Exam 2 Flashcards
kidney stones - most common age group
70% of kidney stones occur between 20-50 yrs old
kidney stones - characteristics of pain
note: intra-renal stone (within the kidney) does not cause pain
kidney stones - types of stones
Calcium oxalate (80%): most common
Struvite (2-20%)
Uric Acid (6%): seen in younger women
Cystine 1(%): occurs only in patients with cystinuria
calcium oxalate stones - characteristic findings
most common
radio-opaque (can see on x-ray)
associated with hypercalcemia (high Ca++ in urine only) - primary hyperparathyroidism, malignancy, sarcoid
associated with hyperoxaluric states (high oxalates) - Crohn’s, jejunal ill bypass, high consumption of sweet tea
struvite stones - characteristic findings
cause staghorn calculi
triple phosphate stones: composed of phosphate, ammonium, magnesium
requires pH >7.2 and ammonia (caused by UTI)
proteus is most common organism
associated with foreign body (chronic catheter) or neurogenic bladder (spastic / not well controlled)
uric acid stones - characteristic findings
caused by super saturation of urine with uric acid
- gout patients get these
Radiolucent
Diet changes, allopurinol (med to dec uric acid), increased water intake prevent further stones
kidney stones - areas of impaction
Renal calyx
- stones get stuck here (cannot pass)
Ureteropelvic junction
UVJ-smallest diameter in the urinary tract
- most common site of impaction
kidney stone - sizes and ability to pass
<4 mm: 75% will pass
4 to 5 mm: 50% will pass
6 mm: 10% will pass
>10mm: require urologic intervention
Note: fully obstructed ureter can cause renal stasis
kidney stones - clinical presentation
colicy, severe pain on affected side
- pain in waves
- patient moves around a lot (cannot escape pain)
visceral pain caused by distention of ureter
nausea, vomiting, and pale color common
usually NOT hypotensive (shocky)
kidney stone location and site of pain
kidney = flank pain
proximal to mid ureter = flank pain, anterior abdomen to lower quadrant
UVJ (ureteral vesical junction) = labia, scrotum, groin region
Note: SUVJ and bladder stones may cause urgency, and dysuria as well as pain, or urinary retention
kidney stones - key history questions
Previous episodes of renal colic
Recurrent or Chronic UTI’s
Family history for hereditary disorders causing stones.
Immunocompromise
Solitary functioning kidney, or transplant (more concerning)
Bone pain, fractures (hyperparathyroidism = claim oxalate)
Gout, PUD peptic ulcer disease): uric acid stones
Diet, antacid use
suspicion of kidney stone - physical exam
vitals: tachycardia, elevated BP, tachypnea and diaphoresis
- hypotensive = concerned (not kidney stone)
Fever: suggests stone is infected
Flank tenderness, CVA tenderness
Abd: no point tenderness, pain not exacerbated with palpation
- must auscultate for bruits (AAA)
colicky flank pain - Ddx
AAA (often misdiagnosed as renal colic)
Renal Artery thrombosis/embolism
- seen in A fib or IV drug use
Testicular torsion
Ectopic pregnancy
Appendicitis
Cholecystitis
AAA - clinical presentation
misdiagnosed as renal colic
Caution: patients > 50 with flank pain, especially H/O tobacco, HTN, PVD (peripheral vascular disease)
A rupturing AAA may cause hydronephrosis (swelling of kidney) due to compression, and hematuria (ureteral irritation)
- white cells and red cells in urine since ureter is compressed and inflamed
renal artery embolus - clinical presentation
pain, hematuria and vomiting (intractable vomiting and pain)
- worse then a stone
risk factors: embolic disease (A-fib, PVD, IVDU)
Image: IVP (intravenous pyelogram, angiogram)
- non contrast CT will not give good info
Definitive study: arteriogram
Labs: CPK (elevated) - creatinine phosphokinase
ED role in renal colic
Relieve pain
Exclude life threatening diagnoses (AAA)
Provide appropriate disposition, follow up and instructions for returning
Not every patient needs a definitive diagnosis
ED treatment - renal colic
Hydration
- only if dehydrated or slightly hypotensive
Pain control before diagnostic tests
Analgesia: narcotics, anti-emetics (Zofran), or NSAIDS
NSAIDS: toradol (IV anti-inflammatory), ketorolac, diclofenac
benefits of NSAIDS to treat renal colic pain
non sedating
no ureteral spasm
no effect on hemodynamics
NSAIDS: toradol (IV anti-inflammatory), ketorolac, diclofenac
urinalysis and urine culture - renal colic
urinalysis and urine culture
- 10-30% will not have microscopic hematuria
- pyuria (WBCs) occurs due to inflammation or w/ bacteria infection
- crystals in urine may correspond to stone type (pH>7.6 proteus infection or RTA (renal tubular acidosis)
microscopic hematuria - what it means in kidney stones and acute cystitis (UTI)
magnitude of blood in urine does not correlate with size of obstruction, pain, or significance of infection
any localized inflammation may irritate ureter (causing hematuria) - e.g. appendicitis
laboratory studies - renal colic
urinalysis and urine culture
CBC: only if concerned about infection
Chem 7: prior to contrast study
SPT (serum preg test): prior to contrast study
passed stone - sent for evaluation
Chem 7 laboratory test
electrolytes, BUN, creatinine
order before contrast study
imaging for suspected renal stones - 4 functions
non-contrast CT
1) Confirms diagnosis
2) R/O other serious disorders
3) defines site of stone
4) Detects or R/O serious complications such as obstruction
imaging for suspected renal stones - who should be imaged
first time stone producers
history of IVDU
suspicion of serious disorder
Note: frequent stone formers who are not infected and symptomatically improve, do not require a study
KUB - role in kidney stones
x-ray of kidneys, ureter, and bladder
- cannot see ureter
stones: radio-opaque will show up, but uric acid won’t (or any radiolucent stones)
limits: gas patterns, fecoliths, phleboliths, small stones (must be 2mm to be visible)
- provides no info on kidney fx
Helpful: pts w/ documented stones presenting to ER
- possibly after CT
Ultrasound - role in kidney stones
Study of choice in pregnant patients
Operator dependant, and anatomy dependent due to overlying pelvic structures
Diagnosis of stones is made through visualizing obstruction (specifically hydronephrosis)
Best at showing stones in the renal calyx and UVJ, - poor for ureteral stones
Can’t size calculi
IVP (intravenous pyelogram)
gold standard for evaluating urolithiasis and its complications
- rarely used in ED
evaluates renal fx, visualizes the entire urinary tract, and degrees of obstruction (IV contrast and sera of films)
contraindications (Chem 7):
- allergy (0.1%)
- pregnancy
- DM
- RI creatinine >1.8
- dehydration
- multiple myeloma
- patients on glucophage
IVP disadvantages
May not directly visualize stone and may not accurately size the stone
Time consuming
Contrast and radiation exposure
helical CT (abdominal CT) - non contrast
standard for renal stone imaging
fast, no contrast
Identifies the stone anywhere along the GU tract
Accurately sizes the stone
Hounsfield typing may differentiate type of stone
Provides info about other intra-abdominal structures (AAA, mass)
helical CT (abdominal CT) disadvantages
Less information about the degree of obstruction as compared with IVP
May not be readily available
Radiation exposure similar to IVP
disposition - dx of kidney stone without infection
Send home w/ education
NSAIDS and narcotics
- anti-emetics
Flomax or calcium channel blocker in select patients
- helps with urinary tract spasm
Adequate hydration to produce clear urine
Strain urine until the stone passes (not always possible)
RTC: uncontrollable pain, vomiting, fever, abdominal pain
outpatient follow-up - kidney stones
Patients need a stone analysis, complete urinalysis, and blood chemistry, 24 hour urine (?)
guidelines to prevent kidney stones
Increase fluids to 3 L/day for u/o of 2 L/day
Normal calcium intake (natural, not suppl.)
Decrease sodium intake
Decrease oxalate (chocolate, nuts, black tea, dark roughage) and avoid excess vitamin C supplements
Decrease protein
medications to prevent kidneys stones
Calcium oxalate stones
- Hypercalciuria: thiazide diuretic + potassium citrate
Uric Acid stones
- Increase urine pH to 6.5-7.0
- Potassium Citrate
- Allopurinol (uric acid / gout tx)
when to admit - renal colic / kidney stones
Intractable vomiting
Uncontrolled pain
Single kidney or transplanted kidney with obstruction
Concomitant UTI with obstruction
High grade obstruction or stones >8 mm (?)
Social issues
procedures for kidney stone removal
ESWL (extracorporeal shock wave therapy)
- stones crushed and passed
Percutaneous Nephrolithotomy
- stent placed through back to drain obstruction and remove stone
- can
Ureteroscopy
- distal ureteral stones; outpatient
Stents
- tube inserted to tx obstruction of urine flow
ESWL (extracorporeal shock wave therapy) - procedure for kidney stone removal
Done under fluoroscopy
Indicated for stones > 2cm
Stones are crushed and passed in 2 weeks
Not indicated for women of childbearing years (? Impact on ovary)
Complications:
- hematoma formation
- ureteral obstruction from stone fragments
Percutaneous Nephrolithotomy - procedure for kidney stone removal
Percutaneous stent placed through back under anesthesia to drain obstruction and remove renal stones > 2cm or proximal ureteral stones > 1cm
Complications:
- bleeding
- injury to collecting system and infection
Ureteroscopy - procedure for kidney stone removal
Indicated for distal ureteral stones
Outpatient procedure, usually requires sedation
May require placement of stent
Complications:
- ureteral stricture
renal stents
tube inserted to tx obstruction of urine flow
May become obstructed
KUB is helpful in verifying placement
Check for UTI
acute cystitis - presentation
bladder infection (UTI) Dysuria Frequency Urgency Suprapubic pain Hematuria Low grade fever
UTI - uncomplicated v. complicated
uncomplicated:
- lower tract sxs
complicated:
- pyelonephritis
- pregnancy (avoid pyelo)
- catheter, stent, or tube in GU system
- male (should not get UTI)
- obstructive stone
- hospital UTI
- DM severe
- treatment failure
- anatomical abnormality
- cancer, immune suppression
acute cystitis - diagnosis
UA dipstick:
- LE (esterase) +, nitrites +
Urine culture (micro):
- pyuria (WBCs): >5 WBC/hpf
- bacteruria
- > 5 RBCs/hpf
Organisms involved: KEEP
acute cystitis - organisms involved
KEEP
Klebsiella
Enterobacter
E. coli
Pseudomonas aeroginosa/ Proteus mirabilis
- Sandy said proteus
suspicion of acute cystitis - Ddx
Non infectious dysuria
- trauma
- decreased estrogen in postmenopausal women, leads to atrophic vaginitis,
- scented soaps or lotions
Kidney stone
Sterile pyuria: WBCs from another process
Unclean specimen
urine culture - use in acute cystitis in ER
gold standard for dx, but does not guide ED tx
- takes long to get results
when to send culture:
- treatment failure
- frequent UTIs
- pregnancy
- complicated UTI (pyelonephritis)
urine culture - what level is positive for UTI
Positive culture is > 105 colony forming units/hpf
UTI treatment
ABX depends on local resistance (7 day course)
- confirm med (Janka)
- longer course (7-10 days) in pregnancy, DM, elderly recurrences
Increase fluid
Analgesic: phenazopyridine
- stains tears (no contacts) and urine orange
Cranberry juice: may help with E. coli infection
pyelonephritis
Fever, flank pain, myalgia, anorexia, N/V, urinary sx
E. Coli 75% of time
Diagnosis:
- CVA tenderness
- UA: dip will show protein, LE (esterase), nitrites
- Micro: WBC’s bacteria, WBC casts (key!)
- Urine Cx +
- CBC: leukocytosis with left shift
pyelonephritis - disposition
impatient:
- child
- pregnant
- acutely ill
outpatient:
- can manage on oral ABX
pyelonephritis - treatment
Inpatient
- IV abx (ampicillin and Gentamycin)
- Consider follow up C&S (culture and sensitivity - ABX resistence)
Outpatient:
- oral fluoroquinolone (Ciprofloxin 500 mg bid) for 14 days (+/- 400 mg IV loading dose)
- 1gm IV Ceftriaxone q 24 hours until oral medication can be tolerated
Note:
Cranberry juice: may help with E. coli infection
urinary retention
Inability to voluntarily pass urine
Usually secondary to obstruction (BPH - benign prostate hypertrophy)
urinary retention - causes
Obstruction:
Men: BPH - prostate
Women: UTI, prolapse of bladder, rectum, or uterus
Post-op hernia surgery
young women (20-30): onset of MS
medications: anti-cholinergic medications, antihistamines, ephedrine and amphetamines
urinary retention - presentation
Straining to void
Decrease in force of urine
Interruption of urination
Sensation of incomplete emptying
Irritative sx: frequency, dysuria, urgency, nocturia
urinary retention - evaluation/treatment
Placement of foley catheter and UA
Imaging only if infection or stones suspected
Patients d/c home with foley in place, urology follow up
No abx unless high risk
Consider alpha adrenergic blockers (tamsulosin) after urologist consult (postural hypotension) 0 help w/ urinary retention
acute renal failure (ARF)
Sudden decrease in Renal function resulting in an inability to maintain fluid and electrolyte balance and excrete nitrogenous wastes
Serum creatinine most useful marker.
Failure is defined as:
- 2-3 fold increase in serum creatinine +/-
- decrease in urine output of < 5 cc/kg/hr for 24 hours
what value is concerning for low urine output
< 5 cc/kg/hr for 24 hours
acute renal failure (ARF) - characteristics and prevalence
Azotemia: nitrogenous waste accumulation
Uremia: symptomatic azotemia (nausea, vomiting, lethargy, altered mental state)
30% of ICU admissions have ARF
25% of hospitalized patients develop ARF
azotemia
nitrogenous waste accumulation
uremia
symptomatic azotemia - nausea, vomiting, lethargy, AMS (altered mental status)
acute renal failure - 3 causes
pre-renal (50%): sudden or severe drop in BP (shock); interruption of blood flow to kidneys
- perfusional
intra-renal (45%): direct damage to kidneys
- glomerular, tubular, interstitial
post-renal (5%): sudden obstruction of urine flow
- obstrcutive
Note: usually rule out pre and post before considering intrinsic casues
ARF - pre-renal causes and lab findings
Shock syndromes implicated: septic, cardiogenic, hemorrhagic, hypovolemic
If you can fix the shock, you fix the kidneys if caught in time
Labs (conc. urine):
- Urine spec grav > 1.030
- Serum Bun/Creatinine > 20
- Urine osmolality >500
- FENA< 1
ARF - renal causes and lab findings
Acute Tubular Necrosis (ATN) (85%)
Interstitial Nephritis (10-15%)
Glomerulonephritis (5%)
Labs (no elevated BUM/creatinine):
- Spec grav < 1.010
- Serum Bun/Creat <10
- Urine osmolality <300
- FENA >1
Acute Tubular Necrosis (ATN)
renal (within kidney) cause of ARF
acute tubular injury from ischemia or toxin
Labs:
- BUN ratio <20:1, FENA>1%
- Microscopic: renal tubular epithelial cells, muddy brown casts
Common drug offenders: aminoglycosides, amphotericin, contrast dye, cyclosporines
Treatment:
- loop diuretics may help in fluid overload
- may require dialysis
Interstitial Nephritis
renal (within kidney) cause of ARF
Causes:
- Immune mediated response
- Drugs: PCN, Ceph, sulfa, NSAID’s rifampin
- Infections: Strep, RMSF(rocky mt spotted fever), CMV, Histoplasmosis
- Immunologic: SLE, Sjogren’s, Sarcoid
Clinical: fever, azotemia (nitrogenous waste accumulation), rash, arthralgias (joint pain)
Urine micro: pyuria, esp. eosinophiluria, WBC casts, hematuria
- see eosinophils in urine since immune response
Diagnosis:
- renal biopsy
Treatment:
- discontinue offending drug
- self limited if found early
- possibly dialysis
- corticosteroids
Glomerulonephritis
renal (within kidney) cause of ARF
Immune deposition causes, vaculitis, anti glomerular basement membrane disease (goodpasture syndrome)
Strep (with edema and HNT) - can get post strep glomerulonephritis
Clinical: dependent edema and hypertension
UA shows red cell casts
Treatment:
- high dose corticosteroids,
- possible exchange transfusions until chemotherapy
ARF - diagnostics
Microscopic UA
BUN, Creatinine, urine sodium and FENA
- FENA helps to differentiate type of renal failure
CBC, Chem 7 ,CXR, EKG
Renal Ultrasound
- may show obstruction upper or lower tract, small kidneys, hydronephrosis
- CT not used as contrast may cause more injury
chronic renal failure - two main causes
2 HTN- small kidneys
#1 DM- normal sized kidneys - why we need aggressive control of blood sugars
chronic renal failure - treatment
Good management of underlying condition
Dialysis
Transplantation
ED evaluation of ARF
Look for life threatening complications
- Hyperkalemia (cardiac, renal failure)
- Pulmonary edema
- Pericardial effusion
Physical Exam
- Evidence of hypovolemia (tachycardia, orthostatic VS, decreased skin turgor)
- Evidence of hypervolemia (S3, JVD, edema, rales)
Percuss the bladder (percussable with 150 ml, palpable with 500 ml urine)
acute abdominal pain in ED - basic facts
1 chief complaint in ED (~10% of all ED visits)
Second leading cause of ED lawsuits
- Inadequate exam
- No follow up
- Inadequate patient instructions
- Data misinterpretation
Often difficult to determine cause/definitive dx
ED approach to acute abdominal pain
Is the patient critically ill?
- sever pain / rapid onset
- abnormal VS
Do sxs fit a known disease pattern?
Special conditions:
- cognitive impairment
- immunocompromised
Is surgical consult needed?
- acute abd, pulsatile abd mass, shock, hemodynamic instability, rigid abd, GI bleeding
vital signs that are worrisome for acute abdominal pain
severe pain of RAPID onset
abnormal vital signs
- inc. HR, dec. BP, inc, RR< fever)
Note: BP would typically be high with pain, so if it’s low, be concerned)
abdominal pain - common causes (< 60 y/o)
Abdominal pain, nonspecific Appendicitis, acute Urologic (kidney stones) - unique to age group Intestinal obstruction Biliary Disease Trauma, abdominal - unique to age group PUD, perforated viscus
abdominal pain - common causes (> 60 y/o)
Biliary Disease Intestinal obstruction Abdominal pain, nonspecific Diverticulitis - unique to age group Appendicitis PUD, perforated viscus Malignancy - unique to age group
abdominal pain - life-threatening conditions
Abdominal aortic aneurysm
Thoracoabdominal aortic dissection
Ectopic pregnancy
Placental abruption
Mesenteric ischemia Perforation of gastrointestinal tract peptic ulcer, bowel, esophagus, or appendix Acute bowel obstruction Volvulus Splenic rupture Incarcerated hernia Myocardial infarction
Note: top 4 will kill you if you do not dx immediately!!
- others have complications that will kill
visceral abdominal pain
direct irritation of involved organs
dull, achy, poorly localized, protracted
signs: distension, inflammation, ischemia
parietal (somatic) abdominal pain
direct irritation of parietal peritoneum of abdominal wall by gastric juice, pus, bile, urine, succus entericus, feces
steady, sharp, better localized
Peritoneal pain signs: guarding, rebound, rigidity
referred abdominal pain
Pain felt at a location distant from the diseased organ/primary stimulus
Examples:
- AAA to lower back
- gallbladder to shoulder
- Ureter to groin
- Pancreatitis to back
- Perforated ulcer to RLQ
misleading abdominal pain
from “extra-abdominal” source
Examples: Intrathoracic diseaseto upper abdomen, uremia, pneumonia, pleural effusions
abdominal pain in elderly
Usually sicker than they look
- under-report sxs
- surgical emergencies more common
- fever not reliable
- do not mount same immune response
Have a low threshold for a bigger workup and to admit
acute abdominal pain in ER - approach to patient
Step 1 – General survey and VS
- Ill appearing, serious pain
- Abnormal VS
Step 2 – History and Physical Exam
Step 3 – Diagnostic Workup
- Labs
- Imaging/Studies
Step 4 – Reexamine
- Do they feel better? Worse? New Sx?
Step 6 – Disposition
- Surgical consult (does someone else need to weight in)
- Admit to hospital
- D/C from ED
history for acute abdominal pain - OPQRST
Onset: abrupt, gradual, protracted
Provoking: eating, fatty foods, coughing, straining
Quality: dull, vague, crampy, steady, sharp, tearing
Region and Radiation: localized, diffuse, where radiates to
Severity: mild, moderate, severe
Time: duration since onset, change, constant, intermittent, prior episodes
history for acute abdominal pain - key components
associated sxs:
- N/V/D, fever, sweating, dyspepsia, dysphagia, tachycardia, chest pain, SOB, LMP, dark urine, heaturia, etc.
PMH: immunocompromised, PUD, DM, CAD, A-fib, IBD, diverticulosis, etc.
PSHx: date of surgery
Medications: anticoag, antibiotic, corticosteroids, NSAIDS
Shx, FHH, allergies, providers/code status
physical exam for acute abdominal pain - inspection
Distention, ascites, masses, surgical scars, ecchymosis, pulsations
- surgical scars
- specific findings: Grey turner’s sign, Cullen’s sign, caput medusa
Grey Turner’s sign
bruising (blueish) flanks
- hemorrhagic pancreatitis or ruptured AAA (bleeding inside)
Cullen’s sign
bruising around umbilicus
- hemorrhagic pancreatitis or ruptured AAA (bleeding inside)
caput medusa
visible dilated abdominal venous vasculature
- sign of portal hypertension (liver failure / obstruction)
physical exam for acute abdominal pain - auscultation
For bowel sounds (all 4Q)
- High-pitched/tinkling or hyperactive: obstruction
- Decreased or absent: ileus, narcotic use, mesenteric ischemia
- Normal
For bruits
Renal arteries, aorta, femoral arteries
ileus
obstruction due to no peristalsis
- decreased to absent bowel sounds
physical exam for acute abdominal pain - percussion
Hollow organs for distention = obstruction
Peritoneal cavity for fluid wave, dullness to tympani ratio
Solid organs (Liver, spleen) for enlargement
CVA tenderness
Note: pain on percussion = worry about peritonitis
physical exam for acute abdominal pain - palpation
Light and deep palpation for tenderness
- voluntary guarding, rigidity, referred tenderness, rebound tenderness
Assessment of solid organ size
- Liver, spleen, kidney
Palpation of vascular pulsations
- Aorta, femoral
peritoneal irritation - signs on palpation of abdomen
rigidity, referred tenderness, rebound tenderness
guarding
voluntary - person pulls away in pain
rigidity
involuntary - spasm and contraction of abdominal wall
physical exam for acute abdominal pain - rectal exam
Anal lesions, tenderness, masses
Detection of grossly bloody or melanotic stools, occult blood
- hypotension: be sure not bleeding from anus
Fecal impaction
physical exam for acute abdominal pain - pelvic/GU exam
Note: unilateral or bilateral abdominopelvic tenderness → ectopic gestation in pregnant women with acute abdominal pain
- SERIOUS
Also palpate for masses
diagnostic workup for acute abdominal pain - labs
Always get:
- CBC, BMP, LFTs, Lipase (common)/Amylase (rare), UA, urine pregnancy
Depend on Ddx: coags, cardiac enzymes, venous lactate (indicator of how sick someone is), ABG (for elderly or very sick)
Note: must get creatinine before imaging study to test kidney fx
diagnostic workup for acute abdominal pain - imaging studies
plain fims: obstruction, perforation (free air)
- abd series (upright, KUB)
- CXR
Ultrasound: gallbladder (RUQ pain), hernias
CT abd/pelvis:
- contrast for most things
- no contrast for kidney stones (cannot see infection or fluid)
Angiography (CTA): mesenteric ischemia, AAA
EKG: anyone w/ epigastric pain (older, concerning)
diagnostic workup for acute abdominal pain - imaging special considerations
special considerations:
- renal disfunction, pregnancy (no CT), pediatric, obese (no U/S)
See summary table
diagnostic workup for acute abdominal pain - imaging supplemental studies
Serial abdominal plain films
- upper GI study (drink contrast, series of x-rays, look for obstruction)
Nuclear medicine studies
- cholescintigraphy (HIDA): gallbladder
MRCP: MRI that looks at ducts
- gallbladder and pancreas
ERCP: camera down mouth, up through common bile duct, can remove stones
- gallbladder and pancreas
acute abdominal pain in ER - disposition (who to admit)
Patients with a specific diagnosis requiring admission
Cannot (reasonably) exclude potentially serious causes of abdominal pain
High-risk patients with acute abdominal pain (elderly, immune compromised, unable to communicate, cognitively impaired)
Appear ill, have intractable pain or vomiting, are unable to comply with discharge or follow-up instructions, or who lack appropriate social support
appendicitis - general info and pathophysiology
most common: age 10-30
misdiagnosis remains as a leading cause of malpractice suits
Causes:
- obstruction by lymphoid hyperplasia or fecalith (most common)
- tumor (carcinoid - most common tumor)
- infection (parasitic)
appendicitis - clinical presentation
onset of pain before GI sxs
poorly localized initially (visceral) - localizes to RLQ
Sxs: range in magnitude; anorexia, nausea, +/- vomiting, low-grade temp / fever
PE:
Periumbilical tenderness ⟹ RLQ tenderness and guarding
McBurey’s point tenderness
Rovsing’s sign: referred pain from LLQ palpation
Obturator sign: pain w/ RLE passive hip flexion (int/ext rotation)
Psoas sign: pain w/ RLE active extension
appendicitis - hints to perforation in hx and PE
Pain free interval and peritoneal signs/sx
appendicitis - location of pain in pregnancy
displaced from RLQ to RUQ
appendicitis - diagnostic work-up
labs:
- Leukocytosis
- UA: normal or RBC and WBC 2ndary to local inflammation
Studies:
- CT (abd/pelvis) w/ contrast
- U/S: kids and pregnant
appendicitis - management
Surgical consult and admission
Preoperative management:
- Hydration with IVF, NPO
- IV analgesics
- IV ABX
Definitive tx is appendectomy (laparoscopic or open technique)
Note: ruptured appendicitis will first need tx for infection (ABX) and then removal
appendicitis - disposition (who can go home)
RLQ pain or tenderness w/ nomral labs, normal CT, stable VS, can eat and keep things down, pain can be controlled on PO meds, talked with surgery, able to return if sx get worse
biliary tract disease - general info and pathophysiology
collection of diseases/conditions (4) involving the gallbladder and biliary tract
primarily related to gallstone disease and complications from gallstone obstruction
- gallstones remain asymptomatic in 80% of cases
pathophysiology:
obstruction or impaired gallbladder contraction → cholestasis → inflammation → infection
biliary tract disease - risk factors
“F” risk factors
Female, Fertile, Forty, Fluffy (fat), Fair
cholelithiasis
gallbladder stones (GS)
biliary colic
intermittent obstruction of the biliary tree by stones
- inflammation w/o obstruction
- transient and self-limiting
- can go home
cholecystitis
gallbladder inflammation
- Acute : obstructed cystic duct most common
- Chronic : GB wall thickening, fibrosis, gas, no infection (no inc. WBC or fever)
- Acalculous: geriatrics, critically ill, trauma, TPN, postpartum
- Emphysematous: high risk gangrene, perforation
choledocholithiasis
common bile duct stone - stones get stuck and and pancreatic enzymes get backed up - pancreas gets angry!
cholangitis
Ascending biliary tract infection due to common bile duct obstruction
- rare but emergent (ICU)
Charcot’s triad: fever, RUQ abdominal pain, and jaundice (look under tounge and in eyes)
Reynolds pentad: Charcot’s triad + AMS and shock
Charcot’s triad
fever, RUQ abdominal pain, and jaundice (look under tounge and in eyes)
Reynolds pentad
Charcot’s triad + AMS (altered mental status) and shock
biliary tract disease - clinical presentation
Acute RUQ pain
- referred to the R scapula or epigastrium
Crampy, colicky pain vs. moderate to severe, unremitting pain
Postprandial pain (fatty food)
Anorexia, N/V, +/- fever
Note: dark urine, light stools, jaundice/pruritus → CBD obstruction
PE:
- RUQ tenderness
- (+) Murphy’s sign (breath in)
- jaundice: CBD obstruction
- jaundice, fever, shock, AMS: cholangitis
biliary tract disease - diagnostic workup
Labs:
- CBC: normal or inc. WBC
- CMP: normal of inc. LFTs, ALP, total bili
- Lipase: inc. lipase (GS pancreatitis)
Imaging:
US Abdomen
- diagnostic study of choice
CT A/P if GS pancreatitis or CBD stone obstruction is suspected
Ancillary studies:
- HIDA, ERCP, MRCP
lipase
tells you health of pancreas
important since pancreatic enzymes are very toxic so need to make sure this is not angry (will release if infected)
biliary tract disease - management
Pain control:
- IV Fentanyl (short-acting) or Dilaudid (longer acting)
- NOTE: Avoid morphine (causes constriction of sphincter of Oddi)
IV Abx
- broad Spectrum ABX to cover Gram (-), Gram (+), and anaerobes
IVF, IV antiemetics
Surgery consult +/- admit to hospital
Cholecystectomy (laparoscopic vs open)
ERCP for choledocholithiasis, cholangitis
HIDA for acalculous cholecystitis
diverticular disease - general and pathophysiology
small herniations (+/- infection) through wall of colon - usually sigmoid colon
common, incidence inc. w/ age, 15-20% develop diverticulitis, 2/3 have uncomplicated disease (tx: high fiber diet)
Pathophysiology:
Diverticulosis: ↑ intraluminal pressures in the colon + weakening of the colon wall → diverticula
Diverticulitis:
Thickened fecal material → erosion of the diverticular wall → inflammation and microperforation → diverticulitis
Complicated diverticulitis: macroperforation, abscess, fistula, peritonitis, sepsis
diverticula
small herniations through the wall of the colon
- usually sigmoid colon
diverticulosis
multiple diverticula
diverticulitis
inflamed or infected diverticula
diverticular disease - clinical presentation
Diverticulosis:
- typically asymptomatic
Diverticulitis:
- LLQ abdominal pain, fever
- LLQ tenderness, tender palpable mass
- RLQ or suprapubic pain → redundant sigmoid colon
- NOTE: peritonitis (rebound and guarding) → perforation
- SERIOUS
diverticular disease - diagnostic workup
Labs:
- CBC: Leukocytosis
- BMP, LFTs, Lipase, UA: r/o other causes
Imaging:
- CT (abd/pelvis): in ER
- PO contrast (Gastrografin): in-patient; swallow contrast and will leak out of holes (takes 3 hrs)
diverticular disease - management of uncomplicated diverticulitis
Bowel rest (liquid diet)
PO Abx x 7-14 days
- Levo/Flagyl or Augmentin
- Colonoscopy after episode subsided
Outpatient f/u with surgery if recurrent episodes
diverticular disease - management of complicated diverticulitis
Admit Bowel rest (liquid diet) - NPO if obstructed (fistula, abscess) IV Abx (broad spectrum) Abscess – IR/CT guided drainage Surgical consult - Perforation or exploration
intestinal obstruction - three types
mechanical
- usually requires surgical intervention
adynamic ileus (paralytic ileus) - surgical intervention uncommon
intestinal pseudo-obstruction (Ogilvie Syndrome)
- surgical intervention uncommon
mechanical obstruction
physical barrier: may be complete or partial
Simple obstruction: blockage of intestinal lumen only, usually one point of blockage
Strangulated obstruction: Blockage of lumen and blood supply, usually two points of blockage (closed loop)
Usually requires surgical intervention
adynamic ileus (paralytic ileus)
Neurogenic failure of peristalsis → Decreased bowel motility and muscular tone
Common: narcotic meds, post-surgery
Surgical intervention uncommon
intestinal pseudo-obstruction (Ogilvie Syndrome)
Colonic dilatation without evidence of a mechanical obstruction
Ileus of large bowel, common in elderly
Surgical intervention uncommon
most common cause of obstruction in:
- small bowel (SBO)
- large bowel (LBO)
- ileus
SBO: adhesions (surgery)
- intussusception caused by neoplasms in adults
LBO: neoplasma
- almost never hernia or adhesions
Ileus: opiates, manipulation of bowel during surgery
intestinal obstruction - clinical presentation
Intermittent, poorly localized, crampy pain
N/V, abdominal distension, decreased bowel movements and/or flatus (passing gas)
PE:
- diffuse abdominal distention/tenderness
- abnormal bowel sounds (high-pitched=SBO, distant or absent sounds=ileus)
- rectal exam: fecal impaction or blood
Peritoneal signs = perforation/ischemia
- cough sign or heel bump sign
Note: more proximal the obstruction = more severe the sxs
peritoneal signs for intestinal obstruction
pain with cough or heel bump = positive peritoneal signs
- indicate perforation or ischemia
intestinal obstruction - diagnostic workup (labs)
Labs: normal in early obstruction
- CBC: Leukocytosis with a left shift
- BMP: inc. hemoglobin and hematocrit, inc. BUM and Cr, abnormal electrolytes (vomit, dehydration)
- venous lactate: increased in strangulation
intestinal obstruction - diagnostic workup (imaging)
abdominal plain films:
- dilated loops of bowel (air-fliud levels, constipation)
- ileus: dilated, fluid filled loops of bowel
CT (abd/pelvis) w/ contrast
- complete vs partial obstruction
- strangulated vs simple
- pneumatosis intestinalis
- pneumoperitoneum: perforation
- “whirl sign”: volvulus
Upper GI series w/ small bowel follow-through
- proximal dilation, collapsed distal bowel
pneumatosis intestinalis
gas in the bowel wall of small or large intestine
- seen on CT
- air bubbles with fecal matter
- emergent surgery!
sigmoid volvulus
Hugely dilated sigmoid that almost fills the entire abdomen
Note the “coffee bean sign” also known as “bent tire tube sign”, extending from the pelvis to the diaphragm
Complete loss of haustral pattern
Disposition: GI consult for endoscopic detorsion
intestinal obstruction - management
Admit to hospital, consult Surgery
- IVF, pain control, NPO
- NG (nasogastric) tube to intermittent suction (if vomiting)
- IV Abx (broad spectrum)
Surgical emergencies:
- Closed-loop obstruction
- bowel necrosis
- cecal volvulus
Ileus: NPO, NGT if vomiting, d/c narcotics, ambulate
Sigmoid volvulus: GI consult for endoscopic detorsion
hernias - general information and locations
protrusion of any viscus from its surrounding tissue walls (i.e. through a fascial defect in abdominal wall)
Anatomical types:
- groin: most common
- inguinal (indirect > direct)
- femoral (prone to strangulation; seen in females) - anterior abdominal wall: incisional, umbilical, epigastric, etc.
inguinal hernias- direct v. indirect
Indirect: abdominal cavity → internal inguinal ring → inguinal canal → into the scrotum
Direct: abdominal cavity → through the posterior inguinal canal wall → inguinal canal
types of hernias
Reducible: hernia contents can be displaced back to their usual position
- hernia sac is soft
Incarcerated: non-reducible by direct pressure (incarcerated tissue may be bowel, omentum, or other abdominal contents)
- hernia is firm
Strangulated: incarcerated with resulting ischemia
- surgical emergency
- hernia sac is hard, tender, indurated, skin changes, peritoneal signs, sepsis (+/-)
hernia - clinical presentation
lump or swelling at hernia site
- size increases with exertion
may be painful/tender
sxs of bowel obstruction = strangulation
hernia - diagnostic workup
Labs:
Normal unless strangulated bowel is present (↑WBC, ↑VL (venous lactate))
Imaging:
- not always needed
- US: identify hernia, doppler to exclude strangulation
- CT A/P: concerned about incarceration and/or strangulation
hernia - management
Reducible: reduce manually under sedation
Incarcerated: try to reduce 1-2 times; observe (abd examinations), if unable to reduce
- consult surgery
Strangulated: surgical consult for emergent repair
- DO NOT try to reduce
- IVF, NPO, IV ABX, IV pain control
Note: surgical repair for definitive treatment
manual hernia reduction in ER
Analgesics and light sedatives administered
Patient in Trendelenburg position
Apply ice or cold compress to the area to reduce swelling/inflammation
Hernia sac is elongated and the contents are compressed in a milking fashion to ease their reduction into the abdomen
Known as “taxis procedure”
ischemic bowel - general information and two types
loss of blood flow to area of bowel due to blockage in artery
mesenteric ischemia: loss of blood flow to small bowel
- emergent
- leads to bowel necrosis
ischemia colitis: loss of blood flow to large bowel
- not emergent
- does not lead to bowel necrosis
mesenteric ischemia - general information, symptoms, treatment
involves superior mesenteric artery -> small bowel
- usually EMBOLIC arterial occlusion
often leads to bowel necrosis
Sxs: sudden onset of severe abd pain out of proportion to exam, ill appearing
Tx: surgical emergency, admit, treat shock
- 50% survival if dx within 24 hrs (poor prognosis)
mesenteric ischemia - risk factors
Age > 60y A-fib CHF hemodialysis hyper coagulable states
- embolus or thrombus in superior mesenteric artery
mesenteric ischemia - clinical presentation
Pain out of proportion to exam
Abdominal distension, absent BS, peritoneal signs, ill appearing
Sudden onset of severe, diffuse, mid to lower abdominal pain
Postprandial pain, gradual onset → thrombotic arterial occlusion
+/- Nausea, vomiting, diarrhea, bloody stool
mesenteric ischemia - diagnostic workup
Labs:
CBC, BMP, venous lactate, ABG, coags
- ↑↑WBC, ARF, ↑lactate, metabolic acidosis
Imaging:
Angiography (CTA or MRA) is diagnostic study of choice
CT A/P + IV contrast to identify additional findings
ischemic colitis - general information, symptoms, treatment
Variant of mesenteric ischemia
- usually involves the inferior mesenteric artery → COLON (splenic flexture)
S/Sx: LLQ pain and tenderness, mild/crampy abd pain, bloody diarrhea
Tx: sigmoidoscopy
- usually transient, 20% need surgical intervention
abdominal aortic aneurysm (AAA) - general information
most lethal pathology if ruptures!!
Thinning of media of aorta (middle layer)
90% infrarenal
- below kidney
Infrarenal aortic diameter
- normal: 2 cm
- aneurysmal: > 3cm
- need repair: > 5cm
Men:Women = 4:1
More common in age >65y
AAA - clinical presentation
most are asymptomatic - become symptomatic when they leak / rupture
Severe, abrupt onset of abdominal or back pain, hypotension, syncope, AMS (lack of cerebral profusion) → Leaking or ruptured
Signs of shock, unstable hypotension
Palpable midline abdominal pulsation or mass
- tender = leaking or ruptured
Periumbilical ecchymosis (Cullen sign) or flank ecchymosis (Grey Turner sign)
AAA - diagnostic workup
Labs:
CBC, BMP, type and cross (get blood ready), coags, VL (venous lactate)
Imaging:
1. plain films 9CXR, AbXR): calcified or bulging aorta
- abdominal U/S: ideal for unstable puts who cannot undergo CT
- CT A/P w. contrast: can see anatomical details of aneurysm and associated hemorrhage b/f surgery
AAA - management
ALL PATIENTS with the clinical triad → emergent eval by a Vascular surgeon
IV access (2 large-bore IV’s), cardiac monitoring, supplemental O2
IVF, +/- blood products, control of VS
- target HR 60-80 bpm
- target BP 100-120 mmHg (permissive hypotension)
Surgical repair: transabdominal approach vs endovascular repair
AAA - clinical triad
abdominal and/or back pain, a pulsatile abdominal mass, and hypotension
- high suspicion of AAA
- emergent eval by a xascular surgeon
post abdominal surgery complications
Fever
Abdominal pain, GI complaints
Wound complications (hematomas)
Drug-therapy related complications
causes of fever - post abdominal surgery
Five W’s
wind: atelectasis (24 hrs) or pneumonia (3-7d)
water: urinary tract infection (2-5 d)
wound: infection (5-10d)
Walking: deep vein thrombosis (since not walking) (4-6d)
- PE (anytime)
Wonder drugs: drug fever, thrombophlebitis (blood clots block veins), C. diff colitis
causes of abdominal pain - post abdominal surgery
Intestinal obstruction - adhesions (takes time to develop) - Ileus Intraabdominal abscess Anastomotic leaks Bowel injury
wound complication - post abdominal surgery
Hematomas – pain, pressure, swelling of the wound, bloody wound drainage
- usually dark blood; worry if bright red blood (something has been nicked)
Seromas – painless swelling below the wound
- gravity dependent
Infection – increasing pain, erythema, swelling, drainage, tenderness at incision site, systemic s/sx of infection
Wound dehiscence – wound ruptures along a surgical suture
drug-therapy related complications - post abdominal surgery
Opiates: constipation, urinary retention
Antibiotics: C. diff colitis
cholecystectomy - common post-surgical complications
Bile leak, bowel injury, pancreatitis, retained CBD (common bile duct) stones, abscess
laparoscopic surgery -common post-surgical complications
Atelectasis, GI tract injuries, bowel injury
colonoscopy - common post-surgical complications
Hemorrhage, perforation, retroperitoneal abscess, volvulus
most important aspect of the evaluation of the patient with abdominal pain in the ED
history
- then serial exam to evaluate how pain changes in ED
- can give pain meds (will not mask all serious pain)
common causes of post-surgical fevers
24 hours: atelectasis, necrotizing fasciitis
72 hours: PNA, UTI
5 days: DVT
7-10 days: wound infections
approach to GI bleed
upper or lower?
- ligament of Treitz separates
- EGD v. colonoscopy (tell GI doc)
sick or not sick
MUST do rectal exam for presence of blood!!
separation of upper and lower GI tract
ligament of Treitz: suspensory ligament of duodenum (b/t duodenum and jejunum)
GI bleed fake-outs
Hematemesis
- Nosebleeds
- Dental bleeding
- Tonsil bleeding
- Red drinks
- Red food
Melena
- Charcoal
- Pepto-bismol
Hematochezia
- Partially digested red grapes
- Red food (beets)
- Vaginal bleeding
- Gross hematuria
False + occult blood testing
- Red meat, turnips, horseradish, vitamin C
clinical signs of liver disease
petechiae, jaundice, spider angiomata
causes of dysphagia (difficulty swallowing)
acute:
Food Impaction
Esophageal Perforation
chronic:
Poorly controlled GERD
Esophagitis
esophageal emergencies: Coin/button battery ingestion Sharp Objects Swallowed FB Narcotic packets
Mallory Weiss tear
Tear of the gastric mucosa from retching
Painless hematemesis from violent vomiting
Self limited
Boerhaave’s
painful, esophageal perforation
what foreign body in esophagus must be removed immediately
button batteries (can burn/perforate in 6 hours)
acute pancreatitis - diagnosis
requires 2 of 3:
- characteristic abdominal pain (severe stabbing epigastric pain or LUQ, radiates to back, begins abruptly, N/V common)
- serum Amylase/Lipase levels > 3x normal
- CT or US findings c/w pancreatitis (rely on labs more than imaging)
Ranson’s Prognostic Criteria for pancreatitis
3 positives = severe disease (helps to determine if sending pt to ICU v. admit)
Admission:
- Age over 55
- Blood sugar > 200 mg/dl
- WBC > 16,000
- AST > 250
- LDH > 350 IU/dl
Test other criteria 48 hours later
anal fissure
tear at rectal sphincter
most common cause of rectal pain
fecal impaction
Bolus of stool sits in rectal vault only allows liquid stool to pass
- commonly misdiagnosed as an obstruction by providers who don’t perform a rectal exam
Treatment:
manual disimpaction, enemas, may require sedation
concerning complaints for vomiting
vomiting plus: blood abd pain headache female diabetes
vomiting plus:
- blood: esophageal varicies, UGI bleed
- abd pain/distention: bowel obstruction
- HA: migraine, inc. ICP (brain bleed)
- Female: pregnant
- Diabetes: DKA, diabetic gastroporesis (slowing of gut)
cyclic vomiting syndrome
idiopathic disorder characterized by recurrent, stereotypical bouts of vomiting with intervening periods of normal health, without organic cause identified
cannabis hyperemesis syndrome
daily vomiting with MJ use
- hot shower makes feel better (clue)
must stop using for 1 month since MJ stays in system to know if cause
pseudomembranous colitis
Membrane like yellowish plaques overlay and replace necrotic intestinal mucosa
- complication of C. Diff
Progression of symptoms to include increasing pain, severe leukocytosis, lactic acidosis, hypovolemia/hypoalbuminemia
pneumonia disposition - criteria for admitting
Hypoxia Immunocompromise Ill Appearing Extremes of age Co morbid diseases Curb-65, PSI
CURB-65
C-confusion U-Urea >7mmol/L R- RR > 30/minute B-B/P <90/60 65-Age >65 years old
criteria to helpt to determine if admit for pneumonia
Ddx for wheeze
all the wheezes is not asthma: Pneumonia Bronchitis Croup COPD CHF PE Allergic reactions FB aspiration
when to intubate and asthmatic in ER and what sedative to use
Absolute indications: Coma and respiratory arrest Otherwise clinical changes suggest need: - Increased work of breathing - Increased PCO2 - decreased PO2 - decreased mental status
Ketamine: good induction agent for asthmatics - bronchodilates
when to admit for acute COPD exacerbations
Note: not every exacerbation requires hospitalization
Criteria for admission: AMS (altered mental state) Co-morbid conditions Inability to eat or sleep due to dyspnea Inability to walk between rooms if previously mobile Social situations Worsening hypoxemia No response to outpatient management
signs of respiratory distress
Tachypnea Tripod posture Use of accessory muscles Diminished breath sounds Altered mental status Hypoventilation Hypoxia Physical exhaustion
when to admit for croup
Persistent hypoxia
Recurrent symptoms after 3 hours
>WOB (stridor at rest, tachypnea, retractions)
>2 rounds of racemic epi
ER levels
Level 1: nearly dead Level 2: sepsis, STEMI Level 3: Level 4: sprained ankle Level 5: pain meds filled
anatomy of penis
vasculature on “dorsal” side (if erect) - opposite urethra
- this is the front of the penis
Must avoid when puncturing / draining - needles in corpora cavernous (2 and 10 o’clock) - priapism
cremasteric reflex
This reflex is elicited by lightly stroking or poking the superior and medial (inner) part of the thigh -normal response is an immediate contraction of the cremaster muscle that pulls up the testis ipsilaterally (on the same side of the body)
- lost in testicular torsion
- 30% of population just does not have normally
