, Ca, Phos, Uric acid, LDH, Cr)
- alkaline diuresis = D5 1/2NS - to keep urine pH > 7
- keep urine output high - through lasix, mannitol
- allopurinol - to keep uric acid production down
- Rasburicase = also helps with uric acid level
- **If calcium too low = must give…MAGNESIUM
- During treatment = remember that high K and low Ca kill people
- keep alkaline urine output high (lasix / mannitol)
- check lytes, phos, UA, Ca, LDH, Cr
- try to keep phosphate < 7, calcium > 6, potassium < 6
- if calcium low = remember to give magensium too**
- if phosphate > 7 = switch NaHCO3 to NS to prevent calcium phosphate deposits in kidney
- acute potassium = always good, but insulin/D-50 is preferred over IV calcium
- may need dialysis
LEUKOSTASIS
- mostly in AML with WBC > 100,000
- altered mental status, coma common, but other organs also involved; dizziness, lethargic, etc.
- hypoxia
- renal insufficiency
- may worsen during induction chemo for AML
TREATMENT
- hydrate the patient!!!
- Quinton access (renal) & Chemotherapy (oncology)
- gen an LP for cytology to rule in/out CNS leukemia
- steroids may help here too (like with decadron for cord compression)
HYPERCALCEMIA FROM MALIGNANCY
- MC causes = breast cancer, lung cancer, and MM
- squamous cancers from multiple sites often make PTH-rP (like a fake parathyroid hormone) - causes increased osteoclast activity and decreases osteoblast activity
- usually gradual in onset
- fatigue, N/V, constipation, anorexia, apathy
- MC = DECREASED CONSCIOUSNESS***
Patients are always volume depleted due to calcium-induced renal tubular defects
TREATMENT
- volume replete the patient
- Furosemide (lasix)
- ** IV PAMIDRONATE** - or if renal function is okay = IV Zoledronic Acid (Zometa)
- dialysis, calcitonin and steroids = can be used as adjunctive therapy
Hypercalcemia = predicts short survival with cancer
SIADH
- Syndrome of Inappropriate ADH
- SMALL CELL LUNG CANCER
- lots of ADH –> lots of water retention –> HYPONATREMIA
Na+ < 120 = anorexia, irritability, N/V, constipation, muscle weakness, myalgia
Na+ < 110 = seizure, coma / death, abnormal reflexes, papilledema
decreased BUN / osmolarity (dilute from water absorption)
increased urine osmolarity & sodium levels (concentrated urine)
TREATMENT
- treat underlying tumor
- limit fluid intake to 500-1000mL/day
- furosemide (lasix)
- parenteral sodium replacement with severe neurological symptoms
- monitor electrolytes: Mg, K, Ca
NEUTROPENIC FEVER
- MOST URGENT-
- may initially be very subtle; then rapid development of hypotension, dyspnea, sepsis
⦁ gram negative»_space;gram positive = short-term
⦁ fungal / viral / opportunistic infxn = long-term (weeks)
Most patients are neutropenic due to chemotherapy, not due to malignancy in the marrow
- Most neutropenia occurs 10-15 days after chemo
Do blood culture to find out which infection, then start broad spectrum abx
- fully evaluate patient for a source: blood, CXR, sputum, urine, skin, LP?
- if suspectied source = treat it
- if no suspected source = treat empirically for gut flora
⦁ cefipime, moxifloxacin, Pip/gent, aztreonam
- TX = predninsone, IVIG if thrombocytopenia
SPONTANEOUS ABORTIONS (MISSCARRIAGE) = < 20 WEEKS
o THREATENED MISCARRIAGE ⦁ no cramping ⦁ slight bleeding ⦁ closed os ⦁ no passed products of conception ⦁ Unpredictable prognosis ⦁ US = + fetal cardiac activity - 90-96% will go on to term - expectant management (wait for tissue products to pass or to carry to term) = bed rest, gradual resumption to normal activities, no sex, hydration, no meds
o INEVITABLE MISCARRIAGE
⦁ cramping, lower back pain
⦁ increased bleeding
⦁ open cervical os (dilated)
⦁ products have not passed, but inevitable; can’t be saved, poor prognosis
⦁ US = cardiac activity or fetal demise
- Management = expectant (natural passage) or surgical (D&C) or Misoprostol (Cytotec) = can help pass fetal tissue early
o INCOMPLETE MISCARRIAGE
- fetus has passed, but placenta remains
- heavy bleeding - can be enough to cause hypovolemic shock
- mod/severe cramping & low back pain
- cervical os is open (dilated)
- uterus feels “boggy” on palpation
- US shows tissue in uterus (placenta)
- surgery usually necessary to remove retained tissue
ECTOPIC PREGNANCY
implantation of fertilized egg outside the uterus
- MC location = fallopian tube
- can also be implanted in cervix, ovary or abdominal cavity
RISK FACTORS ⦁ hx of ectopic pregnancy ⦁ hx of genital infections - PID ⦁ hx of tubal surgery ⦁ hx of infertility = on infertility treatment ⦁ IUD
What can happen
1) can rupture –> hemorrhage
2) can result in abortion –> tissue absorbed
3) can spontaneously resolve
PRESENTATION ⦁ MC symptom = Abdominal pain ⦁ vaginal bleeding ⦁ amenorrhea (1-2 months) ⦁ hypovolemic shock ⦁ morning sickness, breast tenderness ⦁ diarrhea / urge to defecate ⦁ malaise / syncope ⦁ sudden severe lower abdominal / pelvic pain - can radiate to shoulder
PHYSICAL EXAM = check hemodynamic status***
- tachycardia
- hypotension
- cervical motion tenderness / abdominal or pelvic tenderness
- normal appearing cervix - but tender
- may find adnexal mass or may be unremarkable
- vaginal vault = brick red to brown in color
LABS
⦁ beta hCG = will be lower than normal for gestation
⦁ CBC = may show anemia or slight leukocytosis
IMAGING
⦁ TRANSVAGINAL ULTRASOUND*** - can determine if intrauterine pregnancy is present; should be seen if serum hCG > 2000
- if ectopic pregnancy = usually seen in fallopian tube (97%)
- if TVS = inconclusive and patient is stable = obtain serial quantitative hCGs to follow
Heterotopic pregnancy = have both Intra-uterine pregnancy and extrauterine pregnancy at same time
TREATMENT
- laparoscopy = surgery
- if patient has a positive hCG and is hemodynamically unstable = is considered to have a RUPTURED ECTOPIC PREGNANCY = needs immediate surgical intervention
- if patient is stable = can treat with MTX - terminates fetus prior to rupture
PLACENTA PREVIA
- the placenta implants on lower part of uterus - either extends over the cervical os or lies close to it
⦁ total/complete = entire os is covered
⦁ partial = internal os partially covered
⦁ marginal or low-lying = edge is at the os, but doesn’t cause an obstruction
RISK FACTORS ⦁ previous placenta previa ⦁ multiparity (multiple births) ⦁ multiple gestations ⦁ previous C-section ⦁ trauma ⦁ smoking ⦁ old mom ⦁ infertility treatment ⦁ previous uterine surgery
SYMPTOMS
- PAINLESS VAGINAL BLEEDING in 3rd trimester = bright red blood
DON’T DO VAGINAL / SPECULUM EXAM - can do transvaginal US - to determine if placenta previa and to rule out placenta abruptiae
- have normal fetal heart tones and stable fetal activity
TREATMENT =
o If acutely bleeding
- 2 large bore IVs NS, oxygen
- foley for following urine output (goal = 30cc/hour)
- CBC, coag studies (can develop DIC)
- type & cross match 4 units of packed RBCs
- maintain maternal hgb > 10
- if platelets < 100,000 = give platelets
- monitor fetal status - consult OB for possible emergent delivery
o If patient has minimal bleeding or bleeding stops or is hemodynamically stable
- monitor mom & baby
o If baby < 34 weeks gestation = consult with OB about giving antenatal steroids
o If contracting = consult about tocolysis - magnesium sulfate
o if not in facility where immediate c-section / neonatal capabilities are present = consider transfer
- Magnesium sulfate & steroids if in labor
- if no FHR, if hemorrhaging, or significantly bleeding = C-section
- most carry to term and have a scheduled C-section
PLACENTA ABRUPTIAE
- partial or complete detachment of placenta prior to delivery
- more frequently in 3rd trimester - fatal!
RISK FACTORS ⦁ previous abruption* ⦁ abdominal trauma* ⦁ cocaine* ⦁ smoking* ⦁ eclampsia ⦁ pregnancy induced HTN*** ⦁ multiple gestation* ⦁ polyhydramnios*
PRESENTATION ⦁ PAINFUL VAGINAL BLEEDING - dark red ⦁ abdominal or back pain ⦁ contractions ⦁ uterine tenderness ⦁ non-reassuring fetal heart rate - bradycardia (fetal distress)*
MATERNAL COMPLICATIONS
- hemorrhagic shock, DIC, rupture, renal failure, necrosis of distal organs
FETAL COMPLICATIONS
- hypoxia, anemia, growth retardation, CNS anomalies, death
LABS
- evaluate for DIC = D-dimer
IMAGING
- ULTRASOUND: classic finding = retroplacental hematoma
TREATMENT
- stabilize mother: oxygen, IV fluids
- monitor fetus
- tocolysis with magnesium sulfate
- consult with OB & neonatal services: immediate delivery**
PLEURAL EFFUSION
- not all pleural effusions need to be drained with a needle (thoracentesis); often will resolve on their own
- there are capillaries in visceral and parietal pleura through which interstitial fluid leaks out and into pleural space; lymphatic vessels then drain the pleural fluid in a equal balance
- can be either transudative issue (too much fluid leaks out of capillaries either due to increase in hydrostatic pressure or decrease in oncotic pressure) or exudative issue (too much fluid leaks out of capillaries due to inflammation of pulmonary capillaries –> makes them more leaky - creates larger spaces in capillary membrane)
TRANSUDATIVE
⦁ hydrostatic pressure = like BP - the force that blood exerts on the walls of the vessels (pushing force) - like with heart failure. If there is an increase in hydrostatic pressure…
- Heart failure: heart can’t effectively pump blood to body, so blood backs up into the lungs –> increased hydrostatic pressure in pulmonary vessels, which forces fluid out of pulmonary capillaries and into the pleural space
⦁ oncotic pressure = due to solute concentrations; if there is a decrease in solute concentration in pulmonary vessels, fluid will leak into pleural space, as solutes cannot cross capillary walls (cirrhosis, nephrotic syndrome)
- Cirrhosis = not making enough proteins –> low oncotic pressure in vessels
- Nephrotic syndrome = proteins lost in urine –> low oncotic pressure in vessels
o Transudative fluid = clear
EXUDATIVE
- inflammation of capillaries –> larger spaces in capillary membrane, allowing fluid, immune cells and large proteins (LDH) to leak out of capillaries and into pleural space
⦁ trauma
⦁ malignancy
⦁ inflammatory conditions (SLE, RA, sjogrens - autoimmune conditions)
⦁ infection (pneumonia)
o Exudative fluid = cloudy (full of immune cells)
LYMPHATIC PLEURAL EFFUSION
= chylothorax = lymphatic fluid accumulates in the pleural space due to an disruption in the thoracic duct, preventing drainage
⦁ damage to thoracic duct during surgery
⦁ tumors in mediastinum that compress thoracic duct
o Lymphatic fluid = filled with fat (looks like milk)
**biggest way to distinguish between transudative & exudative fluid = is that exudative fluid will have high amounts of protein & LDH from leaking out of inflamed capillaries
- use LIGHT CRITERIA- exudative if > 1 of the following
⦁ fluid protein : serum protein > 0.5
⦁ fluid LDH : serum LDH > 0.6
⦁ fluid LDH > 2/3 of upper limit of serum LDH
- exudative also has high cholesterol level > 45
SYMPTOMS
- small effusion may go unnoticed
- large effusions ==> pain with inhalation (pleurisy) and SOB, worse when laying flat
PE = decreased breath sounds, dullness to percussion, and decreased tactile fremitus
- if large enough, can put pressure on lungs and therefore push trachea to other side
XRAY = standing - fluid will settle in costophrenic angle (bottom is white)
laying flat = will settle all over chest wall, creating a layering effect (whole side is white)
TREATMENT = thoracentesis if needed
PATHOPHYSIOLOGY OF PLEURAL EFFUSION
- The abnormal accumulation of fluid in the pleural space
- generally the entrance & exit of fluid into pleural space is about equal
- fluid accumulation occurs when either the entry or exit rate of fluid is altered (increase in entry of fluid or decrease in exit of fluid)
MOST COMMON CAUSES OF PLEURAL EFFUSION ⦁ heart failure (transudative) ⦁ bacterial pneumonia ⦁ PE (exudative) ⦁ Malignancy ⦁ viral infections (not as common as bacterial) ⦁ cardiac surgery ⦁ pancreatitis
TYPES OF PLEURAL EFFUSION OR ASSOCIATED CONDITIONS
o Empyema = infection of pleural space
o Parapneumonic = pleural effusion secondary to bacterial pneumonia
o Hemothorax = gross blood (from chest trauma or malignancy)
o Chylothorax = lymph fluid due to impaired lymphatic drainage
TRANSUDATIVE VS EXUDATIVE o TRANSUDATIVE EFFUSIONS ⦁ heart failure ⦁ cirrhosis ⦁ nephrotic syndrome ⦁ atelectasis
- Mechanism of Transudative Effusions
⦁ increased hydrostatic pressure (CHF)
⦁ decreased oncotic pressure (albumin - cirrhosis or nephrotic syndrome)
⦁ increased negative intrapleural pressure (atelectasis)
⦁ ascites
o EXUDATIVE EFFUSIONS
⦁ cancer
⦁ inflammatory processes (trauma, autoimmune, infection)
- Mechanism = increased vascular permeability due to infection or inflammation
MEDICATIONS THAT CAN LEAD TO PLEURAL EFFUSION ⦁ Methotrexate ⦁ Amiodarone ⦁ Phenytoin ⦁ Nitrofurantoin ⦁ Beta blockers
BETty sold her FUR coat for METH/AM/PHEtamines
- beta blockers
- nitroFURantoin
- METHotrexate
- AMiodarone
- PHEnytoin
SYMPTOMS OF PLEURAL EFFUSION
- Asymptomatic
- dyspnea (common)***
- cough (generally pretty dry, unless also have pneumonia or pulmonary edema)
- pleuritic chest pain***
- fever (infection)
- hemoptysis
- weight loss (malignancy)
PHYSICAL EXAM
- dullness to percussion
- decreased or absent tactile fremitus
- decreased breath sounds
- reduced vocal fremitus and/or resonance
- +/- pleural friction rub
- may cause lung collapse & mediastinal shift if massive effusion or hemothrax (can have so much fluid accumulate that it causes pneumothorax or pushes trachea over)
DIAGNOSTIC TESTING
⦁ CXR (standing & laying flat)
⦁ CT scan can help determine lung disorders and presence of loculation
⦁ Ultrasound can determine presence of loculation and fibrin stranding; also aids in thoracentesis procedure
- loculation & fibrin stranding can’t be drained - coagulates - has to be scraped out
CXR - blunted costophrenic angles ⦁ > 175cc to obscure lateral costophrenic angles ⦁ > 500cc to obscure the diaphragm - may see meniscus sign - lateral decutibus films ⦁ can detect smaller effusions ⦁ can differentiate loculations & empyema (whether fluid shifts when laying down or not)
if effusion is large enough = will have tracheal deviation away from effusion
TREATMENT FOR PLEURAL EFFUSION
- the treatment of underlying conditions may often resolve pleural effusions (don’t drain all of them!)
- Thoracentesis = diagnostic & therapeutic
- Remove fluid via thoracentesis (max amount removed at one time = 1.5L - don’t want to remove too much, because relieving too much pressure at once can lead to compensatory pulmonary edema)
- may have placement of chest tube for continued drainage
- chronic effusion may require pleurodesis (induced scarring - with talc or doxycycline)
- empyema may require surgical removal
hemothorax can cause mediastinal shift and can lead to collapse
ANALYSIS OF PLEURAL FLUID ⦁ differential cell count ⦁ cytology ⦁ protein (helps determine transudate vs exudate) ⦁ LDH (helps determine transudate vs exudate) ⦁ gram stain ⦁ culture ⦁ pH ⦁ glucose
EXUDATIVE EFFUSION WILL HAVE HIGH AMOUNTS OF PROTEIN & LDH IN PLEURAL FLUID
LIGHT’S CRITERIA: EXUDATE IF >/= 1
o fluid protein : serum protein > 0.5
o fluid LDH : serum LDH > 0.6
o fluid LDH > 2/3 the upper normal limit of serum LDH
ALTERNATIVE CRITERIA: EXUDATE IF ⦁ LDH% of serum ULN = > 45% ⦁ cholesterol > 45 mg/dL ⦁ protein > 2.9 g/dL
TRANSUDATE IF
⦁ LDH % of serum ULN = 45%
⦁ cholesterol = 45 mg/dL
⦁ protein = 2.9 g/dL
