Abdomen Flashcards
PEDIATRIC PRESENTATION
A child between the ages of 6 months and 6 years who ingested a coin, as witnessed by or reported to a caregiver.
Followed by coughing, choking, drooling, refusal to eat, and/or difficulty swallowing.
Initial symptoms are often transient and self-resolving.
Up to 50% of children may have no signs or symptoms of ingestion at all.
ADULT PRESENTATION
Adult patient will typically have a sudden onset of pain or dysphagia during a meal. Often, the patient is an elderly individual who is attempting to swallow inadequately masticated food.
Common symptoms include retrosternal pain, dysphagia, odynophagia, and drooling.
This condition is commonly associated with an underlying pathology in adults, such as strictures, eosinophilic esophagitis, dysmotility disorders, esophageal diverticulum, esophageal web, Schatzki ring, or malignancy
esophageal FB
-80% of all cases are pediatric
-Peds = often objects like coins (MC), toys, pen caps, magnets
-Symptoms: Coughing, choking, drooling, refusal to eat, vomiting, painful swallow
-Possible perforation: Neck swelling, pain, or crepitus
-Possible airway compression by foreign body: Wheezing or stridor
-Adults = Often food impaction (meat) and bones
-Retrosternal chest pain, retching, odono-/dys-phagia, choking, coughing
-PE may include oropharyngeal erythema, neck tenderness, or swelling.
-Possible perforation: Crepitus
-Intentional ingestions are more likely to occur in those with psychiatric disorders, intellectual disability, prisoners, body packers
-Psych and prisoners -> Razors, spoons, etc.
-90% of esophageal foreign bodies will pass through the GI system spontaneously
esophageal FB: Where do objects tend to get stuck?
Cricopharyngeus muscle (C6/T1) (MC peds)
Aortic arch (T4)
GE junction (T11) (MC adults)
esophageal FB: dx
-Diagnostic tests
-History and physical alone are enough to make diagnosis
-Laboratory tests are not often needed in uncomplicated cases
-XR imaging: helpful, but many objects are not radio-opaque
-AP/Lateral soft tissue neck
-AP/Lateral chest xray
-AP/Lateral abdominal xr
-Serial XRAYS for monitoring progression
-CT is preferred for locating small, radiolucent objects or if there is concern for perforation
-Chicken or fish bone
-Small plastic pieces
-Endoscopy = locates / removes the FB, procedure of choice!
diff dx: esophageal FB
Tracheal foreign body
Esophageal spasm- nutcracker
Infectious esophagitis
Pill esophagitis
Reflux esophagitis
Globus pharyngeus (globus sensation)
esophageal FB: when do we do endoscopy
-Urgent GI consult for endoscopy within 4-6 hrs if:
-*Button battery – most dangerous
-Persistent or Severe symptoms (cannot tolerate secretions or airway compromise)
-Multiple magnets, or, single magnet PLUS metallic objects
-> 24 hours without passing the pylorus
-Sharp objects in esophagus that can perforate
-Large size (width>2.5 or length>6 cm)
-Multiple objects
-Coin at the criopharyngeous
-Urgent EGD can be performed within 24 hours in patients without concerning symptoms or history
coin ingestion
-35% asymptomatic
-Trachea = sagittal plane
-Esophagus = frontal plane
-Tx: Endoscopy
-Prior to endoscopy, protect the airway =ET tube
-Asymptomatic= within 24 hours
-Symptomatic (respiratory symptoms, drooling) = emergent
button battery
-TRUE EMERGENCY
-Burns within 4 hours
-Perforation within 6 hours
-XR: “double halo” (sometimes)
-Consult GI for EMERGENT endoscopy
-Start broad spectrum antibiotics
-!Honey can be given at regular intervals to patients with button battery ingestion
-Honey acts by neutralizing the tissue pH, which helps to reduce the severity of tissue damage by the button battery.
-If passed pylorus and asymptomatic can monitor
-Should pass within 2-3 days!
objects pass the pylorus
-2 year old swallowed two nails approximately 4cm in length
-XR showed passed pylorus
-No evidence of perforation
-Opted for medical management
-Successful passing after 4 days
-lets the kid poop it out…if it perforates you need surgery anyways -> wait
esophageal food impaction
-Meat = give time and sedation, often passes spontaneously, do not allow to sit > 12 hours in esophagus
-Treatment options
-!Endoscopic retrieval
-!Glucagon: 0.5-1mg IV relaxes lower esophageal sphincter (side effect: nausea + vomiting)
-Nitroglycerin SL 0.4mg has been described in case reports to resolve impaction in adults
-Nifedipine: 10mg SL reduces lower esophageal tone (caution: hypotension)
-Not recommended:
-Carbonated beverage: gaseous distension to push it down
-Meat tenderizer – causes perforations!
-Consider WHY they had an impaction
-Esophageal dysmotility?
-Anatomic barriers such as schatzkis ring, strictures, malignancy?
disposition for esophageal FB
-Admission
-Those with esophageal foreign bodies and related complications require immediate consultation with a gastroenterologist or surgeon and may need retrieval within 6 hours.
-These patients likely require admission to the operating room or ICU:
-Patients with inability to tolerate oral intake
-Patients with persistent symptoms
-Discharge home
-Patients who pass their foreign body or have removal without complication can be safely discharged home.
-Follow-up with primary care and gastroenterology should be considered in all patients, especially those with food impaction, due to the high rate of underlying pathology.
-Caregivers should have education on home safety and avoidance of high-risk objects.
approach to N/V
-MC in adults: Gastritis, Gastroenteritis, Febrile systemic illness, Drug effects
-MC in peds: Infections
-Expand your differentials past GI
-Alcohol
-Drug toxicities
-Infections – Viral syndromes, Sepsis
-Neuro – brain bleeds, pseudotumor
-Cardiovascular – MI
-Endocrine – DKA
-Pregnancy – Hyperemesis gravidarum
-Vestibular system
-Cancer side effects
-Miscellaneous – Glaucoma, psychiatric, cannabinoid hyperemesis syndrome
key concepts for abdominal pain
-Acute abdominal pain = pain of non traumatic origin for max 5 days
-Abdominal pain accounts for 7-10% of all ED visits in the US
-dx challenge:
-dx of “non-specific abdominal pain” (31%)
-dx of renal colic (31%)
-Conventional plain film is of limited utility as routine investigation
-Only valuable in patients with suspected perforated viscus and LBO
-Surgery begets surgery
-After an appropriate evaluation showing no emergent cause of abdominal pain, a trial of oral intake, a repeat abdominal physical exam … a clear timeline for follow up and strict return to ED precautions should be discussed. Remind the patient that some causes of abdominal pain only reveal themselves in time.
top 5 CANT MISS causes of abdominal pain
-aortic dissection
-ruptured AAA
-mesenteric ischemia
-intestinal obstruction
-perforated viscus
-ectopic pregnancy
-extra-abdominal diseases
-ALWAYS consider a pelvic exam in females, and a testicular exam in males
-ALWAYS consider pulmonary or cardiac cause for upper abdominal pain
general lab eval
-Basic Labs are generally within normal limits
-Lipase =
-Lactate is often elevated in sepsis and bowel ischemia / mesenteric ischemia
-Troponin consideration in epigastric pain
-UA
-Hematuria is found in cystitis, nephrolithiasis, renal vein occlusion, AAA
-Pyuria is found in UTI and sometimes appendicitis
-Pregnancy testing
imaging in abdominal pain
-Plain radiography
-Not generally helpful. Can be a good screening for bowel obstruction, bowel perforation (upright CXR), and radioopaque foreign bodies
-Ultrasound
-Initial study of choice for pregnancy women, suspected AAA (unstable at bedside), gallbladder disease, pediatric appendicitis.
-CT is the study of choice for undifferentiated abdominal pain in patients not expected to have biliary or reproductive disease
-MRI
-Consider in pediatric appendicitis, pregnancy appendicitis
acute abdominal pain management
-Antiemetics for nausea vomiting
-In a pinch: Isopropyl alcohol swabs
-Ondansetron (Zofran) is generally first line
-Metoclopramide (Reglan) with -Benadryl to decrease dystonia risk
-Haloperidol (Haldol) is good for intractable N/V in gastroparesis, cannabinoid hyperemesis syndrome, and acute on chronic abdominal pain
-Topical capsacin : For cannabinoid hyperemesis syndrome or gastroparesis (applied to abdomen)
-Pain control
-Typically patients are kept NPO until sure there is no surgical intervention
-Acetaminophen
-Opioids: morphine, hydromorphone, fentanyl
-Ketorolac (Toradol) is an NSAID, used for renal colic, but not generally due to contraindications if patient goes for surgery
-“GI Cocktail”
-Antacid such as Maalox or Mylanta, viscous lidocaine, and H2 block famotidine
-Treatment for likely dyspepsia and gastritis
abdominal pain the ER
-After a thorough workup, the large majority of discharged patients with abdominal pain of unknown origin are found to have a benign condition and discharged.
-In a retrospective study of discharged ED patients with abdominal pain, only 7.9% re-presented with abdominal pain, and 76% of these patients were once again given the same diagnosis of non-specific abdominal pain
acute abdomen
-Acute abdomen = urgent attention and treatment
-Often due to: infection, inflammation, ischemia, obstruction, free air
-ILL-APPEARING
-Peritoneal signs: rigid abdomen, guarding, rebound, absent bowel sounds
-Diagnosing a patient with a full-blown acute abdomen is easy!!!
-It’s the early presentations that are hard to detect
CL is a 71M hx HLD, squamous cell CA of tonsil diagnosed 11/12/18, admitted 11/20-11/30/18 from ENT clinic for oncology workup and PEG tube placement on 11/26, BIBEMS from home for severe abdominal pain on attempted use of PEG tube. The last time it was used normally was yesterday morning (12/1). Around 4pm today, a helper at home tried to push water and then tube feed through the tube, but it caused excruciating pain. Patient also endorses nausea but no vomiting. Has been passing gas but has not had a bowel movement in a few days. Currently has LUQ abdominal pain that is non-radiating and severe. +Nausea without emesis.
What do you want to do based off the information so far?
Moved to monitored area, 2 large bore IV placed, fluids given, pain control given
Physical exam:
General: Cachetic, NAD, A&Ox3
HEENT: Normocephalic, non-icteric sclera, normal ROM of neck/supple
CV: RRR, normal heart sounds without murmur
Pulm: Crackles in LLL, diminished on right side. Effort normal, no distress, no stridor, no wheezing.
Abdomen: Generalized tenderness. Rigidity. Guarding. Rebound. PEG tube in place. No surrounding erythema/induration around site. No distension.
Skin: Warm and dry without noted rash. Extremities without edema
-PERFORATED VISCUS
perforated viscus
-causes: inflammation, ulceration, trauma, obstruction
-leads to peritonitis -> life threatening
-anywhere from stomach to the rectum
-Extremely dangerous!
-Peritoneum does not like air
-Peritoneum does not like gut microbes -> sepsis
-Typical presentation:
-!!Abrupt, severe pain
-↑ HR, ↓ BP, ± fever
-Exam: Distress w/ peritoneal signs
-!Rigidity
-!Pain to light palpation
-!Involuntary guarding
-sepsis/shock
-ill appearing
-early -> focal tenderness
-late -> Peritoneal signs, laying still (shake the bed, jump), difuse tenderness and rigidity, rebound and guarding
causes of perforated viscus
-perforated peptic ulcer -MC
-NSAIDs, smoking, ETOH use, gastritis
-hematemesis, melena, hematochezia
-local inflammation
-appendicitis, diverticulitis!!!!, crohns, etc.
-post-instrumentation
-colonoscopy, postop, PEG, foreign body
-bowel perforation/ischemia
-prior abdominal surgery, SBO, cancer
perforated viscus: labs
-Labs will not dx
-Pre operative labs
-Urine hcg
-Lactic acid level
-xray:
-Peritoneal air under diaphragm in upright CXR
-Lateral decubitus -> free air between liver edge and wall
-False neg -> If minimal air, might miss it
-Limitations -> doesnt tell us WHERE
-CT abdomen pelvis
-Both sensitive & specific for free air
-Can localize the perforation
-Evaluates for other cause of pain
-Limitations -> Requires pt to be stable
-Limitations -> Needs IV contrast and if time permits, water soluble PO contrast
left lateral decubitis
-perforated viscus
CT shows free air
perforated viscus: tx
-Resus, Resus, Resus
-2 large bore IV
-Get blood products ready
-NPO, IVF
-Broad spectrum antibiotics
-Definitive treatment is surgical repair
56yoF PMHx HLD, Obesity, PSHx appendectomy, cholecystectomy, tubal ligation, cervical conization, presents with complaint of RLQ pain x 1 week. Seen on 1 week ago for mid-abdominal pain, and diagnosed with UTI and given macrobid (culture shows appropriate sensitivity) +Constipation x 3 days but is passing flatus.
Denies fevers, chills, nausea, vomiting, change in appetite, chest pain, SOB, dysuria/frequency/urgency/foul smell.
BP 119/71 | Pulse 90 | Temp 97.3 °F (36.3 °C) (Skin) | Resp 18 | LMP 09/11/2013 (Approximate) | SpO2 99%
A&Ox3, NAD, CTAB no WRR, RRR no MRG, warm extremities
Abdomen: Soft, non-distended. +Exquisitely tender RLQ without rebound or guarding.
apendicitis
appendicitis stats
-Lifetime risk of appendicitis is 7-8%
-70% of cases occur in people <30 years old
-Missed appendicitis in the leading source of malpractice suits in adults with abdominal pain
-There is no individual sign or symptom that can reliably exclude appendicitis in any patient
-Lack of distress, no rebound/guarding, or having diarrhea are not reasons enough to exclude appendicitis
appendicitis sx
-!!!Periumbilical or epigastric pain initially
-Due to lumen distension which triggers VISCERAL pain fibers
-4-48 hours later the pain migrates to the RLQ
-Due to somatic pain fiber innervation
-Other classic findings:
-!Fever (low grade)
-Nausea, !vomiting (typically after pain started!!!!)!*- GASTRITIS IS BEFORE
-!Loss of appetite (anorexia)
-Pain !worsens with abdominal movement!
-CHILDREN: Diarrhea, Limp, Anorexia, nausea
-ELDERLY: late presentation masking of VS
appendicitis atypical sx
-Retrocecal appendix -> right flank / low back
-Retroileal appendix -> testicle, suprapubic area, or cause dysuria
-Low appendix -> left sided or rectal pain
-Appendicitis in pregnancy -> RLQ or RUQ pain
-Occurs due to enlarged uterus during pregnancy displacing the appendix
-RLQ is still MC
-Sudden significant increase in pain (and possibly a decreased in pain later on) in perforation
appendicitis PE
-Tenderness to palpation in the RLQ
-Special manuevers
-McBurney’s point
-Rovsing sign
-Psoas sign
-Obturator sign
-Involuntary guarding*
-Rebound tenderness
-Fever
-If the peritoneum is affected
-the child will often be laying still
-Rebound tenderness
-Involuntary guarding
appendicitis dx
-XRAY- not useful
-US:
-About 86% sensitive
-No radiation
-1st choice in children or pregnancy
-Obesity, bowel gas, perforation make it less sensitive
-Look for: !Thick, non-compressible appendix ≥6mm in diameter, or >2mm wall thickness!
-CTAP w/ IV contrast
-Most sensitive & specific
-Eval for DDX
-Will need oral contrast in low BMI pts
-Findings: !thickened appendix >7mm diameter, mural enhancement, stranding!
-Perforation will have periappendicial fluid or air
-MRI:
-Used to confirm in pregnancy if ultrasound was non-confirmatory
(non-contrast study, IV gadolinium is toxic to fetus)
appendicitis
appendicitis tx
-NPO with maintenance IVF
-Antiemetics, Antipyretics/Analgesia as appropriate
-Antibiotics with Gram +, Gram -, anaerobes coverage
-Combination therapy: Ceftriaxone + metronidazole
-If perforated (peritonitis), cover pseudomonas and ecoli
-Piperacillin-tazobactam (Zosyn) 4.5g IV q6h as a single agent
-General surgery consult for appendectomy
-If perforated or abscess -> Delayed appendectomy or percutaneous drainage
-In children, reasonable to admit for serial exams for patients in whom early appendicitis is suspected and imaging is non-diagnostic.
what is the best imaging modality that can be used in pregnant pts presenting with signs of appendicitis
-endoscopy
-MRI w/o contrast!!!!!!!!!!
-plain abdominal film
-CT scan
-MRI with contrast
History– This patient had surgery 2 days prior to these images for a ruptured appendix.
Symptoms– Vague abdominal pain, low-grade fever (37.9C), Not passing flatus or stool for 2 days.
Physical– The abdomen was mildly distended. The laparoscopic access sites were normal. There was a paucity of bowel gas sounds. No focal tenderness, guarding or rebound.
ILEUS
ileus
-NO normal peristalsis w/o mechanical obstruction
-Continuous pain, distention, decreased bowel sounds, minimal or no tenderness, no flatus/BM, usually self limited
-MC than obstructions post op!
-XRAY will show dilated fluid filled loops throughout entire bowel (small and large) that are persistent over time
-Many causes (MC post-op) including when there is adjacent pathology: pancreatitis, appendicitis, abscess, medications, lyte abnl
-Mostly supportive care, gastric decompression for relief, IVF
bowel obstruction
-bowel dilation from blockage -> increase intraluminal pressure -> compromised blood flow to bowel wall -> edema and transudation of fluid into the lumen -> compromised arterial flow leads to ischemia and gangrene -> eventually perforation
-partial obstruction = ileus
causes of SBO
-Adhesions (#1 cause)
-Hernia (#1 cause w/o PSH)
-Neoplasm
-Strictures
-Intussusception
-IBD
SBO hx and PE
-History of abdominal surgery*
-Crampy Abdominal pain, colicky
-Nausea, Vomiting
-↓ Flatus = ↑ distension
-Early diarrhea, late constipation or obstipation
-Physical
-Dehydration -> hypotensive and tachycardic
-Distended
-Tympanic to percussion
-Initially hyperactive BS, late is hypoactive BS
-If perforated: peritoneal signs and sepsis
-Look for hernias esp testicular
SBO dx
-Labs (pre-op)
-CBC
-CMP + lipase + mag
-T&S, Coags
-VBG
-↑ Lactate supports strangulation
-Acidosis in bowel infarct
-Plain upright CXR
-Air under the diaphragm can indicate perforation
-Upright abdominal XR
-!Air fluid levels in dilated loops
-These can be seen in ileus too
-String of pearls
-Plicae circulares =
Valvular coniventes
-Supine abdominal XR
-Distended loops of bowel >3cm
-In complete obstruction, no gas in rectum
-CTAP is way more sensitive for obstruction (and perforation)
-Find transition point
-May see pneumatosis intestinalis
SBO
SBO
what do you think the MC metabolic derangement is in early SBO
Metabolic alkalosis
Metabolic acidosis
Respiratory alkalosis
Respiratory acidosis
Answer:
Hypochloremic hypokalemic metabolic alkalosis
At least until bowel infarcts, then acidosis occurs
LBO
-Typically in older pts (73 avg)
-Causes:
-Colorectal malignancy (MC,50%)
-Volvulus
-Diverticulitis
-Strictures from IBD
-Hernia w/ incarceration
-Adhesions
-Rare causes: ischemia, adhesions, intussusception
Dilated loops of small bowel and large bowel to the region of the splenic flexure on the erect projection. Air-fluid level in the region of the distal transverse colon on the erect projection.The distal large bowel is collapsed. No free gas or pneumotosis. No bony mets seen.
volvulus
-Obstruction from !twisting or looping! of the bowel
-Same complications as SBO and mesenteric: infarction, perforation, infection [e.g. peritonitis]
-Types:
-SIGMOID (MC)
-CECAL
-MIDGUT (infants)
what is the imaging modality of choice in the eval of bowel obstruction
CT scan!!!!!!!!
MRI
Plain x-ray radiograph
Colonoscopy
Ultrasound
65yoM with a history of paroxysmal atrial fibrillation, peripheral vascular disease, and HTN presents to the ED with diffuse abdominal pain.
The pain started after dinner last night and has progressed since with nausea and emesis.
He’s previously had these symptoms after eating, but they have usually resolve.
The patient is not currently on any anticoagulation but takes HCTZ-lisinopril. Social history pertinent for 48 ppy tobacco use. ROS pertinent for noted blood in stool.
Vitals: HR 112, BP 98/61, RR 22, T 101.1, SpO2 98% on RA
General: Older male, in mild distress;
CV: Tachycardic, irregularly irregular, no murmur, 2+ pulses in UE, 1+ in LE BL;
Abdomen: Diminished BS, extremely tender diffusely with light palpation;
Skin: Lower extremities without hair;
Rectal: Bloody stool
What do you need to consider, and what’s the next step in your evaluation and treatment?
CT angiography = demonstrated an embolus in his superior mesenteric artery and bowel wall thickening.
IV fluids, antibiotics, and heparin, but still has pain.
OR = exploratory laparotomy. Surgeons note a segment of small intestine that appears ischemic, but no necrosis. The clot from the superior mesenteric artery is removed and the bowel is re-evaluated. The segment of bowel that was ischemic in appearance is now pink.
Your patient has an uncomplicated post-op recovery and is thankful that your early diagnosis of mesenteric ischemia saved him from having any bowel resected.
mesenteric ischemia
-low incidence (0.09%)
-high mortality rate in first 24hrs - 60-80%
-decreased blood flow to bowel can be chronic or acute
-acute- sudden decreased perfusion
-chronic- episodic with digestion (d/t atherosclerosis of mesentery)
-poor perfusion -> ischemia -> infarction/necrosis -> bacterial translocation + possible perforation
mesenteric ischemic: etiologies
-ACUTE MESENTERIC ARTERIAL EMBOLUS (~40-50%)!
-Atrial fibrillation!
-Endocarditis
-MESENTERIC ARTERIAL THROMBOSIS (20-35%)!
-Kind of “myocardial infarction” of the gut from previous atherosclerosis
-NON-OCCLUSIVE (5-15%)
-Low perfusion states!: Hypotension, dehydration, shock, hemorrhage, CHF
-Vasopressor use
-MESENTERIC VENOUS THROMBOSIS (5-15%)
-Hypercoagulable! states: OCPs, Anti-thrombin III, protein C/S def, Factor V Leiden
mesenteric ischemia S&S
-History depends on underlying cause
-Historic triad in embolism:
-!!Severe sudden diffuse abdominal pain
-!N/V
-± GI bleeding or diarrhea
-Hx of cardiovascular dz
-Chronic mesenteric ischemia
-Post-prandial abd pain (30-60 minutes after a meal)
-Food avoidance
-Mesenteric Venous thrombosis
-More gradual symptom onset
-Physical
-Early VS normal, can progress to hypotension, tachycardia, fever
-!Pain out of proportion to exam
-Soft abdomen!- Peritoneal signs: Distension / Guarding / rebound once infarcted
-Signs of PVD
-CV: Murmur if endocarditis
-CV: Irregularly irregular if afib
-Rectal: ± guaiac positive
mesenteric ischemia Dx
-ECG looking for cause
-Labs -ECG, CBC (WBC 25+), CMP, Blood gas (↑ Lactate, lactic acidosis)
-!CT angiography (speak to radiologist for protocol)
-May see abrupt termination of the vessel (cutoff sign) or filing defects
-Early bowel findings are non-specific: ascites, bowel wall thickening, edema
-Late: portal gas (pneumatosis portalis), free air (pneumoperitoneum occurs when the bowel perforates secondary to ishcemia), intramural bowel gas (intestinal pneumatosis)
pneumatosis intestinalis in mesenteric ischemia
mesenteric ishemia
-mesenteric ischemia
-portal gas
-Dilated loops of bowel with thickened, less contrasted, walls seen in ischemic bowel
mesenteric ischemia tx
-NPO, fluids, analgesics, bowel rest
-Broad spectrum antibiotics (ceftriaxone+flagyl, or, zosyn)
-If venous thrombosis, consider starting heparin
-Early surgical consultation
-Possible IR for mesenteric angiogram w/ thrombectomy
-Possible stenting
-Open surgery to bypass the obstruction and remove dead bowel
A 71-year-old female presents to her primary care physician with a four-day history of left lower quadrant abdominal pain. The patient also complains of diarrhea and mild nausea. She continues to tolerate a diet, though reduced in quantity. On exam, her vitals are T 101F HR 86, BP 130/92, RR 15, and SaO2 100%. Abdominal exam is notable for LLQ tenderness to palpation without rebound or guarding. Urine dipstick is normal and complete blood count shows a minor leukocytosis with a left shift. A screening colonoscopy from a year ago is shown. What is the next best step in management?
-Immediate colonoscopy
-Trimethoprim-sulfamethoxazole and a liquid diet
-Abdominal CT with IV contrast
-CTA of the mesenteric vessels
-Laparotomy and surgical management
-Abdominal CT with IV contrast
diverticular disease
-Most patients with DIVERTICULOSIS will be asymptomatic
-5-15% will have painless diverticular bleeding
-4% will develop diverticulitis
-Diverticulitis
-!Abdominal Pain - LLQ
-Can refer to lower back, or cause UTI symptoms
-Localized guarding, rigidity and rebound tenderness
-!± Fever
-± Nausea, vomiting
-!Change in bowel habits (diarrhea or constipation, or altering)
-5% of diverticulitis cases become complicated:
-Perforation, obstruction, abscess formation, fistula
-Dx: !!CT abdomen pelvis with IV contrast may show thickened bowel wall
diverticulitis tx
-Acute, uncomplicated diverticulitis in a patient with a history of diverticulitis, or CT-demonstrated first episode of acute, uncomplicated diverticulitis:
-Analgesia
-Stool softeners
-Consider oral antibiotics for 10-14 days:
-Ciprofloxacin (500 mg oral, BID) + Metronidazole (500 mg oral, TID)
-Amoxicillin-Clavulanate (875 mg oral, twice daily)
-Moxifloxacin (400 mg oral, daily)
-Follow up colonoscopy
-A toxic patient with radiographic, or CT evidence of complicated diverticulitis:
-Fluid resuscitation
-Analgesia
-Surgery consult
-IV antibiotics:
-Piperacillin-tazobactam (3.375 – 4.5 g IV q 6h)
-Imipenem-cilastatin (500 mg IV every 6 hours)
-Levofloxacin (500 mg IV every 24 hours) + metronidazole (500 mg IV every 8 hours)
-Ceftriaxone (1 g IV every 24 hours) + metronidazole (500 mg IV every 8 hours)
-Admission to hospital
You are working in the emergency room when a patient is brought to your resuscitation room. Per the triage nurse, patient is a 55 year old male who was reporting low back pain and collapsed in triage.
BP 65/40, HR 160, RR 14, O2 sat unknown, Temp 37.1C
Pulse ox ; not reading, poor waveform
Decreased LOC
2 large bore IV with 2L saline
ECG revealed sinus tachycardia
Bedside ultrasound showed 8cm AAA
Call vascular surgery team for likely ruptured AAA
2U PRBCs of O- blood
T&S and 6U blood ordered
Straight to OR
AAA
-causes 15,000 deaths in U.S. annually
-Common cause of sudden death men >65 years old
-Mortality rate with ruptured AAA 90%
-Pts with ruptured AAA do not survive to reach the hospital 50%
-Mortality rate elective open operative repair 2-7%
-Frequently missed or delayed dx
-MC misdiagnosed as left sided renal colic, Diverticulitis, MSK pain
-Reasonable indications include all patients >50 years old with unexplained hypotension, dizziness, syncope, cardiac arrest
-Reasonable to consider in all elderly patients with back, flank or groin pain
AAA: anatomy
-AAA is a dilation of all 3 layers of the aortic wall to more than 50% normal diameter
-Normal aorta ~2cm diameter
-Abdominal aorta >3cm is considered a AAA
-MC rupture site: retroperitoneum
-MC rupture site: Infra-renal
-Risk of rupture increases once the AAA >5cm
-Can be fusiform in shape (more common) or Saccular (pedunculated)
AAA: RF
-Smoking** current smokers have a 7x higher chance to develop AAA
-Male > female
-Increased age >50
-Family history (8x increased risk)
-Secondary causes: obesity, HTN, HLD, atherosclerosis, cardiovascular disease , PVD
Which of the following factors does NOT increase the risk for developing an abdominal aortic aneurysm?
Former smoker
Positive family history of aortic aneurysm
Age older than 60
Presence of peripheral arterial disease
Being female!!!!!!!!!!!
AAA: S&S
-ASYMPTOMATIC > 50% Incidental finding -> Require referral
-MC symptom “PAIN”
-!!!ABDOMEN (80%) BACK & FLANK (60%), OR GROIN (22%)
-Classic Triad (only occurs in <50%)
-!Abdominal/back pain + Hypotension + Pulsatile abdominal mass!!
-Rupture can cause syncope alone (rare)
-Non-specific symptoms -> Lightheadedness or dizziness, Sweating, Clammy skin
-Rarely can find pulse deficit, or lower limb ischemia
AAA: workup
-ABCs – especially the circulation!
-Sudden severe blood loss will need transfusion protocol
-Physical exam
-Feel for PALPABLE AORTA
-Sometimes can see retroperitoneal bleeding
-Cullens sign: peri umbilical ecchymosis
-Grey-turner sign: flank ecchymosis
-Ultrasound or other imaging
AAA: unstable? -> US
-Dx test of choice in an UNSTABLE patient – CALL SURGERY
-2013 review in Academic EM shows that bedside US for AAA done by EM physicians have a sensitivity of >97.5% and specificity of >94.1%
-Visualize dilated aorta
-!Cannot distinguish if ruptured since blood goes into retroperitoneal space
-!Cannot detect dissection
-Measure from outside wall to outside wall
-This avoids measuring a false lumen d/ intramural thrombus
-Limitations: Obesity or overlying bowel gas
AAA: CT
-100% sensitivity
-Can tell you where the rupture is and other vessels involved
-Limitations: Patient must be stable, better w/ IV contrast
What is the best imaging modality for the evaluation of a possible abdominal aortic aneurysm in a patient with hemodynamic compromise?
Upright chest film
Non-contrast CT imaging
Contrast CT imaging
Bedside ultrasound
Plain abdominal film
AAA screenings
-Normal aorta < 3cm
-AAA = >3 cm
-!!AAAs between 3cm - 5 cm that are asymptomatic
-Usually monitored with serial ultrasound examinations
-!AAAs > 5 cm
-Repaired with open surgery or endovascular repair
-No proven lifestyle changes can decrease the size of AAAs.
AAA: tx
-Surgical consultation
-As soon as you suspect it, do not delay
-Cannot fix this in the ER
-Two large bore Ivs
-Type and cross
-Permissive hypotension (SBP>90) may have better outcomes
-EKG and Pre-op labs
-Assess for other causes
-UNRUPTURED:
-3-5 cm are less likely to rupture, outpatient follow up -> Surveillance
->5cm require urgent referral to vascular surgeon within 3-5 days -> Elective repair
-Smoking cessation
-B-blockers
-Antihyperlipid agents
-Low dose ASA
-RUPTURED:
-Resuscitate, resuscitate, resuscitate
-2 large bore IV or a central line
-1-2L crystalloids
-2 units of uncross-matched blood
-(while T&S pending as pt will likely need massive transfusion protocol with FFP, PLT, pRBCs)
-Immediate consult with vascular surgeon for surgery -> Endovascular vs. open repair
What is the best initial step for a ruptured AAA?
Transfuse properly typed and cross-matched blood
Allow permissive hypotension
Hydrate the patient
Assess for other causes of symptoms
Immediate surgical consultation!!!!!!!
40 year old female G6P6 with no PMH, moderately obese, presents to the ER with 1 day history of constant epigastric and RUQ pain. Rated 7/10. Began after her dinner last night. Also reports pain in her right scapula. She feels nauseous and has vomited twice. She had 2 similar episodes in the last year that self-resolved within an hour. Both times occurred after eating spicy food.
Temp 100.0F | HR 110 | BP 120/80mmHg | RR 18 | SPO2 100%
Exam notable for RUQ tenderness
WBC 14 (normal 4-10.9)
Total bilirubin 1.0mg/dL (normal 0.1-1.2)
ALP 70 (normal 33-131)
Lipase 30 (normal 7-60)
Troponin <0.1
ECG sinus tachycardia
CXR without lower PNA
U/A negative
HCG negative
+Murphys sign
Fever
Tachycardia
Leukocytosis
Dx…acute cholecystitis!
Why not choledocholithiasis or cholangitis?
Well appearing, normal T bilirubin and ALP makes this less likely
Why not gallstone pancreatitis?
Normal lipase/amylase makes this less
cholecystitis
-History/Symptoms
-Fat, female, fertile, forty
-History of postprandial pain in RUQ
->6 hours pain in RUQ
-± Kehr’s sign
-Nausea, vomiting
-Signs/PE findings
-Fever
-RUQ TTP
-Murphy’s sign
-Voluntary guarding
what is cholecytitis
Calcification of the gallbladder
Inflammation of the gallbladder
Obstruction of the biliary ductal system
Presence of gallbladder stones
Presence of bile sludge
cholecystitis workup
-Pre-op abdominal labs
-CBC for ↑ WBC
-LFTS usually have ↑ ALP
-But normal ALT/bilirubin (unless Mirizzi syndrome)
-Amylase, lipase to assess for evidence of pancreatitis
-U/A for renal pathology
-BHCG for tubo-ovarian pathology
-!!!1st line imaging: Ultrasound
-HIDA if non-diagnostic
-CTAP if complication suspected
-US:
-Gallstone w/ shadowing
-Pericholecystic fluid
-Thickened GB wall >3mm
-Sonographic murphys sign
-GB distension (diameter >5cm, length >10cm)
if dilated CBD, consider choledocholithiasis
-Supportive care:
-IVF, analgesic, anti-emetics, NPO, antibiotics if fever/WBC
In evaluating patients with biliary disease using an ultrasound, what classic finding suggests cholelithiasis?
Gallbladder wall thickening
Common bile duct dilatation
Pericholecystic fluid
Echogenic focus with acoustic shadowing
Intrahepatic duct dilatation
management of cholelithiasis
-pain and symptom control
-outpatient surgery referral
-admission if unable to control symptoms
management of cholecystitis
-pain and symptom control
-bowel rest
-IV antibiotics (pip-tazo)
-surgery- lap cholecystectomy, open chole, or cholecystostomy
choledocholithiasis
-Gallstone in the CBD
-Similar symptoms to cholelithiasis:
-RUQ pain, post-prandial, ± radiation, nausea, vomiting
-!!AND Signs of extrahepatic cholestasis:
-Jaundice & pruritis
-Pale stool / dark urine
40yoF with 24 hours of RUQ pain and epigastric pain, associated with nausea and vomiting. Report similar pain the past, particularly after eating greasy foods. According to her family, over the last few hours, she had become slightly confused. PMH is negative.
Temp 102.5F, HR 110bpm, RR 16/min, BP 90/60mmHg.
She is moderately tender in the RUQ to deep palpation.
She has slight scleral icterus.
She has dark colored urine.
WBC 15 (normal 4-10.9)
Bilirubin 4 (normal 0.1-1.2)
ALP 350 (33-131)
AST 300 (5-35)
ALT 280 (7-56)
GGT 330 (8-88)
Amylase 100 (30-110)
Lipase 90 (10-140)
Urine +bilirubin
Ultrasound:
- Bile duct dilation without stone
Obstructive jaundice!
Any condition which causes occlusion of the biliary tree has the potential to cause cholangitis.
Cholecystitis, choledocholithiasis, gallstone pancreatitis
Viral hepatitis
Mirizzi syndrome
Liver abscess
ascending cholangitis
-MCC:
-Gallstones, ERCP, Cholangiocarcinoma
-!!Charcots triad
-RUQ Pain, fever, jaundice
-Reynolds pentad
-!!Above + confusion (AMS) and shock (hypotension)
-Pre-op abdominal labs should be taken
-CBC will have ↑ WBC
-LFTs will have ↑ ALP, ALT/AST, GGT, bilirubin
-Blood cultures in suspected cases
-Initial investigation: U/S with dilated CBD
-Low sensitivity initial stages
-Low sensitivity for stones
-Gold standard: ERCP
ascending cholangitis management
-Immediate management
-IVF, NPO
-Early Broad-spectrum IV Antibiotics
-Vasopressors if unstable
-Definitive tx: Remove the obstruction
-!ERCP (suction vs. stent)
-Percutaneous cholecystostomy (PTC) if cannot tolerate ERCP
-Call critical care + surgery
-Prevent recurrence! -> Delayed cholecystectomy
which of the following is NOT a typical laboratory finding in cholangitis
Elevated sodium
Elevated alkaline phosphatase
Hyperbilirubinemia
Elevated transaminases
pancreatitis causes
-!!!MC causes: Gallstone, ETOH, ↑ Triglycerides
-Post ERCP, trauma
-Obstructive biliary sludge or tumors
-Drugs: Thiazides, estrogens, salicylates, Tylenol, antibiotics
-Metabolic: HLD, hypercalcemia, DKA, uremia
-Viral / Autoimmune: Mumps, coxsackie B, hepatitis, EBV, adenovirus
-Bacterial: Salmonella, Strep, Myco, legionella
-Scorpion stings
pancreatitis dx
-Labs
-LIPASE is the best
-Amylase
-Imaging
-CT is best
-Ranson’s Criteria on admission:
-Age >55
-Glucose >200
-WBC>16k
-ALT >250
-LDH>350
-3 positives = severe, ICU
65-year-old male with history of liver cirrhosis is brought to the ED for AMS.
Temp 37.4°C (99.3°F), HR 98, BP 113/72, SpO2 92%, RR 20.
He is alert but mildly confused. He has a distended abdomen but denies any tenderness. He has mild asterixis on exam. You wonder if his worsening clinical status could be secondary to hepatic encephalopathy or spontaneous bacterial peritonitis (SBP).
cirrhosis
-Despite not having the classic triad of SBP, a diagnostic paracentesis was performed
A cell count, gram stain and culture was sent
Cell count returned at 297 cells/mm3
You ordered 2g cefotaxime IV and admit the patient to the hospital
hepatic encephalopathy
-Precipitating factors: “LIVER”
-Librium, Infection, Volume loss, Electrolyte d/o, RBCs in gut
-Can also be high protein diet or worsening liver function
-Early signs are sleep inversion -> sleep during day, awake at night
-Asterixis
-Hyperammonia levels
-Check for hypoglycemia
-Treatment: Lactulose, low protein diet
spontaneous bacterial peritonitis
-Life threatening infection that occurs in chronic liver dz or !cirrhotic patients!
-Portal hypertension -> bowel edema -> transmigration of enteric organisms such as e coli or enterococcus
-Classic triad uncommon:
-Fever/chills, abd pain, increasing ascites
-Consider in any patient with ascites AND hepatic encephalopathy, worsening ascites, abdominal pain, fever, leukocytosis, renal failure
-Often generalized abdominal tenderness w/ ascites
-“Masked” peritoneal signs
-Serum blood tests generally not helpful (CBC, ESR, CRP)
-Diagnostic paracentesis*
-Neutrophil count >250 cells/mm³
-+ Gram stain
-Treatment with 3rd gen cephalosporin (CEFOTAXIME)
-Consider adding albumin
approach to critical pt with GI bleed
-AIRWAY:
-Consider intubation for: airway protection, aspiration risk, AMS, or need for further evaluation such as endoscopy or balloon tamponade device
-PPE: Face shield, goggles, mask
-Head up position to prevent aspiration
-2 suction tip catheters
-BREATHING:
-avoid positive pressure ventilation prior to intubation (risk of gastric insufflation)
-CIRCULATION:
-2 large bore Ivs or a large central venous catheter
-Maintain MAP > 65 mm Hg
-Consider massive transfusion protocol (1:1:1 pRBC:FFP:Platelets)
-Consider reversal agents for bleeding if on AC/Anti-platelet
-If variceal bleed suspected, administer:
-Octreotide and antibiotic (ceftriaxone)
-Consider Blakemore tube if endoscopy not immediately available
-DISABILITY:
-Assess GCS as another reason to intubate (hepatic encephalopathy, hypotension, instability)
GI bleed: upper vs lower
-UPPER- proximal to ligament of treitz
-HEMATEMESIS
-COFFEE GROUND EMESIS
-Digested blood, think epistaxis
-MELENA-Black tar-like sticky stools that smell bad, black from digestion
-BRBPR- If brisk UGIB - bright red blood per rectum
-LOWER- distal to ligament of treitz
-HEMATOCHEZIA (90% LGIB)
-Maroon blood mixed with stool (transverse colon or proximal)
-Bright red from anus, rectum, sigmoid
-Rarely from rapid UGIB
-BRBPR
55 year old male with a history of alcoholic liver cirrhosis presents with complaints of weakness, dizziness, syncope, coffee-ground emesis, black tarry stools for two days.
upper GI
causes of upper GI bleed
-Proximal- Epistaxis
-Esophagus
-Esophagitis (common in pregnancy)
-!Mallory Weiss tear
-!Esophageal varices * highest morbidity
-Stomach & duodenum
-!Gastritis / GERD
-Gastric varices
-!Peptic ulcer disease is MC
-Duodenitis
-Aortoenteric fistula
-differentials: nosebleed, hemoptysis, dental bleeding
upper GI bleed hx
-Ask how many episodes of bleeding, and how much blood?
-Ask about liver cirrhosis, alcohol abuse, hepatitis, peptic ulcers, NSAID use, anticoagulation, recent surgical history (fistulas)
-Ask about
-Abdominal pain -> PUD perforation?
-Vomiting -> Mallory Weiss tear?
-PUD -> hx of pain related to eating
-Chronic bleeds -> lightheadedness, fatigue, chest pain, DOE, SOB
-Dizzy/Syncope -> elderly tend to have pre/syncope or AMS in anemiae
eval for UGIB
-Physical exam
-Look for jaundice, scleral icterus, abdominal distension, hematemesis, positive stool guaiac or obvious melena on exam
-Vitals vitals vitals
-Diagnostic tests
-CBC for Hgb level (not an assessment of real-time blood loss)
-Coagulation panel
-CMP: Look for AKI and LFTs
-Lactate to guide therapeutic considerations
-Type and screen and cross match.
-ECG and troponin screening
-± Chest x-ray for perforated viscus
-± CT angiography for continued bleeding
UGIB management
-ABCs
-Administer isotonic crystalloid fluids
-Administer PPI
-Reduces rebleeding and surgical intervention in PUD
-Usually, a bolus followed by a continuous infusion
-Administer blood products as necessary
-Transfusion goal hemoglobin >7g/dL (consider >8 if CAD)
esophageal varices
-OCTREOTIDE (somatostatin)
-Decreases rate of bleeding and incidence of rebleeding
-Decreases portal hypertension -> decreases mortality
-50mg/hr for 72 hours
-Complications: hypoglycemia, hyperglycemia, thrombocytopenia
-PPI and broad spectrum antibiotics
-Emergent control of bleeding:
-!!BALLOON TAMPONADE: Sengstaken-Blakemore, Minnesota
-Complications: sepsis, perforation, 65% rebleed rate
-Deferred management:
-Endoscopic variceal ligation
-TIPS procedure
Balloon tamponade devices
-Indication: The uncontrolled hemorrhage from esophageal or gastric variceal bleeding after medical or endoscopic treatment fails, is not available, or is not technically possible
-These are temporary measures because of frequent rebleeding after deflation
-Contraindications:
-Unprotected airway
-Esophageal rupture (Boerhaave’s syndrome)
-Esophageal stricture
-Uncertainty of bleeding site
-Well-controlled variceal bleeding
A 65-year-old patient presents to the ED with several days of left-lower quadrant abdominal pain and an episode of painless bright red rectal bleeding that occurred 3 hours prior to her presentation. She is currently taking warfarin for a history of paroxysmal atrial fibrillation. She appears pale and is tachycardic on the monitor.
LGIB
LGIB causes
-Common causes of LGIB:
-DIVERTICULOSIS* MC (30%)
-Painless BRBPR
-Arteriovenous malformations (AVMs)
-Ischemic Colitis
-Mesenteric ischemia
-Polyps
-Malignancy
-Hemorrhoids
-Aortoenteric fistula (hx of AAA repair)
-UGIB is the MC cause of guaiac + stool
LGIB diff dx
-upper gi bleed
-external hemorrhoids or anal fissure
-vaginal bleeding
-food: beets, red dyes, iron, pepto-bismol
What is the most SERIOUS condition that can cause lower GI bleeding?
Hemorrhoids
Aortoenteric fistula- tend to be a rapid bleed -> ACT FAST!!
Diverticulosis
Ischemic colitis!!!!!!!!!! - HIGH MORTALITY BUT YOU HAVE MORE TIME
Inflammatory bowel disease
H&P for LGIB
-similar to UGIB
-Ask about signs and symptoms of critical anemia
-Chest pain, palpitations, dyspnea, orthostatic symptoms
-Ask about painless vs. painful rectal bleeding
-External hemorrhoids and anal fissures are typically painful
-Ask about recent surgeries, AC use, NSAIDs, bismuth and iron
-Rectal exam can assess for hemorrhoids, fissures, and gross finding of blood in stool
LGIB workup
-Colonoscopy is the preferred method for diagnosis and treatment but a small subset of patients may benefit from angiographic evaluation and interventional radiology therapy
-CT abdomen pelvis can diagnose varices, perforation, gastritis, fistula, colitis, tumor, diverticulis
-CT Angiography: Recommended for recent (within 4 hours) or ongoing severe bleeding with any hemodynamic instability. Routine CTA is low yield in those with minor bleeding or if bleeding has stopped.
-Endoscopy: within 24 hours for severe bleed
-Colonoscopy: needs bowel prep, difficult in massive bleeds
LGIB tx
-In many cases of LGIB, the bleeding will stop spontaneously or the source of bleeding can be controlled via endoscopic or angiographic approach. Surgical intervention such as colectomy can be considered if endoscopic and angiographic modalities fail.
-Treatment is based on cause
-Infectious colitis -> antibiotic
-Irritable bowel disease -> bowel rest, IVF, steroids
-Ischemia -> bowel rest, antibiotics, surgery depending on cause
-Tumor -> surgery if also obstructed or causing massive bleed
-Diverticulosis -> IR embolization, surgical resection
-Fissures -> nitro/ccb cream
-Hemorrhoid -> steroid cream, long term fiber, short term stool softener
dispo UGIB/LGIB
-UGIB:
-ICU if they have: unstable vital signs, age >75, persistent bleeding, coagulopathy or severe anemia (hematocrit <20%)
-Glasgow-Blatchford bleeding score
-Indices for discharge with follow-up
-LGIB:
-Oakland score for lower GI bleeding is a validated score (do not memorize)
-Discharge home - Young stable, normal indices, no active bleeding, hemorrhoids or fissures
Which blood type is recommended to give a 20 year old female presenting to the ED with massive GI bleeding and unstable vital signs?
What is the medication of choice in patients with variceal bleeding?
What intervention can be used to temporize an unstable patient with an upper GI bleed due to esophageal varices?
- O neg uncross unmatched
- octreotide and PPI
- Blakemore tube
