ER ROTATION Flashcards
NEXUS CRITERIA
NEXUS (National Emergency X-Radiography Utilization Study) is a set of validated criteria used to decide whether trauma patients require c-spine imaging.
The NEXUS criteria states that a patient with suspected c-spine injury can be cleared providing the following:
1) No posterior midline cervical spine tenderness is present.
2) No evidence of intoxication is present.
3) The patient has a normal level of alertness.
4) No focal neurologic deficit is present.
5) The patient doesn’t have a distracting injury
Trauma patients who DON’T require c-spine imaging:
1) alert and stable / no altered level of consciousness
2) no focal neurologic deficit
3) not intoxicated
4) no midline spinal tenderness
5) no distracting injury
The NEXUS criteria has a sensitivity of 99.6% for ruling out cervical spine injury in the original study validating the criteria (95% confidence interval, 98.6-100%)
The NEXUS criteria may not be reliable in patients >65
** If any of the above criteria are present, the C-Spine cannot be cleared clinically **
PECARN CRITERIA
Pediatric Head Injury/Trauma Algorithm
- Predicts need for brain imaging (CT) after pediatric head injury.
A) Age < 2
1) GCS < 15 or signs of altered mental status or palpable skull fracture
- Yes = CT!
- No ==>
2) scalp hematoma or hx of loss of consciousness for 5+ seconds or severe mechanism of injury or not acting normal according to parent
- Yes = Observation vs CT - depending on physician experience, parental preference, age of child < 3 months, worsening symptoms etc.
- No ==> CT not recommended
B) Age: 2+
1) GCS < 15 or signs of altered mental status or signs of basilar skull fracture
- Yes = CT!
- No ==>
2) hx of loss of consciousness, hx of vomiting, severe mechanism of injury or severe headache
- Yes = Observation vs CT - depending on physician experience, parental preference, worsening symptoms, etc.
- No = CT not recommended
PERC CRITERIA
PERC Rule for Pulmonary Embolism
1) age 50+
2) HR 100+
3) O2 < 95%
4) unilateral leg swelling
5) hemoptysis
6) recent surgery or trauma
7) prior PE or DVT
8) hormone use - OCP / hormone therapy / estrogen hormone replacement - males or females
If any are positive = cannot rule out PE
If all are negative = chances of PE are < 2%
CURB-65
for pneumonia
CENTOR CRITERIA
for strep pharyngitis (GABHS = Strep Pyogenes) - Estimates probability that pharyngitis is streptococcal - whether to do rapid strep swab, and that it’s not viral pharyngitis
1) Age: 3-14 = +1 point
- strep in patients < 3 is rare
- age 15-44 = 0 points
- age 45+ = -1 point
2) Tonsillar exudates or Tonsillar swelling = + 1 point
3) Tender / swollen anterior cervical lymphadenopathy = +1 point
4) Fever > 100.4F (38 C) = +1 point
5) Absent cough = +1 point
TREATMENT - Amoxicillin = 250mg TID x 10 days (adults) or 10mg/kg TID x 10 days (peds) - PCN - Azithromycin
RLQ PAIN DIFFERENTIAL DIAGNOSIS
The mnemonic “APPENDICITIS” can be used to remember the differential diagnosis of RLQ pain.
Appendicitis Pelvic Inflammatory Disease (PID) Period (Menstrual cramps) Pancreatitis Endometriosis Ectopic pregnancy Neoplasm Diverticulitis Intussusception Cyst (ovarian) Inflammatory bowel disease (Crohn's / UC) Torsion (ovary) Irritable bowel syndrome Stones (kidney)
OCULAR FOREIGN BODY
1ST CHECK VISUAL ACUITY
Patient will present as → complaining of right eye pain and irritation. He states that he wasn’t wearing glasses, and while trimming his driveway with his weedwacker “something flew into my eye.” Visual acuity is 20/20. Pupils are equal, round, reactive to light and accommodation. Extraocular movements are intact. On physical examination you note a tearing, red, and severely painful eye.
SYMPTOMS ⦁ foreign body sensation ⦁ tearing ⦁ red ⦁ painful ⦁ inability to open eye due to foreign body sensation
Inspect the eye thoroughly to identify if foreign body is present; use fluorescein staining if necessary
Metallic foreign bodies may leave a RUST RING
- If you can’t remove the foreign body easily = refer to the ophthalmologist
DIAGNOSIS
⦁ Full inspection of lids, conjunctiva and cornea
⦁ fluorescein staining may help
⦁ ** SLIT LAMP ** - assists in identification + removal
- X-ray or CT of may be necessary if there is evidence of penetration of the globe
TREATMENT
⦁ FOREIGN BODY REMOVAL = topical anesthetic + try irrigation - 2L of saline or for 20 minutes
- This is particularly helpful in the case of multiple superficial foreign bodies (eg, sand).
⦁ if irrigation doesn’t work, try swab moistened with proparacaine.
⦁ If swab doesn’t work = REFER
⦁ Treat with topical antibiotic ointment (erythromycin) or sodium sulfacetamide
- no patches!
- do NOT send patients home with topical anesthetics
Intraocular foreign bodies require immediate surgical removal by an ophthalmologist
Rust ring — After removal of a foreign body containing iron there is often a residual rust ring and reactive infiltrate. Patients with rust ring should be treated as patients with corneal abrasions. The rust ring itself is not harmful and will usually resorb gradually.
If patient was working with metal and metal piece is in eye or corneal abrasion present or patient has foreign body sensation = needs TETANUS VACCINE = every 5 years
THEN REFER TO OPHTHO…ALWAYS
CORNEAL ABRASION
Corneal abrasion is a medical condition involving the loss of the surface epithelial layer of the eye’s cornea.
Corneal abrasion is the most common ophthalmologic visit to the emergency department and is a commonly seen problem in urgent care.
CAUSE
- MC cause of corneal abrasion = ** trauma **
Corneal abrasions most commonly result from accidental trauma (e.g., fingernail scratch, makeup brush): Dirt, sand, sawdust, or other foreign body gets caught under eyelid.
FIRST STEP = CHECK VISUAL ACUITY
In corneal abrasion cases, visual acuity is usually fine
SIGNS / SYMPTOMS ⦁ Pain ⦁ Conjunctival injection (red) ⦁ Blurry vision (+/-) ⦁ Trouble with bright lights ⦁ Foreign body sensation ⦁ excessive squinting ⦁ reflex production of tears
In cases of corneal abrasions, the pupil is normal
Corneal abrasions are common and recurrent in people who suffer from corneal dystrophy.
- check for foreign body
- make sure to evert eyelids
DIAGNOSIS
- ** pain relieved with ophthalmic analgesic drops ***
- if not relieved = something else, suspect iritis
⦁ Fluorescein staining of cornea
- apply numbing drops: Tetracaine or Proparacaine
- use saline on fluorescein strip - apply to conjunctiva
- use wood’s lamp to check for abrasion
- rule out corneal ulcer
⦁ Slit Lamp ** = technically best diagnostic test for corneal abrasion. If no slit lamp available = use fluorescein
TREATMENT
⦁ Sulfacetamide 10% solution drops / ointment
⦁ Erythromycin ointment
⦁ Polytrim
Ophthalmic antibiotics include ciprofloxacin 0.3%, ofloxacin 0.3%, gentamicin 0.3%, erythromycin 0.5%, polymyxin B/trimethoprim (Polytrim), and tobramycin 0.3%
- then f/u with ophtho
** ointment is preferred over drops for the management of corneal abrasions due to added benefit of lubrication **
Ointment is preferred over drops in children because it lubricates better and because the may drops sting
DO NOT PRESCRIBE TOPICAL ANESTHETIC AGENTS TO PATIENTS - Repeated use of these agents can cause corneal injury and vision loss.
- can also mask pain that could be due to a serious issue
if DIABETIC OR CONTACT LENS WEARER = need to cover for pseudomonas = can give CIPROFLOXACIN (Ciloxan) or TOBRAMYCIN (aminoglycoside) drops
Prophylactic broad-spectrum antibiotic eye drops are recommended in treatment of post-operative corneal abrasion = POLYTRIM (polymyxin B Trimethoprim)
In corneal abrasion, to reduce photophobia from corneal abrasion, anticholinergics like cyclopentolate or homatropine are prescribed to enhance mydriasis and reduce the pain caused by miosis.
- These drops are anticholinergic or parasympatholytic, meaning that they will block the parasympathetic system and enhance the sympathetic nervous system thereby preventing miosis, or pupillary constriction, and enhances mydriasis, or dilation. The mitotic action actually produces the pain in the eye due to the bright light and the ciliary body contracting to constrict the pupil.
It is critical to distinguish an abrasion from a corneal ulcer. Ulcers are deeper infections of the cornea that develop from corneal epithelial defects (ie: abrasions). Contact lens wearers are also at high risk for corneal ulcers. The hallmark of a corneal ulcer is a shaggy, white infiltrate within the corneal epithelial.
Corneal abrasions may be common after a surgery - The most common intra-operative and post-operative cause of corneal abrasions is due to patients rubbing their eyes during emergence from general anesthesia.
REGARDING PATCHING A CORNEAL ABRASION
- Sensory deprivation, such as patching an elderly patient’s eyes, may lead to an acute case of delirium.
- Even small alterations in the elderly patient’s environment can lead to confusion.
- In cases of corneal abrasions, an elderly patient should receive topical ophthalmic antibiotics. Although eye patching traditionally has been recommended in the treatment of corneal abrasions, multiple well-designed studies show that patching does not help and may hinder.
Patching of the eye after abrasion associated with organic material contamination is contraindicated due to increased risk of infection
EX: An 85-year-old nursing home patient was seen in a local physician’s office during the day for a corneal abrasion. The patient had antibiotic drops instilled, and the eye was patched. At 10: 00 p.m., the nursing staff calls reporting the patient is very confused. The most appropriate action is to
a) Remove the eye patch
b) Prescribe haloperidol
c) Have the patient taken to the emergency room
d) Reassure nursing staff and see patient next day
= A - REMOVE EYE PATCH!
ACUTE OTITIS MEDIA
Inflammatory condition of the middle ear, with or without effusion
Otitis media = Infection of the middle ear caused by a virus or bacteria
Infection of the middle ear, temporal bone + mastoid air cells
** MC PRECEDED BY A VIRAL URI **
Is characterized by the presence of fluid in the middle ear, along with symptoms of inflammation
MC occurs in children due to straighter / shorter / narrower eustachian tube in childhood
Often time frame = 6 months - 3 years
6-18 months = peak age
- **Most commonly preceded by a viral URI –> causes eustachian tube edema –> negative pressure –> transudation of fluid + mucus in the middle ear from sinuses –> secondary colonization of bacteria + flora
Acute otitis media = rapid onset + signs / symptoms of inflammation
Otitis Media with Effusion = asymptomatic - no inflammation, but has drainage/discharge
Common bacterial causes include
⦁ Streptococcus pneumoniae** (MC) - 50%
⦁ Haemophilus influenzae - 30%
⦁ Moraxella catarrhalis - 10-15%
⦁ Strep pyogenes (GABHS - same organism as with strep throat, impetigo, acute sinusitis)
usually viral, but if bacterial, most likely strep pneumo.
RISK FACTORS
- Eustachian Tube (ET) Dysfunction
- young age (shorter / narrower / more horizontal ET)
- caretaker smoking
- bottle propping - bottle feeding while supine
- pacifier use
- day care attendance
- formula feeding / not being breastfed
- family hx
- male gender (MC in boys)
** Children with an upper respiratory infection or those regularly exposed to smoke = at increased risk of developing ear infections
- breastfeeding = protective against OM
COMPLICATIONS = ** Conductive Hearing Loss **
- hearing loss may occur due to chronic inflammation, perforation of TM, or damage to anatomy of inner ear
CLINICAL MANIFESTATIONS
⦁ ear pain (otalgia)
⦁ fever (more often afebrile though)
⦁ accompanying URI symptoms
- may present with abrupt onset ear pain in young children along with
⦁ pulling/tugging at the ear
⦁ increased crying
⦁ poor sleep
⦁ conductive hearing loss / stuffiness
⦁ decreased appetite (sucking / chewing can aggravate inner ear pain)
PHYSICAL EXAM
⦁ red, bulging TM with effusion
⦁ decreased TM mobility with pneumatic otoscopy
** if bullae seen on TM = suspect MYCOPLASMA pneumoniae
- multiple ear infections can cause scarring of middle ear structures
- If TM perforation occurs = Rapid relief of pain + otorrhea (usually heals in 1-2 days)
TREATMENT
- 1st line = Amoxicillin (90mg/kg BID) x 10-14 days
- 2nd line = Augmentin (if resistant to amoxicillin) - SE = diarrhea
- If allergic to PCN = Azithromycin or
- Cephalosporin (ceftriaxone/Rocephin) if mild allergy to PCN (SE / reactions)
- if received Amoxicillin in last month = give Augmentin
- if not seeing any clinical improvement = switch to Augmentin
- can give ibuprofen / Tylenol for pain + fever
H. flu + M. cat = produce beta lactamases = PCNs won’t work
- if under 2 = just give abx
- educate parents with kids over the age of 2 about waiting prior to using antibiotics
symptoms usually spontaneously resolve in 2/3 of children by 24 hours, and` 80% in 2-10 days
- irrigation, then lay on affected side
for chronic / recurrent cases
- myringotomy (incision in eardrum) to help relieve pressure / fluid buildup
- tympanostomy tubes
EPISTAXIS
NOSEBLEED
Patient will present as → a 14-year-old who is brought to your Emergency Department (ED) with an intractable nosebleed. Pinching of the nose has failed to stop the bleed. In the ED a topical vasoconstrictor is tried but also fails to stop the bleeding.
MC AGE
⦁ young = 2-12
⦁ adults = 45-65
RISK FACTORS FOR ANTERIOR EPISTAXIS
⦁ nose picking / nasal trauma (blowing nose forcefully)
⦁ intranasal steroids
⦁ chronic oxygen use
⦁ getting hit in the face
⦁ inhaling nasal irritants
⦁ low humidity in a hot environment (dries nasal mucosa)
⦁ rhinitis
⦁ alcohol
⦁ antiplatelet medications (aspirin / ibuprofen)
RISK FACTORS FOR POSTERIOR EPISTAXIS
⦁ hypertension
⦁ atherosclerosis
MC LOCATION = KIESSELBACH PLEXUS
Most difficult to control = POSTERIOR bleeds from INTERNAL MAXILLARY ARTERY
ANTERIOR VS POSTERIOR NOSEBLEEDS
o ANTERIOR
⦁ MC site = Kiesselbach’s Plexus
o POSTERIOR
⦁ MC site = Woodruff’s Plexus
⦁ MC site = PALATINE ARTERY
- posterior epistaxis may cause bleeding in both nares + posterior pharynx (down back of throat - swallowing blood) –> N / V
The SPHENOPALATINE ARTERY is generally the source of severe posterior nosebleeds causing bleeding from both nares and posterior pharynx.
Patients should always be asked about aspirin or ibuprofen use.
Posterior epistaxis is more common in elderly patients, especially with hypertension. Posterior nasal packing is the treatment of choice.
DIAGNOSIS
⦁ direct visualization
⦁ Patients with symptoms or signs of a bleeding disorder and those with severe or recurrent epistaxis should have CBC, PT, and PTT
⦁ CT may be done if a foreign body, a tumor, or sinusitis is suspected.
TREATMENT
⦁ Most nosebleeds are anterior and stop with direct pressure
⦁ 1st line = Apply direct pressure at least 10-15 minutes, seated leaning forward
⦁ Short-acting topical decongestants (two sprays of oxymetazoline (Afrin), phenylephrine, cocaine) - caution in patients with HTN
⦁ cautery with silver nitrate = if above measures failed, and bleeding site can be seen
o Anterior nasal packing if still bleeding
⦁ Patients with nasal packing = consider treating with antibiotics (Keflex - cephalosporin or clindamycin) prevent toxic shock syndrome and patient has to return to take the packing out.
⦁ Follow up with ENT
If there is no packing in the nose, place a small amount of petroleum jelly or antibiotic ointment inside the nostril 2 times a day for 4–5 days
Posterior balloon packing is used to treat posterior epistaxis. These patients must be admitted to the hospital and prompt consultation with an otolaryngologist is indicated
Recurrent epistaxis: Must rule out hypertension of hypercoagulable disorder
ADJUNCT THERAPY
⦁ avoid exercise for a few days
⦁ avoid spicy foods (cause vasodilation)
⦁ bacitracin + humidifiers = help to moisten nasal mucosa
** SEPTAL HEMATOMA = ASSOCIATED WITH LOSS OF CARTILAGE IF HEMATOMA IS NOT REMOVED **
OVARIAN TORSION
Ovarian torsion refers to the rotation of the ovary at its pedicle to such a degree as to occlude the ovarian artery and/or vein
- complete or partial rotation of ovary on its ligamentous supports
⦁ ovary typically rotates around both the infundibulopelvic ligament (connects ovary to fallopian tube) + utero-ovarian ligament (connects ovary to uterus)
Ovarian torsion (OT) is when an ovary twists on its attachment to other structures, such that blood flow is decreased
Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain
70% of cases accompanied by nausea and vomiting
Complications may include infection, bleeding, or infertility
- this often results in loss of blood supply
- the fallopian tube often twists along with the ovary = adnexal torsion
Ovarian torsion = rare event
- reported with both normal + pathologic fallopian tubes
- 50-60% = SECONDARY TO OVARIAN MASS
- MC cause = ovarian cyst
- Ovarian torsion usually occurs in ovarian masses measuring > 5 cm in diameter.
- RIGHT ovarian torsion = MORE COMMON than left (perhaps because right utero-ovarian ligament is longer than the left, or that presence of sigmoid colon on left side helps prevent it)
SIGNS / SYMPTOMS
⦁ abrupt onset of acute, severe, unilateral, lower abdominal + pelvic pain with guarding
⦁ pain is NON-RADIATING
⦁ often associated with N/V
⦁ often the severe pain comes on suddenly with a change in position
⦁ a unilateral, extremely tender adnexal mass is found in > 90% of patients
⦁ many patients noted intermittent previous episodes of similar pain for several days to several weeks
PELVIC EXAM = adnexal tenderness - no cervical motion tenderness - no change in discharge - no urinary discomfort - no bleeding (ectopic)
** often confused with appendicitis **
- ** severe acute unilateral lower abdominal or pelvic pain with N/V
- brought on by changing positions
- tender adnexal mass
- Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain
70% of cases accompanied by nausea and vomiting
DIAGNOSIS
⦁ color flow Doppler US - transvaginal - presence of spikes
Transvaginal doppler ultrasound is the diagnostic test of choice and will show no flow in the ovary*****
- but doppler flow is not always absent with ovarian torsion
A negative pregnancy test in conjunction with the presence of spikes along the doppler flow graph is diagnostic for ovarian torsion.
⦁ CT with contrast ( to also rule out other causes)
⦁ gold standard for diagnosis = laparoscopy
TREATMENT
⦁ early diagnosis can often be managed with conservative laparoscopic surgery to uncoil twisted ovary
⦁ may perform oophoropexy to fixate the ovary which is likely to twist again
⦁ if necrosis is developing = need unilateral salpingo-oophorectomy = TOC
salpingo-oophorectomy = surgery to remove the ovaries and fallopian tubes. Removal of one ovary and fallopian tube is called a unilateral salpingo-oophorectomy. When both are removed, it’s called a bilateral salpingo-oophorectomy
BACTERIAL VAGINOSIS
Bacterial vaginosis (BV), also known as vaginal bacteriosis or Gardnerella vaginitis, is a disease of the vagina caused by excessive growth of bacteria.
CAUSE
⦁ Gardnerella vaginalis = a pleomorphic, gram-variable rod involved in bacterial vaginosis.
- Decreased Lactobacilli acidophilus (maintains normal vaginal pH) –> causes the overgrowth of NORMAL FLORA (GARDNERELLA VAGINALIS), and other anaerobes
BV = MC CAUSE OF VAGINITIS
BV is not an STD that can be passed on, but it is associated with sexual activity
SYMPTOMS Common symptoms include ⦁ increased vaginal discharge - white or grey ⦁ fishy odor that often smells like fish ⦁ vaginal odor worse after sex ⦁ may have dysuria (burning with urination) ⦁ may be asymptomatic ⦁ may have pruritus, not as common
FISHY, grey, scant, THIN, STICKY discharge
- BV increases the risk of infection by a number of other sexually transmitted infections including HIV/AIDS
- It also increases the risk of early delivery among pregnant women
- Bacterial vaginosis is associated with sexual activity however it is not considered to be sexually transmitted
DIAGNOSIS
⦁ KOH test - release of amine odor (+ whiff test)
⦁ Wet prep = “ CLUE CELLS “
- squamous epithelial cells of the vagina with a stippled appearance from being covered with bacteria
⦁ vaginal pH > 4.5
⦁ Few WBCs (unlike trich / PID)
⦁ Few lactobacilli
TREATMENT
⦁ 1st = Metronidazole (Flagyl) - 500mg bid x 7 days
- safe in pregnancy
- may also use gel (not as effective)
⦁ Clindamycin
- gel or PO
PREVENTION
⦁ avoid douching - promotes loss of lactobacilli
TREATING PARTNER IS UNNECESSARY
- unclear if BV is sexually transmitted, but reduced recurrence if condoms are used
COMPLICATIONS
⦁ premature rupture of membranes (PROM)
⦁ preterm labor
⦁ chorioamnionitis
TRICHOMONAS
Trichomoniasis is a common cause of vaginitis.
most common non-viral STD worldwide
It is a common sexually transmitted infection, and is caused by the single-celled protozoan PARASITE** - Trichomonas vaginalis
⦁ Bacteria = Trichomonas vaginalis (T. vaginalis
⦁ PEAR SHAPED FLAGELLATED PROTOZOA ⦁ sexually transmitted
Produces mechanical stress on host cells and then ingesting cell fragments after cell death.
Trichomoniasis is primarily an infection of the UROGENITAL TRACT
MC site of infection = urethra and vagina in women
SYMPTOMS ⦁ vulvar pruritus ⦁ vulvovaginal erythema ⦁ itching ⦁ burning ⦁ dysuria ⦁ dyspareunia ⦁ post-coital bleeding
⦁ MALODOROUS VAGINAL DISCHARGE
- copious, malodorous discharge
- FROTHY YELLOW-GREEN DISCHARGE
- discharge is worse with menses
⦁ STRAWBERRY CERVIX (cervical petechiae)
Vaginal pH > 5
(normal vaginal pH = 3.8 - 4.5)
DIAGNOSIS ⦁ wet mount = mobile protozoa (trichomonads) = "CORKSCREW" motility - FLAGELLA **** ⦁ elevated WBC count ⦁ vaginal pH 5-6 ⦁ UA = positive for WBCs
** MOBILE WET PREP **
TREATMENT
⦁ Metronidazole (Flagyl)
- either 2g oral x 1 dose or 500mg bid oral x 7 days
- safe to use in pregnancy!
⦁ Tinidazole
** MUST TREAT PARTNER **
COMPLICATIONS
- perinatal complications
- increased HIV transmission
TESTICULAR TORSION
Testicular torsion occurs when the spermatic cord twists, cutting off the testicle’s blood supply, leading to ischemia.
Usually occurs in young males
= ** TRUE UROLOGIC EMERGENCY **
- 65% occur in teenagers (10-20 y/o)
CAUSE
MC underlying cause in adolescents and neonates = congenital malformation known as a “bell-clapper deformity” wherein the testis is inadequately affixed to the scrotum allowing it to move freely on its axis and susceptible to induced twisting of the cord and its vessels.
“Bell-Clapper Deformity” = Inappropriately high attachment of the tunica vaginalis
- tunica vaginalis = serous covering of the testis
Adolescents usually suffer from intra-tunica vaginalis testicular torsion.
Neonates usually suffer from extra-tunica vaginalis testicular torsion.
MC Etiology in Adults = Testicular malignancy
** More common in patients with a history of cryptorchidism **
SYMPTOMS
⦁ principal symptom = rapid onset of testicular pain
⦁ erythematous and swollen scrotum
⦁ ** negative cremasteric reflex **
⦁ may have nausea + vomiting
⦁ Negative prehn’s sign = Lifting of testicle does NOT relieve pain
- patient won’t have fever and pyuria with torsion the way they would with epididymitis
- 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 (lies horizontally)
- if NAUSEA + VOMITING is present = suspect torsion **
- N/V = usually absent in epididymitis
- CREMASTERIC REFLEX = ABSENT*
- *** NEGATIVE PREHN’S SIGN **
- degree of swelling + redness depends on the duration of symptoms
The cremasteric reflex is a superficial reflex found in human males that is elicited when the inner part of the thigh is stroked. Stroking of the skin causes the cremaster muscle to contract and pull up the ipsilateral testicle toward the inguinal canal
Appearance = high-riding testicle, edematous, inflamed
- as the torsion continues = will continue to elevate the testicle
Due to coiling, epididymis becomes more horizontal than vertical, and testicle is elevated
husky blue dot hue to that testicle due to lack of blood supply = indicative of APPENDICEAL TORSION (torsion of appendix of testis)
DIAGNOSIS
⦁ Clinical
⦁ Doppler US - shows absence of the blood flow to the testicle = best initial test
⦁ if US unable to exclude torsion = Emergency surgical exploration***
⦁ Radionuclide scan = not used as frequently
Testicular torsion is a surgical emergency and diagnosis is often made clinically. A doppler ultrasound can be utilized to assess testicular blood flow but should only be done in cases where diagnosis is unclear.
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
TREATMENT
⦁ Manual detorsion - twist out like opening a book = NOT LIKELY due to extreme pain
- 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 with manual detorsion
⦁ surgical detorsion urgently performed to prevent necrosis of the testicle and possible subfertility.
Surgical detorsion = treatment of choice
Surgical treatment of testicular torsion should be performed within 6 hours of the onset of symptoms to avoid testicular necrosis.
⦁ Orchiopexy = to prevent future recurrence = permanently fix the testis in the scrotum and prevent the recurrence of testicular torsion. Usually done to other side as well
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
< 6 hours will bring about the best results (> 90% salvage rate). There is a < 10% chance of salvaging the testicle after 24 hours.
** If young male who is not sexually active is having these symptoms (8-12 y/o) and has a “BLUE DOT SIGN” at the upper pole = torsion of testicular appendix
EPIDIDYMITIS
Epididymitis is inflammation of the epididymis
Epididymitis can be characterized as either acute or chronic. Acute epididymitis is characterized by a swollen and erythematous scrotum with testicular pain, especially upon palpation of the spermatic cord.
Epididymis = a curved structure at the back of the testicle in which sperm matures and is stored, and is then transported to vas deferens
CAUSE
- bacteria from urethra travels to epididymis
- 2 major types
⦁ STIs
⦁ non-STI infections
STIs - associated with urethritis - associated with young men ⦁ gonorrhea - gram-negative intracellular diplococci ⦁ chlamydia - gram negative
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
Chlamydia trachomatis and Neisseriagonorrhea are the most common bacterial causes of epididymitis.
⦁ STD (gonorrhea or chlamydia) > urethritis > sets up shop in epididymis→ inflammation
⦁ non-STI = UTIs/prostatitis (E-coli, pseudomonas, some gram positives)
SIGNS / SYMPTOMS
⦁ swollen / erythematous scrotum
⦁ testicular pain, especially upon PALPATION OF SPERMATIC CORD
⦁ pain develops over days
⦁ positive cremasteric reflex (unlike torsion)
⦁ low-lying testicle*****
⦁ A positive prehn’s sign = relief of pain with lifting of the testicle.
⦁ fever / chills
Epididymitis is an infection of the epididymis that is characterized by testicular pain, inflammation, redness and warmth of the scrotum.
- ** POSITIVE CREMASTERIC REFLEX ***
- ** POSITIVE PREHN’S SIGN ***
- unilateral pain + swelling in the epididymis over a period of days (not acute onset like torsion)
- erythema + edema of overlying scrotal skin - can become extremely large (reactive hydrocele)
- tenderness over the groin or in the lower abdomen
- fever
- dysuria - burning with urination
- could have urethral discharge if gonococcal
Epididymitis can often times be confused with testicular torsion. Differentiating between these two conditions is important as testicular torsion is a medical emergency in which surgical intervention within 6 hours of symptom onset is indicated to save the testicle. Unlike testicular torsion, epididymitis is more chronic and can develop over days.
DIAGNOSIS
** UA + CULTURE **
⦁ Ultrasound - to rule out testicular torsion
Classic ultrasound findings for epididymitis include an enlarged epididymis greater than 17 mm and INCREASED blood flow.
LABS
⦁ CBC (WBCs - left shift)
⦁ UA + culture - positive leukocyte esterases
⦁ urethral culture (or urine NAAT) - GC + chlamydia
⦁ gram stain
The definitive diagnostic tool of the causative agent of epididymitis is urine culture.
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
o Patients < 35
⦁ Ceftriaxone (Rocephin) 250mg IM + Doxycycline 100mg BID x 10 days or Azithro
o Patients > 35
⦁ Fluoroqinolones- Cipro* or Levo
- don’t use Macrobid - only for uncomplicated cystitis
APPENDICITIS
-Inflammation of the vestigial vermiform appendix
Appendix = small one ended tube attached to the cecum (vermiform = “worm-shaped”)
Function of appendix = unknown
- suggested that it might be a safe-house for gut flora, or perhaps plays a part in the lymphatic / immune system
- or perhaps just a useless vestigial organ
- One of the most common causes of acute abdomen
- Approx. 10% of population develops appendicitis at some point
- One of the most frequent indications for emergent abdominal surgery worldwide
Appendicitis = most frequent in 2nd-3rd decade of life (20-30s)
More common in men
** MC CAUSE of appendicitis = OBSTRUCTION **
⦁ Fecalith (hard fecal masses - “poop rock”)
⦁ Calculi or foreign body (ex: undigested seeds)
⦁ Lymphoid hyperplasia
⦁ Infectious process or inflammation
⦁ Benign and malignant tumors**
⦁ Fibrosis
⦁ Parasites (endemic areas) - ex: pinworms
In adults, appendicitis is most often caused by fecalith obstruction of the appendix.
In children, appendicitis is caused by lymphoid hyperplasia obstructing the appendix.
LYMPHOID HYPERPLASIA = more common in children / adolescents = lymphoid follicle growth occurs when young, reaches max size during adolescence - can sometimes obstruct the tube. Can also get inflamed after certain viral infections or even immunizations)
PATHOPHYSIOLOGY
⦁ The intestinal lumen (including appendix) is always secreting mucus and fluids to keep pathogens from entering blood stream and to keep tissue moist
⦁ Even with obstruction, the appendix continues to secrete mucus and fluids within obstruction –> increased pressure + enlarges the appendix –> pushes on afferent visceral nerve fibers nearby, causing abdominal pain
⦁ Gut flora is trapped in appendix and continues to multiply (Ie: E. coli and Bacteroides fragilis) –> signals immune system –> increase in WBC (leukocytosis) and pus accumulation in the appendix
⦁ Increased pressure from mucus / fluids / bacteria / WBCs - can push and compress on blood vessels that supply appendix with oxygen
- without oxygen supply –> ischemia –> necrosis
- no longer secrete mucus / fluids keeping pathogens out, so can invade the wall with bacteria
⦁ As the appendiceal cells die, the wall becomes weaker –> at risk for rupture / perforation –> allows all the bacteria to escape into peritoneum –> causes patients to often experience peritonitis and have rebound tenderness (pain when pressure is removed)
MC complication with Ruptured Appendix
⦁ Periappendiceal Abscess = forms from ruptured appendix and outflow of accumulated bacteria
Common organisms in gangrenous + perforated cases: ⦁ E. coli ⦁ Peptostreptococcus ⦁ Bacteroides fragilis ⦁ Pseudomonas sp.
SYMPTOMS OF APPENDICITIS ⦁ RLQ PAIN ⦁ may have periumbilical / epigastric pain first (50-60%), followed by RLQ pain ⦁ anorexia = lack / loss of appetite ⦁ nausea / vomiting follow pain ⦁ Fever
Initial “atypical” or nonspecific symptoms of indigestion, flatulence, bowel irregularity, diarrhea, generalized malaise
- Inflamed anterior appendix produces localized RLQ pain
- Retrocecal appendix may cause dull abdominal ache
- Appendix tip in the pelvis may cause urinary frequency, dysuria or rectal symptoms such as tenesmus (urgency to have bowel movement) and diarrhea
***There are NO physical findings taken alone or in concert that can definitively confirm a diagnosis of appendicitis!
- in early appendicitis, PE may be unrevealing
- Rectal exam may be helpful when the appendix is recto-cecal
- In women a pelvic exam is a must!!! But it is difficult to differentiate between adnexal tenderness (ovary/fallopian tube) and appendicitis
COMMONLY DESCRIBED PHYSICAL SIGNS
⦁ McBurney’s point - RLQ pain/tenderness
⦁ Rovsing’s sign - pushing on LLQ causes RLQ pain
⦁ Psoas sign—associated with a rectocecal appendix (resisted leg raise)
⦁ Obturator sign—associated with a pelvic appendix
⦁ Rebound tenderness
⦁ Abdominal guarding
The McBurney point is an anatomical landmark located 1/3 (3-5 cm) of the distance from the right anterior superior iliac spine to the umbilicus.
The most sensitive sign for appendicitis is pain at McBurney’s point
A positive obturator sign, pain on passive flexion and internal rotation of either hip, is indicative of acute appendicitis.
Pain on active hip extension constitutes a positive psoas sign, which is indicative of acute appendicitis.
A ruptured appendix results in peritonitis that presents with guarding and rebound tenderness.
first - early = visceral pain - central abdominal pain
later = somatic pain - RLQ pain - McBurney’s point
Pain referral in early appendicitis usually involves the T10 dermatome at the level of the umbilicus - as an inflamed appendix stimulates visceral afferent nerves at the T8-T10 level of the spine, causing periumbilical pain
As inflammation process continues, more local somatic fibers become irritated, focusing pain more to RLQ
LAB FINDINGS
⦁ Mild leukocytosis—WBC > 10,000 and a left shift
⦁ elevated CRP
⦁ Women of child bearing age = pregnancy test
⦁ dehydration / fluid + electrolyte imbalances
MODIFIED ALVARADO SCORE - Diagnostic Criteria ⦁ Migration of pain to RLQ (1 point) ⦁ Anorexia (1 point) - lack or loss of appetite ⦁ Nausea or vomiting (1 point) ⦁ Tenderness in RLQ (2 points)* ⦁ Rebound tenderness in RLQ (1 point) ⦁ Fever > 37.5 C˚ (99.5 F˚) (1 point) ⦁ Leukocytosis > 10,000 (2 points)*
- Score 4 or less = unlikely appendicitis; work up for other dx
- Score > 4 = further work up for appendicitis
DIAGNOSIS
⦁ **Abdominopelvic CT WITH CONTRAST ** = oral and IV contrast = preferred study
- CT without contrast is acceptable - imaging not always required - if high clinical suspicion for appendicitis using Alvarado scale
⦁ ULTRASOUND
- (Test = preferred first choice, then do CT if US is inconclusive)
- Imaging of choice for children < 14 + pregnant women, or if CT cannot be done within 3 hours
- ultrasound can be done at bedside
TREATMENT
- pain meds **
- IV fluids / rebalance electrolyte
- NPO
⦁ ** Appendectomy! **
- preop antibiotics = cephalosporin (cefazolin) or unasyn (ampicillin sulbactam) + metronidazole (flagyl)
- postop antibiotics if perforated appendix - until no longer febrile
Laparotomy vs Laparoscopy
Approach depends on:
⦁ Confidence of diagnosis
⦁ History of prior surgery
⦁ Patient’s age—laparoscope easier on the elderly
⦁ Gender
⦁ Body habitus—Laparoscope generally easier to do on the obese patient
⦁ Skills of the surgeon
laparoscopy = safer, less expensive, and shorter recovery time Laparoscopy = lower rate of wound infections, less pain on post-op day 1, shorter duration of hospital stay, and shorter duration of return to bowel function....
however, laparoscopy = also higher rate of intra-abdominal abscess, longer operative time, and higher operative + in-hospital cost
NEPHROLITHIASIS
Nephrolithiasis = Kidney stone = Renal calculi = Urolithiasis
Kidney stones form when solutes in the urine precipitate out and crystallize
MC form in the kidneys
- but can also form in the ureters, bladder or urethra
URINE
⦁ water = solvent
⦁ particles = solute
- when certain solutes become too concentrated in solvent, they become supersaturated and precipitate out to form crystals
NIDUS = crystal formation that allows more particles to easily attach and enlarge the crystalline structure
CAUSE OF KIDNEY STONES
⦁ decrease in solvent (dehydration)
⦁ increase in solutes
** MAGNESIUM + CITRATE = inhibit crystal formation, preventing kidney stones from forming in first place **
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
CALCIUM OXALATE STONES
⦁ MC stone
⦁ black / dark brown stone
⦁ microscopy = looks like envelope or box with X inside
⦁ RADIOPAQUE = appears white on xray
⦁ more likely to form in ACIDIC urine
⦁ avoid grapefruit juice (makes calcium oxalate stones worse)
CALCIUM PHOSPHATE STONES
⦁ dirty white color
⦁ microscopy = looks like fortress of solitude
⦁ RADIOPAQUE = appears white on xray
⦁ more likely to form in ALKALINE urine (like struvite)
RISK FACTORS FOR CALCIUM STONES
⦁ hypercalcemia (increased GI absorption of Ca+)
⦁ hypercalciuria (decreased renal absorption of Ca+)
⦁ hyperparathyroidism
⦁ hyperoxaluria - genetic defect that decreases oxalate excretion
⦁ diet heavy in oxalate rich foods = rhubarb, spinach, chocolate, nuts, beer
URIC ACID STONES
⦁ red-brown in color
⦁ Radiolucent = transparent on xrays = don’t usually show up
⦁ uric acid –> urate ion + Na –> monosodium urate crystals
⦁ uric acid is a breakdown product of purines, so diet high in purine-rich foods = shellfish, anchovies, red meat…seafood, meat, cheese, alcohol
⦁ can cause gout / gouty arthritis = deposit of uric acid crystals in 1st MCP joint (podagra) = negatively birefringent crystals
⦁ microscope = looks like tear drops or needles
STRUVITE STONES
⦁ “Infection stones”
⦁ MIX of Magnesium + Ammonium + Phosphate
⦁ forms when BACTERIA (such as proteus mirabilis) use enzyme urease to split urea into CO2 + Ammonia
⦁ Associated with chronic UTI with Klebsiella and Proteus species
⦁ Ammonia makes urine more ALKALINE*** - which favors the precipitation of Mg + Ammonia + Phosphate into jagged crystals called (like calcium phosphate)
⦁ STAGHORN CALCULI - because they often branch into several renal calyces
⦁ dirty white in color (like calcium phosphate)
⦁ look like rectangles with a line through it, or hersheys 3D chocolate tomb-stone shape
⦁ RADIOPAQUE = appear white on xray (like calcium stones)
⦁ Risk Factors
- UTIs
- VUR
- Obstructive uropathies
CYSTINE STONES (amino acid) ⦁ yellow or light pink stone ⦁ rare ⦁ genetic ⦁ ex: young boy with kidney stones ⦁ radiolucent = transparent on xray - wont show up ⦁ look like HEXAGONS
XANTHINE STONES
- also a byproduct of purine breakdown (along with uric acid)
⦁ also red-brown in color
⦁ radiolucent on xray
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 patients may have more than one stone type at the same time
SIGNS / SYMPTOMS OF KIDNEY STONES ⦁ dull or localized flank pain - radiates to lower back ⦁ renal colic (sharp cramping pain) - more constant ⦁ N / V ⦁ CVA tenderness ⦁ hematuria ⦁ colicky flank pain radiating to groin ⦁ tachycardia ⦁ may have fever
fever + vomiting + acute flank pain
- Pain is caused by dilation / stretching / spasm of ureter
- Most painful location = UVJ (ureterovesicular junction) = narrowest point of ureter (between ureter and bladder)
- another location where stones can get stuck = UPJ (ureteropelvic junction) = between kidney and ureter
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
- CMP
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, phosphate, electrolytes, creatinine, BUN
⦁ 24 hour urine collection = volume, pH, calcium, uric acid, oxalate, phosphate, sodium, citrate
Stones < 5 mm = usually passed within hours
DIAGNOSIS OF KIDNEY STONES
⦁ hx + pe
⦁ Ultrasound = initial test - may see stone + hydronephrosis
⦁ CT without contrast = ** definitive diagnosis **
⦁ CBC - elevated WBC
⦁ UA = may show microscopic or gross hematuria (RBCs)
⦁ pain may shift in location as stone travels
- 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 and severity (used to be gold standard, not anymore)
Gold standard = CT - noncontrast abdomen/pelvic**
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 or Zofran
⦁ give strainer - cannot determine type of stone from UA, so give strainer to catch urine and bring in for analysis
⦁ 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**
Stones < 5 mm = likely to pass with hydration / flomax
IF STONE IS 5mm+ = NEED SURGERY = lithotripsy
WHEN KIDNEY STONES BECOME A MEDICAL EMERGENCY
= any obstructing stone with an associated infection***
Outpatient management is appropriate for most patients
WHEN TO ADMIT THE PATIENT WITH KIDNEY STONES
⦁ intractable nausea/vomiting or pain that is not controlled with medications
⦁ obstructing stone with signs of infection (emergency!)
⦁ patients with only 1 kidney
⦁ renal colic with UTI or renal colic with fever
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
⦁ ESWL = extracorporeal shock wave lithotripsy
(> 5-10)
⦁ Percutaneous Nephrolithotomy (PNL) = only if in kidney, and is primary tx for struvite stones
⦁ Ureteroscopy with stent placement
PREVENTION OF KIDNEY STONE FORMATION
⦁ increase fluid intake** (most important)
⦁ avoid sodium and protein
⦁ 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)
SPIDER BITE
Most spiders don’t cause bites that are of medical importance.
The effects of most bites are not serious. Most bites result in mild symptoms around the area of the bite. Rarely they may produce a necrotic skin wound or severe pain
Although all spiders in the United States are venomous, only a few can puncture the human skin. The brown recluse spider is of most clinical importance in the United States. Another spider of clinical significance is the Black Widow spider.
TREATMENT
Most spider bites are managed with supportive care such as NSAIDS for pain and antihistamines for itchiness.
PREVENTION
Efforts to prevent spider bites include clearing clutter and the use of pesticides.
BROWN RECLUSE SPIDER BITE
Loxosceles recluse - (brown recluse) spider
Found mostly in the midwestern, southern and southeastern United States
These spiders like to hide in quiet, cluttered places like closets, woodpiles, attics, and storage spaces
Most bites occur when the spider feels threatened by sudden movement, such as when a person puts on clothing or a shoe in which the spider is resting
Brown violin on the abdomen
SIGNS / SYMPTOMS
⦁ Local burning + erythema at bite site x 3-4 hrs
⦁ Brown recluse spider bites often develop a(n) ERYTHEMATOUS HALO around the bite within 24-72 hours, and may develop SURROUNDING NECROSIS
⦁ can cause BLISTERING or NECROSIS at the site of the bite, erythema, and some systemic symptoms
⦁ The classic recluse spider bite possesses the “red, white and blue” sign: red erythema around a rim of blanched skin that encircles a central blue-purple papule, vesicle or bulla.
⦁ Necrosis typically begins 2-3 days after the bite, followed by ESCHAR formation and a deep ULCER
⦁ “Loxoscelism” consists of local vesicle formation, progressing to tissue necrosis and systemic symptoms
o Necrotic wound
- Local tissue reaction causes local burning at the site for 3-4 hours → blanched area (due to vasoconstriction) → central necrosis, erythematous margin around an ischemic center “red halo” → 24-72 hours after hemorrhagic bullae that undergoes Eschar formation → necrosis
SYSTEMIC SYMPTOMS maculopapular rash, fever, headache, malaise, arthralgia, nausea and vomiting. ⦁ maculopapular rash*** ⦁ fever*** ⦁ headache*** ⦁ malaise ⦁ arthralgia ⦁ N / V
TREATMENT
- wound care = clean with soap + water
- apply cold packs to bite site; avoid freezing the tissue
- keep body part in elevated or neutral position
- local symptomatic measures
- sometimes delayed excision
Most wounds heal spontaneously within days to weeks
o Pain Control: NSAIDS***
- opioids if more severe
- tetanus prophylaxis if needed
o Dermal Necrosis
- debridement in some cases if it will lead to better wound healing
- Dapsone (aczone) has been used in past
- antibiotics if secondary infection develops (treat like cellulitis)
Patient with brown recluse spider bite will present as → a 32-year-old man who was cleaning out his dark, undisturbed attic. That day he noticed an erythematous lesion with a clear center on his arm. Since then the lesion has necrosed in the center, giving rise to a crater-like eschar lesion
BLACK WIDOW SPIDER BITE
Black widow spiders are endemic to Eastern and Southwest U.S.A
Usually had a recent event outdoors within last 8 hours: outdoor activities - hiking / camping, outdoor furniture use, gardening, sleeping outside, etc.
These spiders are found mostly along the East Coast and in the Southwestern United States.
The black widow is well known for its black glossy color and red hourglass marking on its abdomen
Red hourglass on the abdomen
They can leave 2 fang marks and their venom, containing α-latrotoxin, can lead to release of acetylcholine, which is responsible for the bite symptoms.
They are not aggressive, prefer dark and quiet habitats like garages, and are WEB-BUILDERS.
Most bites occur during accidental or purposeful provocation of the spider or disruption of its web
SYMPTOMS = Latrodectism These spiders produce a neurotoxic venom (containing α-latrotoxin) that is responsible for the majority of systemic symptoms after a spider bite. The neurotoxin triggers the release of acetylcholine, which may result in ⦁ elevated blood pressure ⦁ muscle cramping / pain / spasms / rigidity **** ⦁ convulsions ⦁ lacrimation ⦁ salivation ⦁ seizures ⦁ headache *** ⦁ fever ⦁ tremors ⦁ N/V *** ⦁ SOB
Muscle pain MC affects extremities, back + abdomen
Neurologic manifestations - May not see much at bite site: toxic reaction = nausea, vomiting, HA, fever, syncope, and convulsions
** May not see much at bite site **
- Deaths are relatively rare
Cutaneous manifestations are usually unimpressive, but may present with significant
⦁ erythema
⦁ pain and
⦁ localized sweating
PHYSICAL EXAM
- blanched circular patch with a surrounding red perimeter and central punctum (target lesion)
Two fang marks can be at the site of the bite.
TREATMENT
⦁ supportive - wound care + symptomatic treatment
⦁ benzodiazepine / muscle relaxers for muscle cramps / spasms / rigidity
⦁ NSAIDS or opioids or other analgesics
⦁ antivenom can be given - after antihistamine - reserved for patients who are not responsive to above medications
Treatment is usually supportive because symptoms self-resolve in most cases within 1-3 days
Treatment involves supportive care, including a benzodiazepine to manage muscular cramps. Black widow spider antivenom may also be administered (pre-medicate with antihistamine to reduce adverse reactions).
- anti-venom available for elderly and kids
Patient with black widow spider bite will present as → a 21-year-old who returns from a camping trip early complaining of a dull numbness affecting his upper left extremity. He recalls a sharp pinprick sensation before the development of symptoms. The patient now describes a cramping pain and muscle rigidity of the back and chest area. A red, indurated area is found on the distal left arm. The patient has profuse sweating, nausea, vomiting, and shortness of breath.
INSECT STING TREATMENT
If an insect sting causes a severe reaction or anaphylaxis = ** EPINEPHRINE ** (adrenaline)
1) 1st LINE = EPI
2) REMOVE THE STINGER - This is necessary as the stinger continues to pump venom from its sack until it is empty or removed
⦁ Place a firm edge such a knife or credit card against the skin next to the embedded stinger
Apply constant firm pressure and scrape across the skin surface to remove the stinger. This is preferred to using tweezers or fingers, which can accidentally squeeze more venom into the patient
3) CLEAN the site with disinfectant
4) Apply ICE or cold pack to reduce pain and swelling
5) A TOPICAL STEROID cream or calamine lotion may be applied several times a day until symptoms subside
- If necessary, oral ANTIHISTAMINES can also be taken
INSECT BITE TREATMENT
The main treatment aim of insect bites is to prevent itching
1) Cool the affected area
2) Apply topical calamine lotion or local anesthetic
3) Oral antihistamine reduces itch and weals
4) Use moderate potency topical steroids for papular urticaria or persistent reactions
Bites from insects carrying disease require specific antimicrobial therapy to treat the disease
ANAPHYLAXIS
Anaphylaxis can be treated with epinephrine 1:1000
0.5-1 mL Epi = given IM or subQ
o INFANTS + CHILDREN
⦁ Infants weighing <7.5 kg (16 lbs) should be given an exact weight-based dose (not estimated), whenever possible
- However, if drawing up an exact dose is likely to cause a significant delay in a rapidly deteriorating patient, the 0.15 mg dose can be given by autoinjector (Epi-Pen Jr.) or by drawing up 0.15 mL of the 1 mg/mL solution
⦁ Infants and children weighing from 7.5 - 25 kg
(16 – 55 lbs) can be given 0.15 mg by autoinjector (Epi-Pen Jr.) or by drawing up 0.15 mL of the 1 mg/mL solution
o ADOLESCENTS + ADULTS
⦁ Patients weighing 25-50 kg (55 – 110 lbs) can be given 0.3 mg by autoinjector (EpiPen) or by drawing up 0.3 mL of the 1 mg/mL solution
⦁ Patients who weigh > 50 kg (> 110 lbs) can be given 0.5 mg (0.5 mL of the 1 mg/mL solution)
⦁ If the patient is obese, this can be administered using a 1.5-inch needle to penetrate the subcutaneous fat. However, if drawing up an exact dose is likely to cause a significant delay in a rapidly deteriorating patient, the 0.3 mg dose can be given by autoinjector
*20% of patients may need a second dose due to ongoing symptoms – you can inject another dose of EpiPen or EpiPen Jr 5 - 15 minutes after first injection
DEEP VEIN THROMBOSIS (DVT)
Deep Veins = refers to the veins that typically runs between muscles as they travel back to the heart
(vs the superficial veins that you can see on surface of skin)
PATHOPHYSIOLOGY
⦁ DVT = deep vein thrombosis = blood clot in the deep veins that are responsible for bringing blood back to the heart
⦁ Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward against gravity
⦁ The surrounding muscle compress the vein and propel blood forward
⦁ One-way valves prevent blood from going backwards
⦁ Deep veins ultimately lead to either SVC or IVC, and dumps blood into the right atrium
- ** MC LOCATION FOR DVT = LOWER LEGS ***
- MC = below the knee
- but blood clot can form in both superficial or deep veins, and in other parts of the body as well
** Most DVTs originate in the CALF **
DVT = MC in Left iliac vein than right iliac vein - because aortic bifurcation crosses and potentially compresses left iliac vein
1) Damage to the endothelium of blood vessel wall usually occurs
2) immediate vasoconstriction response –> limits the amount of blood flow
3) platelets adhere to the damaged vessel wall, and become activated by collagen + tissue factor (which are usually kept separate from blood due to intact endothelium, but now damaged
4) platelets recruit more platelets to create platelet plug = Primary Hemostasis
5) Coagulation Cascade is activated –> clotting factors made by the liver –> final step = fibrinogen getting activated into Fibrin ==> which forms a polymerized mesh around the platelets = Secondary Hemostasis
- results in a hard clot at the site of vessel injury
Only takes a few minutes from injury to clot formation
Usually anticoagulation proteins control coagulation cascade
⦁ Antithrombin = inactivates 9a, 10a, 11a, 12a, 7a, and thrombin
⦁ Protein C = inactivates 5a + 8a
6) As the clot grows in size, it decreased blood flow and decreases lumen size, which increases blood pressure
- the clot may start naturally breaking down due to increased pressure
** PLASMIN (enzyme) breaks down fibrin into fragments called D-DIMERS
7) Sometimes the pressure can cause a part of the main clot to break free = Embolus - can travel to the heart
Thromboembolism can move from leg –> IVC –> RA –> RV –> Lungs - can get lodged, causing a PE
= life threatening emergency, as it blocks blood from getting to the lungs to pick up oxygen
If ASD (atrial septal defect) = thromboembolism can go from RA to LA –> can go to the brain (Embolic Stroke)
In a patient with patent foramen ovale or ASD, DVT is a risk factor for a paradoxical embolism. A paradoxical embolism, also called a crossed embolism, is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin through a lateral opening in the heart, such as a patent foramen ovale.
RISK FACTORS FOR DVT = ** VIRCHOW’S TRIAD **
⦁ 1) venous stasis (slowed blood flow)
- slow or static blood
- long periods of inactivity of skeletal muscle pump (bed rest / post-op, long flights/car rides, pregnancy - baby compresses nearby veins)
- in venous stasis, platelets and clotting factors have more time to contact the endothelium and adhere –> activation of clotting cascade
⦁ 2) Hypercoagulable state
- excess clotting factors - due to genetics, surgery, or taking certain medications like birth control, malignancy, factor V leiden, pregnancy
- during surgery, physical damage activates clotting cascade
- birth control increases clotting factors, and decreases anticoagulation factors like protein C + antithrombin
- just starting warfarin (before it acts as blood thinner)
⦁ 3) Damage to Endothelial lining of blood vessel
- this exposes tissue factor and collagen
- caused by infections, chronic inflammation (DM), toxins (like those in cigarettes), surgery, lower leg injury
VIRCHOW’S TRIAD (Risk factors for DVT)
1) Venous Stasis
2) Hypercoagulability
3) Damage to endothelial lining of blood vessels
SYMPTOMS OF DVT
⦁ MC in lower limbs, especially below the knee
⦁ pain
⦁ swelling
⦁ redness
⦁ warmth
⦁ Phlebitis = warmth, erythema, palpable cord
*** HOMAN’S SIGN = calf pain upon dorsiflexion of foot
MC symptom of DVT = leg swelling
If PULMONARY EMBOLISM OCCURS
⦁ shortness of breath
⦁ chest pain
⦁ hemoptysis
DVT = MC cause of PE
about half of patients with DVT are asymptomatic
** WELL’S CRITERIA ** = scoring system used to stratify the risk of having deep venous thrombosis
low risk (Wells’ Score <2) and a negative d-dimer the clinician can exclude the need for ultrasound (US) to rule out DVT
⦁ Active Cancer
⦁ Bedridden recently >3 days or major surgery in last 3 months
⦁ Calf swelling >3 cm compared to the other leg
⦁ Collateral (non-varicose) superficial veins present
⦁ Entire leg swollen
⦁ Localized tenderness along the deep venous system
⦁ pitting edema of symptomatic leg
⦁ Paralysis, paresis, or recent plaster immobilization of the lower extremity
⦁ previous documented DVT
⦁ Alternative diagnosis to DVT not as likely
** Unilateral swelling / edema of lower extremity > 3cm = most specific symptoms/sign of DVT **
- separate Well’s criteria for PE available
DIAGNOSIS OF DVT
⦁ ** Compression Ultrasound with doppler ** = test of choice = first line imaging
⦁ Venography if US inconclusive = GOLD STANDARD - dye injected into veins, XRAY to identify blockages
⦁ D-dimer can be helpful (fibrin breakdown products are usually higher in presence of a clot)
- normal d-dimer =/< 0.5
D-dimer should only be used as the first line test when the diagnosis seems unlikely
False positive D-dimer elevations = Pregnancy, Liver disease, Inflammation, Malignancy, Trauma, Hospitalized patients
TREATMENT
- main goal = preventing PE
- body will naturally try to break down clots on its own, so small clots may resolve on their own
- for larger clots
⦁ Anticoagulants: LMW Heparin (Lovenox) -> Warfarin
⦁ Thrombolytic enzymes
⦁ Thrombectomy (surgically remove clot)
In Unfractionated Heparin (IV) (Indication = prevents further emboli rather than treating existing one) - need to titrate to PTT 1.5-2.5x normal value
⦁ MOA = potentiates antithrombin III, inhibits thrombin / other coagulation factors
⦁ SE = HIT (heparin induced thrombocytopenia)
⦁ Antidote for Heparin toxicity = Protamine Sulfate
LMWH (Lovenox / Enoxaparin) SQ injection =
- don’t need to monitor PTT
- Safe in pregnancy
⦁ Lower risk of HIT**
⦁ Contraindication = thrombocytopenia, and renal failure if Creatinine > 2.0
⦁ Antidote for Heparin toxicity = Protamine Sulfate
- but not as effective as with UFH
Warfarin (Coumadin)
⦁ MOA = inhibits vitamin K-dependent coagulation factors of EXTRINSIC pathway: 2, 7, 9, 10. Inhibits protein C + S.
- Coumadin should be overlapped with heparin for at least 5 days AND until INR > 2-3 for at least 24 hours
⦁ Antidote for Warfarin toxicity = Vitamin K
⦁ Avoid cruciferous veggies with high levels of vitamin K (spinach, kale, brussel sprouts, greens) and green tea, cranberry juice, ETOH
Thrombolytics/thrombectomy = reserved for failed anticoagulation or massive thrombosis
LONG-TERM TREATMENT TO PREVENT FUTURE DVT
⦁ Anticoagulants (warfarin-coumadin / heparin / Lovenox / Eliquis / Xarelto)
⦁ Antiplatelets (low-dose ASA, Plavix)
⦁ Filters (can be placed in IVC to prevent PE)
IVC filter = reserved for patients with contraindications to anticoagulants, or those with little cardiopulmonary reserve in which an embolic event would kill them
Heparin is an anticoagulant that is preferentially used to prevent and acutely manage DVT
Warfarin = oral vitamin K antagonist that is used for prophylaxis against DVT and has a teratogenic effect.
Ideally, DVT/PE should be confirmed before initiating anticoagulation therapy, but if the clinical suspicion is high or objective confirmatory studies are not forthcoming, anticoagulation therapy may be started, as patients can deteriorate rapidly and die
FIRST LINE TREATMENT FOR DVT = anticoagulation with IV heparin, then switch to warfarin x 3-6 months
Recurrent DVT requires lifetime anticoagulation
PREVENTION
⦁ compression stockings
⦁ calf exercises between long periods of stasis
⦁ ambulation as early as possible after embolization
women older than 35 years who smoke should avoid oral contraceptive pills due to risk of thrombosis. Progestin-Only Hormonal Methods are a reasonable alternative in this population.
AORTIC ANEURYSM
- aneurysma = greek for “dilation”
ANEURYSM = abnormal dilations or bulge in vessel
officially termed aneurysm when the bulge or dilation is 1.5x larger than the normal diameter of the vessel
Aneurysms can occur to any artery in the body: Aorta, Femoral, Iliac, Popliteal, Cerebral, etc.
Aneurysms can occur in veins too, but the likelihood is much lower due to decreased pressure in veins
TRUE ANEURYSMS vs PSEUDOANEURYSMS
o True Aneurysm
- all layers of the blood vessel bulge out together
⦁ Fusiform = the dilation is symmetrical on all sides
⦁ Saccular or Berry = dilation is on one side - because for some reason that side had to put up with higher pressures, or is weaker than other side
o Pseudoaneurysm
⦁ not actually an aneurysm, but really a hole in the vessel wall that allows blood to leak out and look like an aneurysm
- looks like a perfect bulge due to surrounding structures / tissues that hold blood in that one spot - allowing it to look like a fusiform or berry aneurysm
MC Arterial Aneurysms = Aorta
⦁ 60% of aortic aneurysms = Abdominal aortic aneurysm *** (AAA or triple A)
⦁ other 40% of aortic aneurysms = thoracic section
- ** Majority of AAA = located just below where the renal arteries branch off, but above the aortic bifurcation into common iliac arteries
- this is because there is less elastin in this part of the aorta than others = weaker
PATHOPHYSIOLOGY OF ANEURYSMS
- weakness in vessel wall, so anything that causes the vessel walls to weaken can cause an aneurysm
- when a wall is weakened, it struggles to contain the pressure of blood pushing against it
- as the diameter of the weakened section dilates, the pressure on that part increases (Laplace’s Law), making the diameter of the aneurysm even bigger –> cycle of continuous bulging until rupture!
(this is why blowing up a balloon is tough at first, but gets easier as it stretches = due to positive feedback loop of increased diameter and increased pressure)
CAUSES OF ANEURYSMS / WEAKENED VESSEL WALL
⦁ Hypertension
⦁ Hyperlipidemia / plaques
⦁ Mycotic aneurysms = caused by bacterial infections
⦁ smoking
⦁ genetic conditions - affect collagen / fibrillin (Marfans or Ehlers-Danlos)
o Hypertension
- vessels get blood supply as blood runs through them, but for thicker vessels, like descending aorta (thicker in order to handle high pressure from heart) = have own blood vessels in tunica media + tunica externa (tunica intima still gets supply from lumen blood) called VASA VASORUM
- Hypertension causes hyaline arteriosclerosis of vasa vasorum –> narrows lumen of vasa vasorum –> ischemia + atrophy of tunica media/externa smooth muscle –> weakens aorta wall –> aneurysm
o Plaques
- plaque buildup in tunica intima (atherosclerosis) –> that section of tunica intima doesn’t get oxygen –> ischemia (common in abdominal aorta - pressure is high, and vessel wall is nourished by flowing blood)
RISK FACTORS FOR ANEURYSMS (same as atherosclerosis) ⦁ male ⦁ > 60 ⦁ hypertension ⦁ family history ⦁ smoking ⦁ tertiary syphilis
Risk factors of abdominal aortic aneurysm include history of tobacco use, older age, male gender, and family history.
ENDARTERITIS OBLITERANS = inflammation of vasa vasorum (occurs with tertiary syphilis) -> fibrosis -> constricts the lumen of the vessels supplying oxygen to vessel wall - particularly of thoracic aorta (thicker vessels, so have vasa vasorum) –> atrophy
Thoracic aortic aneurysms are a common finding in tertiary syphilis.
MYCOTIC ANEURYSMS
- bacteria (or fungi) from an infection somewhere else in body can break off and travel elsewhere in the blood (embolic bacteria)
- usually gets stuck in intercranial arteries, visceral arteries or arteries feeding arms / legs
- bacteria weakens the vessels –> aneurysm
- commonly caused by
⦁ bacteroides fragilis
⦁ pseudomonas aeruginosa
⦁ salmonella
- Mycotic aneurysms = also a complication of infective endocarditis
- fungal causes
⦁ aspergillus
⦁ candida
⦁ mucor
MARFAN SYNDROME
- impaired elastic properties of fibrillin –> weak blood vessel walls
EHLERS - DANLOS SYNDROME
- disrupted ability to form collagen proteins
Thoracic aortic aneurysms are associated with connective tissue disease such as Marfans + ED
SIGNS / SYMPTOMS OF ANEURYSMS
- intact aneurysms = okay - usually don’t cause any symptoms
- but bulging vessel can compress nearby organs or vessels
- ex: bulge in aortic arch can compress SVC –> decrease amount of blood going to the heart
MOST CONCERNING COMPLICATION
- ** RUPTURE of aneurysm ***
- blood spills out of vessel, and less blood is getting to tissues / cells downstream that need it –> ischemia
- ** AORTIC INSUFFICIENCY ***
- particularly occurs when there is an aneurysm in thoracic aorta, right above aortic valve
- the dilation causes the aortic valve itself to expand and not close properly together, allowing blood to flow back into LV during diastole (Aortic regurgitation)
- Aortic insufficiency can also cause a high-pitched BRASSY COUGH due to aneurysm compressing on left recurrent laryngeal nerve that wraps around aorta
A bicuspid aortic valve is a known risk factor for thoracic aortic aneurysms.
BRAIN ANEURYSM
- if cerebral artery aneurysm ruptures = will bleed into SUBARACHNOID space –> puts pressure on brain tissue / irritates the meninges
⦁ sudden / intense HEADACHE
⦁ inability to flex neck forward
ANOTHER COMPLICATION OF ANEURYSMS
⦁ ** formation of BLOOD CLOTS **
- as blood is pooling into aneurysm prior to rupture, stasis of blood can form clots
- clot can become so big it blocks off entire artery –> ischemia…or
- part of clot can break off (thromboembolism) and travel elsewhere –> ischemia
ABDOMINAL AORTIC ANEURYSM SIGNS /SYMPTOMS
- sometimes asymptomatic, even if it has ruptured
⦁ severe flank pain / abdomen / chest / lower back / groin
⦁ pulsating mass that is in time with heartbeat
⦁ hypotension (in about 50%) - more indicative of rupture
Ruptured abdominal aortic aneurysm should be suspected in patients with abdominal pain radiating to the back and associated with hypotension (from retroperitoneal bleeding) and a pulsatile abdominal mass.
A presentation of hypotension, abdominal pain, and a pulsatile abdominal mass is characteristic of an abdominal aortic aneurysm which is in the process of rupturing.
AAA can be asymptomatic until further progression. AAA rupture is life-threatening and can present with abdominal pain, back pain, syncope, hypotension, tachycardia, pulsating abdominal mass, abdominal bruits, and severe pain.
THORACIC AORTIC ANEURYSM SIGNS / SYMPTOMS
- usually asymptomatic
⦁ severe chest / back / abdominal pain
⦁ respiratory difficulties
⦁ trouble swallowing
⦁ brassy cough / hoarseness (compression of left recurrent laryngeal nerve)
⦁ cardiac disease
⦁ rupture
⦁ may hear abdominal bruit as blood moves past aneurysm
Thoracic aortic aneurysm can lead to coughing and hoarseness due to compression of the left recurrent laryngeal nerve.
DIAGNOSIS OF ANEURYSMS
- because many are asymptomatic, they are often diagnosed incidentally
⦁ Ultrasound = initial study of choice
⦁ CT with contrast*** = test of choice
⦁ Angiography - Gadolinium = GOLD STANDARD
Acutely, AAA can be visualized and sized with an abdominal ultrasound.
CT and MRI are used to more accurately localize and determine size.
In the emergent setting, (actively rupturing) an abdominal ultrasound should be done because it is quick, noninvasive, sensitive, and has the ability to show free peritoneal fluid.
MC IV contrast = Iodine
Barium sulfate used for digestive system, Iodine = 2nd line if barium cannot be used
Possible adverse effects of iodinated contrast include warmth, contrast-induced neuropathy, and thyroid dysfunction
LABS / VITALS IF RUPTURED ⦁ hypotensive ⦁ tachycardic ⦁ leukocytosis (elevated WBC) - infection, malignancy, inflammation ⦁ anemia (decreased hematocrit)
Hematocrit = the ratio of the volume of red cells to the volume of whole blood. Normal range for hematocrit is different between the sexes and is approximately 45% to 52% for men and 37% to 48% for women.
TREATMENT
⦁ surgery
Treatment of non-rupturing AAA’s depends on aneurysm size:
⦁ < 5 cm diameter and asymptomatic - monitor with periodic ultrasound
- annual ultrasound if 3.0-4.0 cm
- q6m ultrasound if 4.0 - 4.5 cm
- q3m ultrasound if 4.5 - 5.4 cm + vascular surgeon referral
⦁ > 5.5 cm diameter or symptomatic or grew by 0.5 cm in 6 months - surgical repair using open or endovascular stenting.
⦁ BETA BLOCKER** = reduces shearing forces, decreases expansion and rupture risk.
Abdominal aortic aneurysm does not indicate surgery in asymptomatic patients until the aneurysm reaches a diameter of ≥5 cm.
In aneurysm cases of larger than 5 cm, EVAR
(Endovascular aneurysm repair) is more commonly used because it is less invasive than open aneurysm repair (catheter-based therapy).
⦁ Thoracic aortic aneurysms = surgery if 6cm+
Emergent surgery needed if aneurysm has ruptured or if symptomatic
the USPSTF recommends screening in any male 65-75 with a hx of smoking - 1 time screening via ultrasound
- screening also recommended in those with Marfans + Ehlers Danlos
HYPERKALEMIA
hyperkalemia = higher than normal potassium levels in the blood
normal K+ range = 3.5 - 5.0
Hyperkalemia = > 5.0 or 5.5 mEq/L
Levels > 7.0 can be life-threatening due to its effect on heart muscle
Total body potassium can be split into intracellular and extracellular
o Extracellular = Intravascular space + Interstitial space
⦁ Intravascular = in blood vessels + lymphatic vessels
⦁ Interstitial = space between cells where other proteins and carbohydrate chains are found
o Intracellular = within the cell
MAJORITY OF K+ = INTRACELLULAR (98%) = 150mEq/L
- about 2% = extracellular = 4.5 mEq/L
o INTERNAL POTASSIUM BALANCE
⦁ K+ has a charge, so having much more K+ in the cells creates an electrochemical gradient, called the Internal Potassium Balance, which is maintained by the Na / K pump - pumps 3 Na+ out for every 2 K+ in
⦁ There are also potassium leak channels and inward rectifying channels that are scattered throughout the membrane
⦁ This electrochemical gradient is VERY IMPORTANT for setting the resting membrane potential of excitable cell membranes = needed for normal contraction of SMOOTH, CARDIAC + SKELETAL MUSCLES
o EXTERNAL POTASSIUM BALANCE
= potassium that you get externally through diet daily
- daily basis = typically get 50-150mEq/L = WAYY more than the extracellular K+ level of 4.5 mEq/L
⦁ so body has to excrete most of what it takes in = KIDNEYS - excreted via urine. Small amount of K+ is excreted via GI (poop) and sweat too
HOW DO YOU GET HYPERKALEMIA IN THE BLOOD?
1) decreased potassium excretion via kidneys = external balance shift
⦁ kidney failure / acute kidney injury
⦁ hypoaldosteronism (adrenal insufficiency)
⦁ drugs: ACEI / ARBs / Potassium-sparing diuretics
KIDNEY FAILURE
- potassium is normally freely filtered out of blood and into urine via glomerulus
- about 67% of K+ is reabsorbed in proximal convoluted tubule
- additional 20% reabsorbed in thick ascending limb
- distal tubule + CT can then either secrete or reabsorb remaining 13% depending on what the body needs
- ALDOSTERONE increases Na channels for Na to be reabsorbed and increases K channels for K to be excreted, as well as Na/K pumps
- Hypoaldosteronism (ADDISON’S)–> hyperkalemia
or increased potassium intake = external balance shift
⦁ IV fluids - rapid, excessive intake = iatrogenic cause
2) too much potassium moving out of cells and into interstitium + blood = internal balance shift
⦁ insulin deficiency (type I DM)
⦁ acidosis
⦁ beta adrenergic antagonists (beta blockers)
⦁ alpha agonists
⦁ succinylcholine - causes K efflux from muscles
⦁ hyperosmolarity
⦁ cell lysis
⦁ exercise
TYPE I DM
- after eating, glucose increases in the blood, so insulin is released. Insulin binds to cells and stimulates the uptake of glucose into cells
- insulin increases the activity of the Na / K pump - pulls potassium into cells / pulls sodium out of cells
- people with Type I DM don’t make insulin, so if they eat a meal, especially high in potassium, and don’t take insulin –> don’t have increased potassium intake into cells, so potassium sits in blood –> hyperkalemia
ACIDOSIS
- higher concentration of hydrogen ions in blood = low blood pH
- body can lower blood pH by moving H+ ions out of blood and into cells = use H+/K+ pump to move H+ into cell and move K+ out of cell and into extracellular space (blood / interstitium)
- so in order to help compensate for acidosis, end up with hyperkalemia
- only the case in certain acidosis, NOT respiratory acidosis, as CO2 is lipid soluble and is able to freely move from blood into cell without affecting potassium, and NOT metabolic acidosis of organics such as lactic acid or ketoacids
BETA-2 ADRENERGIC RECEPTORS
- stimulate Na+ / K+ pump - increase intracellular K+
- so Beta-Blockers do the opposite –> hyperkalemia
ALPHA-ADRENERGIC RECEPTORS
- cause potassium to shift out of cells and into blood via calcium dependent K+ channels
- so Alpha-agonists cause more hyperkalemia
HYPEROSMOLARITY
- hyperosmolarity in extracellular space causes water to shift out of cells –> excess potassium in cells –> potassium to shift out of cells –> hyperkalemia
CELL LYSIS - so much potassium is kept in the cell that with cell lysis --> potassium released from cells --> hyperkalemia ⦁ severe burns ⦁ rhabdomyolysis ⦁ tumor lysis (chemo)
EXERCISE
- during exercise, excess ATP is used for energy
- the depletion of ATP triggers potassium channels to open = allows potassium to move down its gradient and out of the cell –> hyperkalemia
- usually the exercise shift is small, but if combined with beta blockers and/or kidney issues –> can lead to hyperkalemia
SYMPTOMS
- need normal K+ levels inside and outside the cell to maintain resting membrane potential to allow muscle cells to depolarize and contract
- if too much extracellular K+ levels = increases resting membrane potential and can cause contraction –> abdominal / intestinal cramping
- eventually the resting membrane potential gets so high that it’s above the threshold potential, once the muscle depolarizes and contracts, it can’t repolarize to allow for another muscle contraction -> weakness
⦁ abdominal / intestinal cramps - increased activity of smooth muscles in peritoneal cavity
⦁ muscle weakness - decreased intracellular K+ for skeletal muscle - ascending muscle paralysis / flaccid paralysis
⦁ diarrhea - increased activity of smooth muscle - peristalsis
⦁ heart arrhythmias / arrest - decreased cardiac myocyte conduction (tends to occur at K+ of 7-8)
DIAGNOSIS
⦁ labs: K > 5.5 mEq / L
- also check glucose, creatinine, cortisol
⦁ EKG
- peaked T waves - best seen in precordial leads (V1 - V6)
- shortened QT interval
- ST segment depression
- in severe cases = can also cause prolonged PR interval, absent P wave, and widened QRS complex
could be PSEUDOHYPERKALEMIA - lab error or
** MC due to Venipuncture **
TREATMENT
⦁ potassium-wasting diuretics (Loop + thiazide - Lasix)
⦁ calcium gluconate- to stabilize myocardial cell membrane = 1st line if severe symptoms, EKG changes or > 6.5/7 mEq/L
⦁ insulin + glucose - insulin shifts K+ into the cell. Glucose given to prevent hypoglycemia from insulin
⦁ sodium bicarb - not given unless metabolic acidosis also present
⦁ beta-2 adrenergic agonists
⦁ resins -binds K in GI tract for excretion (kayexalate = sodium polystyrene sulfonate)
⦁ severe cases = dialysis
Rapid acting therapies (calcium gluconate, insulin and glucose, β2-adrenergic agonists) are indicated in patients with ECG changes, or those with serum potassium greater than 7 meq/L.
Calcium gluconate is used in cases of hyperkalemia because it antagonizes the effect of potassium on the myocyte cell membrane
Calcium gluconate or chloride, followed by measures to reduce serum K+ levels, is the immediate treatment to stabilize cardiomyocytes and reduce the risk of arrythmias when hyperkalemia is present
ex: if patient on lisinopril and have hyperkalemia = likely developed hyperkalemia due to lisinopril, due to reduction in aldosterone
CLEARING CERVICAL SPINE
⦁ A cervical spine MRI scan is the definitive way to diagnose and clear a cervical spine injury on patients of all ages
MRI allows for clear visualization of the ligaments, intervertebral disc spaces, spinal cord, and bones.
o When a patient presents with a cervical injury, protecting the area with a cervical collar is important in order to maintain spinal alignment and prevent further injury
o it is difficult to clinically clear the cervical spine if patient is
⦁ young
⦁ unable to communicate
⦁ unconscious
o Obtaining a cervical spine X-ray should be the initial course of action to determine whether or not there is movement between the bones
o An X-ray, however, is unable to visualize the spinal cord and ligaments
o A CT scan of the cervical spine would be the next ideal imaging technique, but this is best to further investigate the bones and not the ligaments or spinal cord
o To determine injury to the spinal cord or ligaments, determine the presence of hemorrhage or edema, and to evaluate the intervertebral disc spaces, an MRI of the cervical spine provides the most amount of information and therefore is the best tool to definitively clear the cervical spine before cervical collar removal.
Clinical clearance is a useful technique to clear the cervical collar, but should be reserved for patients who are conscious, able to appropriately provide information, and respond appropriately. Young children should not be expected to adequately answer questions or perform instructed movements and therefore clinically clearing a cervical spine is not appropriate in a young and unconscious patient
A cervical spine CT scan is a good technique to evaluate bony injury of the cervical spine, but because it is not an adequate test to evaluate the ligaments and spinal canal, it cannot be used as the definitive test to clear the cervical spine
- If plain X-rays are inconclusive or if there is a high suspicion for fracture despite negative X-rays, a CT scan of the cervical spine should then be performed for further evaluation.
Cervical spine radiographs are the INITIAL test to determine the presence of a bony injury in a patient suspected of a cervical spine injury, but cannot be the definitive test to clear the cervical spine in a patient with a poor neurologic examination.
Even if xray is negative for a bony process, the cervical collar should not be removed until further investigation of the spinal ligaments and spinal cord have occurred
BILATERAL FACET DISLOCATION
Bilateral facet dislocation is an unstable injury that occurs from ** FORCEFUL HYPERFLEXION OF THE NECK ***
Mechanism = Forced Hyperflexion
- It occurs when the articular masses of one vertebra dislocate anteriorly and superiorly from the articular surface of the vertebra below it causing anterior displacement of the spine
- This injury involves forceful disruption of multiple structures at the level of the injury, including all ligamentous structures, the articular facet joints, and the intervertebral disc
This is commonly associated with a COMPLETE SPINAL CORD INJURY due to TRANSECTION of the cord at the level of the injury.
DIAGNOSIS
⦁ XRAY - displacement of superior vertebral body anteriorly more than 1/2 of its width
- Lateral view = best
SYMPTOMS
⦁ severe neurological sequelae
⦁ Loss of all motor and sensory function**
ANTERIOR CORD SYNDROME
Prognosis = poor
Most commonly results from interruption of the anterior spinal artery, resulting in damage to the anterior two-thirds of the cord with sparing of the dorsal columns
syndrome caused by ischemia of the anterior spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord.
PATHOPHYSIOLOGY
⦁ The posterior columns carry tracts responsible for ipsilateral position and vibratory sensation
⦁ The lateral spinothalamic tract carries fibers for contralateral pain and temperature
⦁ The lateral corticospinal tract is responsible for ipsilateral motor function
Syndromes may be incomplete depending on how much of the cord is affected by the injury
In the anterior spinal cord syndrome, just the posterior columns are preserved and so patients lose all pain and temperature sensation as well as motor function
⦁ loss of all motor function
⦁ loss of pain sensation
⦁ loss of temperature sensation
⦁ still have position + vibratory sensation
CAUSES
⦁ Most cases of anterior cord syndrome follow
** AORTIC SURGERY **
but it has also been reported in the setting of
⦁ hypotension
⦁ infection
⦁ vasospasm
⦁ anterior spinal artery ischemia or infarct
⦁ In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord.
SUMMARY
Anterior Cord Syndrome
o PE will show loss of motor, pain, and temperature below injury
o Most commonly caused by flexion injury
o Comments: proprioception and vibration intact
CENTRAL CORD SYNDROME
Prognosis = average
Mechanism = Forced Hyperextension
SYMPTOMS
⦁ ** Upper greater than lower motor weakness **
BROWN-SEQUARD SYNDROME
hemicord syndrome
Prognosis = good
Mechanism = penetrating trauma
SIGNS / SYMPTOMS
⦁ results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side
Ipsilateral loss of Proprioception and Vibration + Paralysis (hIP ViP and walk with a Limp)
loss of all sensation at level of lesion
Below level of lesion = spastic paralysis and positive ipsilateral Babinski
Contralateral loss of Temperature and Pain (ConTemplate the Pain I make)
Brown-Séquard Syndrome
Patient with a history of penetrating trauma
PE will show ipsilateral loss of motor, position and vibration and contralateral loss of pain and temperature
Most commonly caused by spinal cord hemisection
BETA BLOCKER TOXICITY
Beta adrenergic antagonists, more commonly referred to as beta-blockers, inhibit beta-adrenoceptors
They are used in the treatment of a number of disorders including hypertension, heart failure, arrhythmias, ischemic heart disease, migraine headaches, tremor, aortic dissection and portal hypertension
Beta-blockers competitively inhibit epinephrine and norepinephrine, which results in the blunting of multiple metabolic and cardiovascular effects normally regulated by these circulating catecholamines. Both the beta-blockade and the differing properties of toxicity among beta-blocking agents have influence on the adverse cardiovascular effects.
Beta-blocker poisoning should be considered when patients present with overdose of an unknown medication.
The most commonly seen clinical manifestations of beta-blocker overdose include
⦁ hypotension
⦁ bradycardia
DIAGNOSIS
- history + PE
- Labs = hypoglycemia**
- EKG = Bradycardia, PR and QRS prolongation.
After stabilization in the emergency department, patients with a beta-blocker overdose who have altered mental status or hemodynamic instability should be admitted to the critical care unit for cardiac monitoring and management
TREATMENT
⦁ glucagon + insulin
ALVEOLAR OSTEITIS (DRY SOCKET)
dry socket, also known as acute alveolar osteitis
Patients undergo dental extraction and after the procedure a hemostatic blood clot forms in the socket
Pain is common for 24 hours post-procedure and then improves
When the healing blood clot is lost from the socket, the patient develops acute severe pain
Most commonly, EXCRUTIATING PAIN occurs 3-5 days after the extraction and is associated with a foul odor
Pain is related to inflammation and a localized infection of the bone
EXAM = Exposed bone and no clot in extraction site
Treatment includes packing the open socket with iodoform gauze. The gauze is saturated with either a medicated dental paste or eugenol (oil of cloves)
Patients will require analgesia and may benefit from a nerve block.
Alveolar Osteitis (Dry Socket)
Patient will be 3 - 5 days post extraction
PE will show inflammation and local osteomyelitis with a clean extraction site
Most commonly caused by loss of healing clot
Treatment is pack socket with iodoform gauze and eugenol oil
EPIGLOTTITIS
TRUE EMERGENCY!!!!
- Inflammation of the epiglottis => can interfere with breathing
- MC CAUSE = HIB (haemophilus influenza B)*
- gram negative rod
- has been a decrease in incidence due to vaccination
- other causes ⦁ strep pneumo* ⦁ staph aureus ⦁ GABHS ⦁ strep agelectiae ⦁ strep pyogenes ⦁ M. cat
Non-HIB seen more commonly in adults (esp crack, cocaine use)
MC in children 3 months - 6 years*
Males = 2X more common
DM = risk factor
generally sudden in onset (acute)
SYMPTOMS
⦁ DROOLING
⦁ MUFFLED, HOT POTATO VOICE*
3 D’s = DYSPHAGIA, DROOLING, DISTRESS
⦁ fever
⦁ odynophagia (difficulty / painful swallowing)
⦁ inspiratory stridor (also with croup)
⦁ dyspnea
⦁ hoarseness
often in TRIPOD POSITION - leaning forward
Patients sit with neck hyperextended and chin protruding (sniffing dog position)
DO NOT EXAMINE THE PATIENT - could cause spasm
BE PREPARED TO INTUBATE - do not give IV ABX prior to intubation, as this could also cause spasm
DIAGNOSIS
⦁ ** LARYNGOSCOPY ** = definitive diagnosis - provides direct visualization, however, could induce bronchospasm!
⦁ LATERAL NECK XRAY - STAT - THUMBPRINT SIGN
TREATMENT
Secure airway - call anesthesiology and prepare to establish airway, transfer to OR to perform exam
- tracheostomy if necessary to maintain airway
⦁ maintain airway + supportive management = place child in comfortable position and keep them calm.
Admit for observation ==> humidified O2, IV antibiotics (ceftriaxone + clindamycin), and IV corticosteroids
⦁ Dexamethasone to decrease airway edema, and be prepared to intubate
⦁ IV ABX = Ceftriaxone (most likely HIB) or Vanco for anti-staph - call ID specialist for regional coverage/most likely etiology
EX:
Your patient is a 45 year old male that is not immunized. He presents with a fever of 102, dysphagia, drooling, and shortness of breath. Lungs are clear. O2 Sat 100%. Pulse 102. RR-24. Soft tissue neck reveals a thumb sign. All of the following are acceptable management plans except:
A Give a Racemic Epinephrine aerosol treatment and discharge the patient home on steroids = NO
B Begin Vancomycin and Ceftriaxone
C Intubate the patient in the operation room
D Consult anesthesia or ENT
Question 36 Explanation:
In the treatment of epiglottitis racemic epinephrine can help momentarily, but ultimately the patient needs to be intubated and admitted to the hospital. Airway protection is the mainstay of treatment. The patient usually needs to be intubated for 2-3 days prior to weaning attempts. The role of steroids is controversial. Vancomycin helps with anti-staph coverage and Ceftriaxone covers the most common organism haemophilus influenza type B. Anesthesia and/ or ENT should be consulted for airway management.
Patient will present as → a 3-year-old who is brought into the emergency room by her parents. The child has had a high fever, sore throat, and stridor. She has a muffled voice and is sitting up on the stretcher drooling while leaning forward with her neck extended. The patients parents are adamantly against vaccinations, claiming that they are a “government conspiracy.” You order a lateral neck x-ray, which shows a swollen epiglottis.
ANTERIOR + POSTERIOR FAT PAD ON XRAY
Anterior fat pad = “sail sign” and Posterior fat pad = Radial head fracture in adults (even if not seen on xray)
and Supracondylar fracture in children
RADIAL HEAD FRACTURE
Anterior fat pad = “sail sign” and Posterior fat pad = Radial head fracture in adults (even if not seen on xray)
Patient will be an adult with a history of fall on an outstretched hand (FOOSH)
PE will show localized swelling, tenderness, and decreased motion
X-ray will show fat pad ‘sail sign’
fat pads = Supracondylar fracture in children
