Note the sharp angle of the anterior vertebral line and associated asymmetric widening of the interspinous space.
Note the sharp angle of the anterior vertebral line and associated asymmetric widening of the interspinous space.
A 45 year-old female with a history of ureterolithiasis s/p bilateral percutaneous nephrostomies, hypertension and diabetes presents to the emergency department with flank pain and dysuria for two days. She noted that output from her right nephrostomy had diminished. On evaluation, her vital signs are notable for fever and tachycardia but are otherwise normal. Examination demonstrates right costovertebral angle tenderness to percussion. Drain sites appeared normal, without overlying erythema. Urinalyses from both nephrostomy collection bags were submitted. Computed tomography of the abdomen and pelvis was obtained to evaluate for nephrostomy malposition.
The patient was treated with parenteral antibiotics based on prior culture data and was admitted to the intensive care unit with urology consultation and plan for interventional radiology percutaneous drainage. The patient underwent uncomplicated perinephric drain placement and nephrostomy exchange and was discharged on hospital day five to complete a course of oral antibiotics.
A middle-aged male with no past medical history presents with blurred vision. He reported that he was hammering while at work approximately 3 days prior to presentation and felt something enter his left eye. He denies eye pain, has noted some eye redness and increased tearing. Denies prior eye surgery or procedures. Physical examination demonstrates normal visual acuity, minimal left nasal conjunctival injection sparing the limbus, and an irregular left pupil that is minimally reactive. A no-pressure ocular ultrasound was performed and demonstrated a hyperechoic structure in the globe suggestive of foreign body which was confirmed on computed tomography of the orbit. The patient was taken to the operating room for removal.
Prospective observational study evaluating patients presenting with ocular trauma or acute vision complaints underwent ocular ultrasound. Ultrasound findings agreed with the confirmatory test: ophthalmology consultation or advanced imaging (usually computed tomography) in 60 of 61 cases3.
Appears as a highly reflective membrane floating in the substance of the vitreous body, moves within vitreous body with eye movement. Remains anchored at the optic nerve and ora serrata.
Both retinal detachments and posterior vitreous detachments show a linear hyperechoic line in the posterior chamber. However, posterior vitreous detachments are not tethered to the optic nerve and will appear to cross midline.
Seen more easily with high-gain, enhanced by eye movements which demonstrate hyperechoic particles swirling around in the vitreous body.
Identified by the presence of a hypoechoic structure posterior to the globe. Should prompt a measurement of intra-ocular pressure if simultaneous globe rupture is not suspected.
Usually secondary to blunt trauma, lens displaced from normal position and appears as an echogenic ovoid structure floating freely in the vitreous or over the retina.
If the diagnosis of globe rupture is obvious, ultrasound should be avoided. However, the “no-pressure” technique described above likely does not significantly impact intra-ocular pressure and should be safe11,12. Globe rupture can be identified by scleral buckling, anterior chamber collapse, or globe collapse/irregularities.
Though not a direct assessment of ocular pathology, evaluation of the optic nerve sheath diameter (ONSD) serves as a reliable surrogate for elevated intracranial pressure – emulating fundoscopy for papilledema. See normal measurements and image acquisition above.
The preferred imaging modality for evaluation of intraocular foreign body is orbital computed tomography. Ultrasonographically, foreign bodies are typically hyperechoic.
A more advanced technique, the addition of color Doppler over the central retinal artery may reveal decreased systolic amplitude and diastolic flow in embolic or thrombotic occlusion.
A 43-year-old female with a history of hypertension, diabetes and obesity presents with right-upper quadrant abdominal pain for the past 1 week. The pain is characterized as burning, non-radiating, intermittent (with episodes lasting 10-30 minutes), resolving spontaneously and without apparent provoking features. She notes nausea but no vomiting, no changes in bowel or urinary habits. She similarly denies fevers, chest pain or shortness of breath. Vital signs were normal, and physical examination was notable only for right upper quadrant tenderness to palpation without rigidity or guarding.
An ECG demonstrates normal sinus rhythm, laboratory tests including liver function tests and lipase were normal and a bedside ultrasound of the right upper quadrant was performed demonstrating gallstones and a positive sonographic Murphy sign. The patient was diagnosed with acute cholecystitis, antibiotics were initiated, the patient was maintained NPO while general surgery was consulted.
The initial evaluation of a patient presenting with right-upper quadrant (or adjacent) abdominal pain typically includes laboratory tests such as a complete blood count, chemistry panel, liver function tests and serum lipase. In patients at risk for atypical presentations for an acute coronary syndrome or with other concerning symptoms, electrocardiography and cardiac enzymes may be indicated.
The differential diagnosis is broad. A systematic approach proceeds anatomically from superficial to deeper structures centered around the site of maximal pain.
Herpes zoster, erysipelas, or cellulitis
Intercostal muscle strain, myositis, fasciitis
Rib contusion or fracture
Hepatitis (infectious, toxin-mediated), perihepatitis (Fitz-Hugh-Curtis), hepatic abscess, symptomatic cholelithiasis, acute cholecystitis, ascending cholangitis, pancreatitis
Peptic ulcer disease, gastroesophageal reflux, gastritis, gastroparesis
Duodenal ulcer, small bowel obstruction
Retrocecal appendicitis, inflammatory bowel disease
Acute coronary syndrome, lower-lobe pneumonia, pulmonary embolus
The diagnosis is unlikely to be made based on laboratory tests alone 1. However, the addition of bedside ultrasound, particularly for the evaluation of gallbladder pathology, is both rapid and reliable 2-8. The algorithm below provides a pathway for the incorporation of bedside ultrasound of the right upper quadrant in the evaluation of suspected gallbladder disease.
A normal-appearing gallbladder absent gallstones should prompt a traversal of the anatomic approach to the differential diagnosis detailed above. If gallstones are identified, the association with a positive sonographic Murphy sign is highly predictive of acute cholecystitis 2,5,6,9. Acute cholecystitis may be associated with inflammatory gallbladder changes such as wall-thickening (>3mm) or pericholecystic fluid 3,5,6,10-13. However, in the absence of cholelithiasis or a positive sonographic Murphy sign, these features are non-specific and may be the result of generalized edematous states such as congestive heart failure, renal failure, or hepatic failure and critically-ill patients may develop acalculous cholecystitis 7,11,14. Finally, common bile duct dilation may be due to intra-luminal obstruction as in choledocholithiasis, luminal abnormalities such as strictures, or extra-luminal compression from masses or malignancy. Dilation is generally described as a diameter >6mm – allowing an additional 1mm for every decade over 60 years-old as well as more vague accommodations for patients with prior cholecystectomy 3,5,7,15.
A 27 year-old female is brought in by ambulance with syncope. Pre-hospital providers report that the patient developed pelvic pain, vaginal bleeding and lost consciousness. On their arrival, her blood pressure was 80mmHg systolic, point-of-care glucose was normal – a peripheral IV was started, fluids were administered and the patient was transported to the emergency department. On arrival, vital signs were notable for tachycardia and hypotension. The patient was lethargic, maintaining arousal only with constant verbal or noxious stimulation. Her abdomen was markedly tender throughout with rebound and involuntary guarding. Her last menstrual period was 5 weeks ago and she suspected that she was pregnant. Peripheral venous access was expanded and uncrossmatched blood products were rapidly transfused. Whole blood on a point-of-care pregnancy test was positive1, and a bedside FAST demonstrated free intraperitoneal fluid in the hepatorenal recess with large free pelvic fluid. Gynecology was consulted for emergent operative management of suspected ruptured ectopic pregnancy with hemorrhagic shock and the patient was taken to the operating room.
The evaluation of suspected ectopic pregnancy, as with all complaints in the emergency department, begins with an assessment of patient stability: airway, breathing and circulation. The unstable patient requires immediate interventions to secure each critical component, all temporizing measures until the patient can be taken to the operating room for definitive management.
The evaluation and management algorithm for stable patients is dependent on findings of transabdominal & transvaginal ultrasonography, quantitative hCG level (relative to the institution-dependent discriminatory zone), and the identification of high risk historical and examination features that would prompt specialist consultation despite otherwise benign diagnostic tests.
If ultrasonography demonstrates a definite ectopic pregnancy (extrauterine live embryo, adnexal mass containing yolk sac), gynecology consultation is warranted – the table below details candidates for attempts at pharmacologic therapy.
If an intrauterine pregnancy is identified such as a live embryo or yolk sac, barring the presence of risk factors for heterotopic pregnancy (namely, the use of assisted fertilization methods 2, 4-6), then an alternative cause for the patient’s symptoms should be sought.
If the ultrasound is non-diagnostic, patients should be stratified according to risk based on historical features, examination findings and quantitative hCG. If the hCG is above the institutional discriminatory zone, the absence of a definitive IUP is concerning, elevating suspicion for a non-visualized ectopic and warrants gynecology consultation. If the hCG is below the discriminatory zone, then certain features such as the presence of abdominal, adnexal or cervical motion tenderness, or high-risk ultrasonographic features including greater-than-moderate free pelvic fluid, complex fluid, or complex adnexal masses may be secondary features of ectopic pregnancy – again warranting consultation. If no high-risk features are present, close follow-up with repeat hCG and ultrasonography is reasonable.
|Previous tubal surgery||21|
|In utero exposure to diethylstilbestrol||5.6|
|History of PID||3.4|
|Advanced maternal age||1.4-2.9|
|Cervical motion tenderness||4.9|
|Ectopic cardiac activity||>100|
|Ectopic gestational sac||23|
|Ectopic mass and fluid in Pouch of Douglas||9.9|
|Fluid in Pouch of Douglas||4.4|
A 68 year-old male with a history of hypertension, diabetes, hyperlipidemia, chronic obstructive pulmonary disease and congestive heart failure (CHF) with depressed ejection fraction presents via ambulance with a chief complaint of shortness of breath. EMS reports that the patient was tachypneic and saturating 80% on ambient air on their arrival. En route, he received nebulized albuterol, nitroglycerin and was started on non-invasive positive pressure ventilation (NI-PPV).
On arrival, he remains uncomfortable-appearing with a respiratory rate of 35 breaths/min and accessory muscle use. His heart rate is 136bpm, blood pressure is 118/85mmHg, and he is saturating 95% on an FiO2 of 100%. Attempts to obtain a history are limited due to difficulty comprehending his responses with the PPV mask on, and prompt desaturation with it off. Lung auscultation is similarly challenging due to ambient and transmitted sounds, although basilar crackles and diffuse expiratory wheezing are appreciated. Cardiovascular examination reveals a rapid and irregularly irregular rhythm. Assessment of jugular venous distension is limited due to the patient’s body habitus and the presence of mask straps around the patient’s neck. Lower extremities demonstrate 2+ pitting edema, symmetric bilaterally. Intravenous access is established and laboratory tests are sent. The ECG technician and portable chest x-ray are called.
The case presentation above demonstrates a common emergency department scenario: a critically-ill patient with undifferentiated dyspnea. Specifically, the scenario reveals a situation where the physical examination is either obfuscated by technical challenges or otherwise indeterminate. The patient is at risk for deterioration and targeted intervention is mandatory. If a COPD exacerbation is assumed, additional nebulized breathing treatments are indicated – a potentially costly jolt of beta agonists if the patient’s atrial fibrillation and rapid ventricular response are the consequence of decompensated systolic heart failure. Take the route of decompensated CHF and prompt afterload reduction with diuresis would be next – if incorrect, not only would the primary cause go untreated, but his tenuously-maintained blood pressure may suffer.
An approach incorporating point-of-care ultrasonography may be useful. First, a thoracic ultrasound is performed where certain causative etiologies might be identified immediately – for example absent lung sliding suggesting pneumothorax, or signs of generalized or subpleural consolidation.
Other findings on lung ultrasound may point to causes that are not primarily pulmonary. For example, if diffuse B-lines are encountered a focused cardiac ultrasound can be performed to grossly evaluate ejection fraction and estimate right atrial pressure.
Finally, if the lung ultrasound is largely unremarkable (A-lines), a sequence of ultrasonographic findings including right ventricular dilation and the presence of a deep venous thrombosis would point to pulmonary embolism as the diagnosis.
The emergency physician should be adept at the interpretation of computed tomography of the head, particularly for life-threatening processes where awaiting a radiologist interpretation may unnecessarily delay care.
As with the approach detailed previously for imaging of the abdomen and pelvis, a similar structured method for interpretation of head imaging exists and follows the mnemonic “Blood Can Be Very Bad”.
Evaluate the brain parenchyma, including an assessment of symmetry of the gyri/sulci pattern, midline shift, and a clear gray-white differentiation.
Evaluate the ventricles for dilation or compression. Compare the ventricle size to the size of cisterns, large ventricles with normal/compressed cisterns and sulcal spaces suggests obstruction.
Switch to bone windows to evaluate for fracture. The identification of small, linear, non-depressed skull fractures may be difficult to identify as they are often confused with sutures – surrogates include pneumocephalus, and abnormal aeration of mastoid air cells and sinuses. The Presence of fractures increases the suspicion for intracranial injury, search adjacent and opposing parenchyma and extra-axial spaces.
As with the systematic approach preferred for the evaluation and management of other processes explored on this site, a similarly structured method for the interpretation of imaging commonly obtained in the emergency department may afford the same benefits – namely, the timely identification of pathology while avoiding costly missed diagnoses. In this post, I propose an approach to the interpretation of computed tomography of the abdomen and pelvis.
Start with the descending thoracic aorta
Follow the abdominal aorta down including its branches (celiac, SMA, paired renal arteries, IMA)
Continue to the bifurcation of the abdominal aorta to the left and right common iliac arteries
Start with the left and right femoral veins
Follow the inferior vena cava up
The inferior vena cava gains contrast from the renal veins
The inferior vena cava empties into the right atrium
Evaluate for the presence of a pericardial effusion or cardiomegaly
Heterogenous contrast-enhancement is normal
The tail of the pancreas lies in the hilum of the spleen
Evaluate the intrahepatic bile ducts for dilation or pneumobilia, portal venous system for gas, and liver parenchyma for vascular abnormalities or abscesses
Evaluate for radioopaque stones, pericholecystic fluid or surrounding fat stranding
A wishbone-shaped structure superior to the kidneys
Evaluate for hydronephrosis or hydroureter
Continue down into the pelvis; in a female patient the evaluation should include the uterus and adnexa
Having reached the inferior-most portion of the image following solid organs, move upward again from the rectum
Evaluate the sigmoid colon for diverticulitis
Continue following the sigmoid colon up the descending colon to the transverse colon and the hepatic flexure
Continue down the ascending colon to the cecum
At the cecum, attempt to identify a small tubular structure (the appendix) - evaluate for periappendiceal fat stranding, perforation or abscess
Start at the esophagus, evaluate for perforation or hernia
Continue to the stomach and duodenum
Evaluate the small bowel for obstruction (dilation, air-fluid levels)
Switch to lung window to evaluate the lung parenchyma and continue through the abdomen to identify intraperitoneal free air
Use the bone window to identify fractures or lytic lesions
A 50 year-old male with a history of colonic mucinous adenocarcinoma on chemotherapy presented with a chief complaint of “vomiting”. He was unwilling to provide further history, repeating that he had vomited blood prior to presentation. His initial vital signs were notable for tachycardia. Physical examination showed some dried vomitus, brown in color, at the nares and lips; left upper quadrant abdominal tenderness to palpation; and guaiac-positive stool. Point-of-care hemoglobin was 3g/dL below the most recent measure two months prior. As his evaluation progressed, he developed hypotension and was transfused two units of uncrossmatched blood with adequate blood pressure response – he was started empirically on broad-spectrum antibiotics for an intra-abdominal source. Notable laboratory findings included a normal hemoglobin/hematocrit, acute kidney injury, and elevated anion gap metabolic acidosis presumably attributable to serum lactate of 10.7mmol/L. Computed tomography of the abdomen and pelvis demonstrated pneumoperitoneum with complex ascites concerning for bowel perforation. The patient deteriorated, was intubated, started on vasopressors and admitted to the surgical intensive care unit. The initial operative report noted extensive adhesions and perforated small bowel with feculent peritonitis. He has since undergone multiple further abdominal surgeries and remains critically ill.
This process for the evaluation of hypotension in the emergency department was developed by Dr. Ravi Morchi. In the case above, a systematic approach to the evaluation of hypotension using ultrasonography and appropriately detailed physical examination may have expedited the patient’s care. The expertly-designed algorithm traverses the cardiovascular system, halting at evaluable checkpoints that may contribute to hypotension.
Non-compressible tubular structure in the RLQ of a patient with focal abdominal tenderness. >6mm in diameter.
A tubular structure typically anterior to the portal vein without flow. Normally measures <4mm, increases by 1mm per decade after 40yrs.
"Cobblestone" appearance of soft tissue suggesting infection/edema.
Placing the M-Mode marker over the most visibly active portion of the fetal heart allows for measurement of the fetal heart rate.
Free fluid in the hepatorenal recess.
Subxiphoid view of thoracic aorta, markedly dilated (>3cm) with thrombus.
Mild pericardial effusion in a patient with pleuritic chest pain.
IVC without significant respiratory variation.
B-lines extending deep from pleura suggestive of interstitial fluid accumulation (pulmonary edema).
Irregular, "shredded" pleural line suggestive of consolidation.
Transition point with loss of lung sliding in a patient with a small spontaneous pneumothorax.
- Noncontrast axial images through the head demonstrate no evidence of skull fracture.
- Large lentiform-shaped mixed density extra-axial acute epidural hematoma in the right parietal occipital
- Associated subdural hematoma tracking along right convexity toward the right temporal lobe.
- There is no evidence of midline shift.
- Significant interval increase in the size of the right hemispheric subdural hematoma
- There is now midline shift from right to left at the level of the septum pellucidum measuring 10 mm, partial effacement of the right lateral ventricle and subfalcial herniation.
- Scattered subarachnoid blood is redemonstrated.
- Comminuted fractures of the nasal bone are present and there is overlying and associated periorbital soft tissue swelling.
- Interval gross total evacuation of right hemispheric subdural hematoma.
- Moderate anterior bifrontal subdural and right epidural air is present.
- Small scattered subarachnoid and intraventricular blood is redemonstrated.