Brief HPI:

A 34-year-old male with a history of rheumatoid arthritis and interstitial lung disease presents to the emergency department with joint pain unimproved with home medications. He suspects the precipitant is a recent illness, describing cough and nasal congestion. He also noted a “crunching” sensation when turning his neck not otherwise associated with fevers, recurrent vomiting, chest pain, abdominal pain or difficulty breathing.

A chest radiograph was obtained which demonstrated pneumomediastinum.

Chest x-ray showing pneumomediastinum

Imaging from several months prior to presentation is shown below:


Prior CT Chest:

Extensive peripheral reticular and ground glass opacities and traction bronchiectasis predominates in the lower lobes. Imaging findings are most suggestive of usual interstitial pneumonia. Small focus of pneumomediastinum at carina.

The patient was placed on supplemental oxygen, a repeat chest CT was obtained.


Current CT Chest:

Large pneumomediastinum extends superiorly into the bilateral lower neck and bilateral anterior and posterior chest walls. It extends inferiorly to the anterior diaphragmatic space. This most likely represents spontaneous pneumomediastinum in the clinical setting of interstitial lung disease. Pneumorrhachis is seen, related to pneumomediastinum.

The etiology of the patient’s spontaneous pneumomediastinum was deemed to be related to his underlying interstitial lung disease provoked by viral respiratory tract infection related coughing. He was observed for two days without decompensation and was discharged with outpatient follow-up.

Pathophysiology of Pneumomediastinum

Spontaneous pneumomediastinum results from the rupture of terminal alveoli with subsequent tracking of gas along the bronchovascular tree through interstitial lung tissue to the mediastinum and adjacent structures (pleural, pericardial, retropharyngeal, retroperitoneal, intraperitoneal and subcutaneous spaces)1.

Secondary pneumomediastinum arises from non-alveolar sources including the gastrointestinal tract (most gravely, esophageal rupture though also from other intraperitoneal sources2), and upper respiratory tract (including facial fractures3).

Management of Pneumomediastinum5-7

The management of spontaneous pneumomediastinum focuses on treatment of the underlying precipitant, supportive care, administration of supplemental oxygen (to promote gas reabsorption) and observation for complications including rare progression to tension pneumomediastinum4.

Secondary pneumomediastinum is of significantly more concern and should be suspected in patients with any of the following features:


  • History of forceful vomiting
  • Dysphagia


  • Fever
  • Hemodynamic instability
  • Left-sided pleural effusion
  • Abdominal tenderness
  • Leukocytosis

Management is aggressive including resuscitation, maintenance of NPO status, broad-spectrum antibiotics, and emergent surgical consultation.

Differential Diagnosis of Pneumomediastinum5-11

An Algorithm for the Evaluation of Pneumomediastinum


  1. Macklin, M., Macklin, C. (1944). Malignant Interstitial Emphysema of the Lungs and Mediastinum as an Important Occult Complication in Many Respiratory Diseases and Other Conditions: an Interpretation of the Clinical Literature in the Light of Laboratory Experiment Medicine 23(4)
  2. Fosi, S., Giuricin, V., Girardi, V., Caprera, E., Costanzo, E., Trapano, R., Simonetti, G. (2014). Subcutaneous Emphysema, Pneumomediastinum, Pneumoretroperitoneum, and Pneumoscrotum: Unusual Complications of Acute Perforated Diverticulitis Case Reports in Radiology 2014(), 1-5.
  3. Luca, G., Petteruti, F., Tanga, M., Luciano, A., Lerro, A. (2011). Pneumomediastinum and Subcutaneous Emphysema Unusual Complications of Blunt Facial Trauma Indian Journal of Surgery 73(5), 380-381.
  4. Shennib, H., Barkun, A., Matouk, E., Blundell, P. (1988). Surgical Decompression of a Tension Pneumomediastinum Chest 93(6), 1301-1302.
  5. Bakhos, C., Pupovac, S., Ata, A., Fantauzzi, J., Fabian, T. (2014). Spontaneous pneumomediastinum: an extensive workup is not required. Journal of the American College of Surgeons 219(4), 713-7.
  6. Iyer, V., Joshi, A., Ryu, J. (2009). Spontaneous Pneumomediastinum: Analysis of 62 Consecutive Adult Patients Mayo Clinic Proceedings 84(5), 417-421.
  7. Takada, K., Matsumoto, S., Hiramatsu, T., Kojima, E., Shizu, M., Okachi, S., Ninomiya, K., Morioka, H. (2009). Spontaneous pneumomediastinum: an algorithm for diagnosis and management. Therapeutic advances in respiratory disease 3(6), 301-7.
  8. Al-Mufarrej, F., Badar, J., Gharagozloo, F., Tempesta, B., Strother, E., Margolis, M. (2008). Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. Journal of cardiothoracic surgery 3(1), 59.
  9. Takada, K., Matsumoto, S., Hiramatsu, T., Kojima, E., Watanabe, H., Sizu, M., Okachi, S., Ninomiya, K. (2008). Management of spontaneous pneumomediastinum based on clinical experience of 25 cases Respiratory Medicine 102(9), 1329-1334.
  10. Bejvan, S., Godwin, J. (1996). Pneumomediastinum: old signs and new signs. American Journal of Roentgenology 166(5), 1041-1048.
  11. Langwieler, T., Steffani, K., Bogoevski, D., Mann, O., Izbicki, J. (2004). Spontaneous pneumomediastinum The Annals of Thoracic Surgery 78(2), 711-713.

Hepatobiliary Ultrasound

Brief H&P:

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.

Evaluation of Right-Upper Quadrant Abdominal Pain

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

Connective Tissue

Connective Tissue

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

Small Bowel

Small Bowel

Duodenal ulcer, small bowel obstruction

Large Bowel

Large Bowel

Retrocecal appendicitis, inflammatory bowel disease



Pyelonephritis, ureterolithiasis



Acute coronary syndrome, lower-lobe pneumonia, pulmonary embolus

Ultrasound in the Evaluation of Right Upper Quadrant Abdominal Pain

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.

Algorithm for the Use of Ultrasound in the Evaluation of Right Upper Quadrant Abdominal Pain

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.


The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas


Many gallstones

Gallbladder wall thickening

Pericholecystic fluid


Common bile duct dilation

All illustrations are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

Downloads Page License


  1. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289(1):80-86.
  2. Scruggs W, Fox JC, Potts B, et al. Accuracy of ED Bedside Ultrasound for Identification of gallstones: retrospective analysis of 575 studies. West J Emerg Med. 2008;9(1):1-5.
  3. Ross M, Brown M, McLaughlin K, et al. Emergency physician-performed ultrasound to diagnose cholelithiasis: a systematic review. Acad Emerg Med. 2011;18(3):227-235. doi:10.1111/j.1553-2712.2011.01012.x.
  4. Jang T, Chauhan V, Cundiff C, Kaji AH. Assessment of emergency physician-performed ultrasound in evaluating nonspecific abdominal pain. Am J Emerg Med. 2014;32(5):457-460. doi:10.1016/j.ajem.2014.01.004.
  5. Kendall JL, Shimp RJ. Performance and interpretation of focused right upper quadrant ultrasound by emergency physicians. J Emerg Med. 2001;21(1):7-13.
  6. Summers SM, Scruggs W, Menchine MD, et al. A prospective evaluation of emergency department bedside ultrasonography for the detection of acute cholecystitis. Ann Emerg Med. 2010;56(2):114-122. doi:10.1016/j.annemergmed.2010.01.014.
  7. Rubens DJ. Ultrasound Imaging of the Biliary Tract. Ultrasound Clinics. 2007;2(3):391-413. doi:10.1016/j.cult.2007.08.007.
  8. Rosen CL, Brown DF, Chang Y, et al. Ultrasonography by emergency physicians in patients with suspected cholecystitis. American Journal of Emergency Medicine. 2001;19(1):32-36. doi:10.1053/ajem.2001.20028.
  9. Shea JA. Revised Estimates of Diagnostic Test Sensitivity and Specificity in Suspected Biliary Tract Disease. Arch Intern Med. 1994;154(22):2573-2581. doi:10.1001/archinte.1994.00420220069008.
  10. Miller AH, Pepe PE, Brockman CR, Delaney KA. ED ultrasound in hepatobiliary disease. J Emerg Med. 2006;30(1):69-74. doi:10.1016/j.jemermed.2005.03.017.
  11. Shah K, Wolfe RE. Hepatobiliary ultrasound. Emergency Medicine Clinics of NA. 2004;22(3):661–73–viii. doi:10.1016/j.emc.2004.04.015.
  12. Matcuk GR, Grant EG, Ralls PW. Ultrasound measurements of the bile ducts and gallbladder: normal ranges and effects of age, sex, cholecystectomy, and pathologic states. Ultrasound Q. 2014;30(1):41-48. doi:10.1097/RUQ.0b013e3182a80c98.
  13. Engel JM, Deitch EA, Sikkema W. Gallbladder wall thickness: sonographic accuracy and relation to disease. American Journal of Roentgenology. 1980;134(5):907-909. doi:10.2214/ajr.134.5.907.
  14. Gerstenmaier JF, Hoang KN, Gibson RN. Contrast-enhanced ultrasound in gallbladder disease: a pictorial review. Abdom Radiol (NY). 2016;41(8):1640-1652. doi:10.1007/s00261-016-0729-4.
  15. Becker BA, Chin E, Mervis E, Anderson CL, Oshita MH, Fox JC. Emergency biliary sonography: utility of common bile duct measurement in the diagnosis of cholecystitis and choledocholithiasis. J Emerg Med. 2014;46(1):54-60. doi:10.1016/j.jemermed.2013.03.024.

Ultrasound in Ectopic Pregnancy

Brief HPI:

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.

Algorithm for the Evaluation of Suspected Ectopic Pregnancy

Algorithm for the evaluation of ectopic pregnancy


The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas

Ruptured Cornual Ectopic

Tubal Ectopic Pregnancy

Tubal Ectopic Pregnancy

Ectopic Pregnancy

Ectopic Pregnancy

Positive FAST in Ruptured Ectopic

Positive FAST in Ruptured Ectopic

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.

Requirements for methotrexate administration2,3

Hemodynamic stability
Ultrasound findings consistent with an ectopic pregnancy
Willingness of the patient to adhere to close follow-up
No existing organ dysfunction: hepatic, renal, pulmonary, hematologic, immune
Unruptured ectopic mass <3.5cm
No fetal cardiac activity detected
hCG <5000 mIU/L

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.

Risk factors for ectopic pregnancy3

Risk factor OR
Previous tubal surgery 21
Sterilization 9.3
Previous ectopic 8.3
In utero exposure to diethylstilbestrol 5.6
Current IUD 5.0
History of PID 3.4
Infertility 2.7
Advanced maternal age 1.4-2.9
Smoking 1.5-3.9

Examination Findings in Ectopic Pregnancy6

Finding LR+
Cervical motion tenderness 4.9
Peritoneal irritation 4.2
Adnexal mass 2.4
Adnexal tenderness 1.9

Ultrasound Findings in Ectopic Pregnancy 7

Finding LR+
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
Ectopic mass 3.6
No IUP 2.2
Normal adnexa 0.55

Algorithm for the Evaluation of Vaginal Bleeding

Algorithm for the evaluation of vaginal bleeding


  1. Fromm C, Likourezos A, Haines L, Khan ANGA, Williams J, Berezow J. Substituting whole blood for urine in a bedside pregnancy test. J Emerg Med. 2012;43(3):478-482. doi:10.1016/j.jemermed.2011.05.028.
  2. Bhatt S, Ghazale H, Dogra VS. Sonographic Evaluation of Ectopic Pregnancy. Radiol Clin North Am. 2007;45(3):549-560. doi:10.1016/j.rcl.2007.04.009.
  3. Barash JH, Buchanan EM, Hillson C. Diagnosis and management of ectopic pregnancy. Am Fam Physician. 2014;90(1):34-40.
  4. Lin EP, Bhatt S, Dogra VS. Diagnostic Clues to Ectopic Pregnancy. Radiographics. 2008;28(6):1661-1671. doi:10.1148/rg.286085506.
  5. Winder S, Reid S, Condous G. Ultrasound diagnosis of ectopic pregnancy. Australas J Ultrasound Med. 2011;14(2):29-33. doi:10.1002/j.2205-0140.2011.tb00192.x.
  6. Crochet JR, Bastian LA, Chireau MV. Does this woman have an ectopic pregnancy?: the rational clinical examination systematic review. JAMA. 2013;309(16):1722-1729. doi:10.1001/jama.2013.3914.
  7. Mol BW, van Der Veen F, Bossuyt PM. Implementation of probabilistic decision rules improves the predictive values of algorithms in the diagnostic management of ectopic pregnancy. Hum Reprod. 1999;14(11):2855-2862.
  8. First-Trimester Emergencies: A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. October 2003:1-20.
  9. Paspulati RM, Bhatt S, Nour S. Sonographic evaluation of first-trimester bleeding. Radiol Clin North Am. 2004;42(2):297-314. doi:10.1016/j.rcl.2004.01.005.
  10. Anderson FWJ, Hogan JG, Ansbacher R. Sudden Death: Ectopic Pregnancy Mortality. Obstet Gynecol. 2004;103(6):1218-1223. doi:10.1097/01.AOG.0000127595.54974.0c.
  11. Lozeau A-M, Potter B. Diagnosis and management of ectopic pregnancy. Am Fam Physician. 2005;72(9):1707-1714.
  12. Stone MB. Emergency Ultrasound Diagnosis of Ruptured Ectopic Pregnancy. Academic Emergency Medicine. 2009;16(12):1378-1378. doi:10.1111/j.1553-2712.2009.00538.x.
  13. Stein JC, Wang R, Adler N, et al. Emergency Physician Ultrasonography for Evaluating Patients at Risk for Ectopic Pregnancy: A Meta-Analysis. Ann Emerg Med. 2010;56(6):674-683. doi:10.1016/j.annemergmed.2010.06.563.
  14. Fromm C, Likourezos A, Haines L, Khan ANGA, Williams J, Berezow J. Substituting whole blood for urine in a bedside pregnancy test. J Emerg Med. 2012;43(3):478-482. doi:10.1016/j.jemermed.2011.05.028.
  15. Alkatout I, Honemeyer U, Strauss A, et al. Clinical diagnosis and treatment of ectopic pregnancy. Obstet Gynecol Surv. 2013;68(8):571-581. doi:10.1097/OGX.0b013e31829cdbeb.
  16. Arleo EK, DeFilippis EM. Cornual, interstitial, and angular pregnancies: clarifying the terms and a review of the literature. Clinical Imaging. 2014;38(6):763-770. doi:10.1016/j.clinimag.2014.04.002.
  17. Rodgers SK, Chang C, DeBardeleben JT, Horrow MM. Normal and Abnormal US Findings in Early First-Trimester Pregnancy: Review of the Society of Radiologists in Ultrasound 2012 Consensus Panel Recommendations. Radiographics. 2015;35(7):2135-2148. doi:10.1148/rg.2015150092.
  18. Diagnosis and Management of Ectopic Pregnancy: Green-top Guideline No. 21. BJOG. 2016;123(13):e15-e55. doi:10.1111/1471-0528.14189.
  19. Hahn SA, Promes SB, Brown MD, et al. Clinical Policy: Critical Issues in the Initial Evaluation and Management of Patients Presenting to the Emergency Department in Early Pregnancy. Ann Emerg Med. 2017;69(2):241–250.e20. doi:10.1016/j.annemergmed.2016.11.002.
  20. Lee R, Dupuis C, Chen B, Smith A, Kim YH. Diagnosing ectopic pregnancy in the emergency setting. Ultrasonography. 2018;37(1):78-87. doi:10.14366/usg.17044.

Pneumobilia: Hepatic Gas Applied

Brief HPI

A 45 year-old female with a history of pre-diabetes and gastroesophageal reflux disease presents with 3 days of epigastric abdominal pain. She describes constant, burning abdominal pain which worsened on the day of presentation associated with two episodes of non-bloody and non-bilious emesis. The patient was tender to palpation in the epigastrium and right upper quadrant.

Right upper quadrant ultrasound

Laboratory studies were largely normal. A complete blood count demonstrated minimal leukocytosis (11.6 with normal differential), and liver function tests were normal.

A right-upper quadrant ultrasound was obtained which demonstrated “strongly shadowing structures in the gallbladder fossa which might represent a wall-echo-shadow, calcified gallbladder wall, or air within the gallbladder”.

The patient underwent contrast-enhanced computed tomography of the abdomen and pelvis which is shown below.



CT Abdomen/Pelvis with Contrast

Pneumobilia, intra- and extra-hepatic biliary duct dilation, pericholecystic fat stranding, and an air-fluid level within a contracted gallbladder. Mildly dilated loops of ileal bowel with a possible transition point in the right lower quadrant. Findings suggestive of possible gallstone ileus.

The patient was taken to the operating room for exploratory laparotomy, possible cholecystectomy and possible small bowel resection for presumed gallstone ileus. Intra-operative findings were notable for a cholecystogastric fistula which was repaired.

Differentiation between Portal Venous Gas and Pneumobilia

The patient’s CT demonstrated mostly central hepatic gas. This finding combined with the presence of an air-fluid level in the gallbladder was most consistent with pneumobilia. This case demonstrates an application of the previously-developed algorithm for the evaluation of hepatic gas in a relatively unique pathologic process.
Hepatic Gas: Pneumobilia vs. Portal Venous Gas

Pediatric Foreign Body Ingestion

Brief H&P

XR Chest: Circular radioopaque foreign body likely in the antrum of the stomach.

A healthy 5 year-old boy is brought to the pediatric emergency department after he informed his parents that he accidentally swallowed a coin just prior to presentation. He has no complaints and on evaluation appears to be breathing comfortably and is tolerating secretions normally. A plain radiograph was obtained and is shown below.

The patient remained well-appearing and was discharged with primary care follow-up.

Indications for Emergent Endoscopy

  • Esophageal button battery
  • Severe symptoms
  • Sharp foreign body in esophagus
  • Multiple magnets in esophagus or stomach

Radiographic Findings

Esophageal foreign bodies typically orient coronally. For example, a coin will appear as a circle on an anteroposterior projection.

Tracheal foreign bodies typically orient sagitally. For example a coin will appear as a line on an anteroposterior projection.

Algorithm for the Evaluation and Management of Pediatric Foreign Body Aspiration

Algorithm for the Management of Pediatric Foreign Body Ingestion


  1. Sahn, B, et al. Foreign Body Ingestion Clinical Pathway. 1 Aug. 2016, Accessed 26 Aug. 2017.
  2. Wyllie R. Foreign bodies in the gastrointestinal tract. Current Opinion in Pediatrics. 2006;18 N2 -(5).
  3. Uyemura MC. Foreign body ingestion in children. Am Fam Physician. 2005;72(2):287-291.
  4. Chung S, Forte V, Campisi P. A Review of Pediatric Foreign Body Ingestion and Management. Vol 11. 2010:225-230.
  5. Louie MC, Bradin S. Foreign Body Ingestion and Aspiration. Pediatrics in Review. 2009;30(8):295-301. doi:10.1542/pir.30-8-295.
  6. Green SS. Ingested and Aspirated Foreign Bodies. Pediatrics in Review. 2015;36(10):430-437. doi:10.1542/pir.36-10-430.

Acute Urinary Retention

Brief H&P:

A 62 year-old male with no significant medical history, presented to the emergency department with several days of vomiting. Examination showed suprapubic fullness with tenderness to palpation and a bedside ultrasound was performed:



Right upper quadrant ultrasound with moderate hydronephrosis.



Left upper quadrant ultrasound with moderate hydronephrosis.



Relatively non-distended bladder.

Bladder Volume
Bladder Volume

Bladder Volume

Post-void bladder volume.

Ultrasound revealed moderate bilateral hydronephrosis with a relatively non-distended bladder. Labs were notable for new renal failure and the patient was admitted for continued evaluation. He was ultimately diagnosed with idiopathic retroperitoneal fibrosis with bilateral distal ureteral obstruction requiring stenting.

Anatomy of Acute Urinary Retention:

Differential Diagnosis of Acute Urinary Retention:1,2,3

Algorithm for the Evaluation of Acute Urinary Retention


Brief H&P:

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.



CT Abdomen/Pelvis

Free air is seen diffusely in the non-dependent portions of the abdomen: in the anterior abdomen and pelvis, inferior to the diaphragm, and in the perisplenic region. There is complex free fluid in the abdomen.

Algorithm for the Evaluation of Hypotension1

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.

  1. The process begins with the cardiac conduction system to identify malignant dysrhythmias (bradycardia, or non-sinus tachycardia >170bpm), which, in unstable patients are managed with electricity.
  2. The next step assesses intravascular volume with physical examination or bedside ultrasonography of the inferior vena cava. Decreased right atrial pressure (whether due to hypovolemia, hemorrhage, or a distributive process) is evidenced by a small and collapsible IVC. If hemorrhage is suspected, further ultrasonography with FAST and evaluation of the abdominal aorta may identify intra- or retroperitoneal bleeding.
  3. If a normal or elevated right atrial pressure is identified, evaluate for dissociation between the RAP and left ventricular end-diastolic volume. This is typically caused by a pre- or intra-pulmonary obstructive process such as tension pneumothorax, cardiac tamponade, massive pulmonary embolism, pulmonary hypertension, or elevated intra-thoracic pressures secondary to air-trapping. Thoracic ultrasonography can identify pneumothorax, pericardial effusion, or signs of elevated right ventricular systolic pressures (RV:LV, septal flattening).
  4. Assuming adequate intra-vascular volume is arriving at the left ventricle, rapid echocardiography can be used to provide a gross estimate of cardiac contractility and point to a cardiogenic process. If there is no obvious pump failure, auscultation may reveal murmurs that would suggest systolic output is refluxing to lower-resistance routes (ex. mitral insufficiency, aortic insufficiency, or ventricular septal defect).
  5. Finally, if the heart rate is suitable, volume deficits are not grossly at fault, no obstructive process is suspected, and cardiac contractility is adequate and directed appropriately through the vascular tree, the cause may be distributive. Physical examination may reveal dilated capillary beds and low systemic vascular resistance.

Algorithm for the Evaluation of Hypotension

Guided Lecture

Watch “The Transiently Hypotensive Patient: Who Cares?” from EM Ed. In this lecture Dr. Basrai reviews the diagnostic pathway for a patient who presents with transient hypotension.


  1. Morchi R. Diagnosis Deconstructed: Solving Hypotension in 30 Seconds. Emergency Medicine News. 2015.

Pediatric Emergencies

Diseases by Age

  • 1 week – 1 month: Ductal dependent cardiac lesions
  • 1st month: Malrotation with volvulus
  • 1 – 2 months: Pyloric Stenosis
  • 2 – 6 months: CHF
  • 3 months – 2 years: Intussusception
  • 6 months – 2 years: Croup
  • <2 years: Bronchiolitis
  • 2 years: Meckel’s
  • 2 years – 6 years: Epiglottitis


Ductal Dependent Lesions

  • Present 1st week to 1st month
  • Normal duct seals by 3 weeks
  • If dependent on shunt for pulmonary flow  cyanosis
  • If dependent on shunt for systemic flow cold shock (may be worse w/ fluids)
  • Prostaglandin E1
    • 1 mg/kg/min
    • Side effects include apnea, bradycardia, hypotension, seizure
      • Consider intubating prior to administration
    • IVF, cover for sepsis

Congestive Heart Failure

  • Present 2nd to 6th month
  • Presents with respiratory symptoms (wheezing, retractions, tachypnea)
  • Difficulty with feeding (the infant stress test)
  • Treatment: Supportive

 Tetrology of Fallot

  1. Calm the child, knee to chest
  2. O2 = reduction in PVR
  3. Analgesia: morphine 0.1mg/kg, fentanyl 1.5 mcg/kg, ketamine 0.25 mg/kg
  4. Establish Access: 10-20cc/kg bolus
  5. Phenylephrine 0.2 mg/kg IV (to increase SVR)
  6. +/- HCO3 1mmol/kg (if acidosis)
  7. +/- beta blocker (with cardiology consultation)
  8. PGE1 0.05mcg/kg/min titrating to 0.1mcg/kg/min


Slapped Cheek/5th Disease

  • Parvo B19
  • Slapped cheeks, lacy reticular pattern of rash on body
  • Complications:
    • Pregnancy hydrops
    • Sickle Cell Disease  aplastic crisis


  • Koplik spots, conjunctivitis, fever
  • Can cause blindness


  • Different stages of development
  • Treat with acyclovir if > 12 years old
  • Give VZIG in neonates and immunocompromised

Scarlet Fever

  • Erythematous rash, palatal petechiae, pastia’s lines
  • Strawberry tongue
  • Trunk to periphery
  • Treat with Pen VK: 50mg/kg BID x10d or Amox 20mg/kg BID x10d
  • Pen allergic: Azithro 10mg/kg day 1 then 5mg/kg 2-5

Staphylococcal Scalded Skin Syndrome

  • Toxin mediated, negative Nikolsky, good prognosis
  • Treatment: Anti-staphylococcal antibiotics
    • Nafcillin 25mg/kg/d IV
    • Augmentin 45mg/kg/d PO in 2 divdied doses 7-10d
    • Keflex 10mg/kg/d QID x7-10d

Henoch-Schonlein Purpura

  • Palpable purpura in dependent areas
  • Arthralgia/Arthritis (50-84%)
  • Abdominal pain (50%): vascular lesions in bowel, may be intussusception lead point
  • Renal Disease (20-50%) may develop within 2 months
  • Treatment: Supportive, NSAIDs

Kawasaki Disease

  • 5 days of fever + 4/5 of criteria
    • Diffuse polymorphous diffuse rash
    • Conjunctivitis
    • Mucous membrane change (strawberry tongue)
    • Cervical LAD (usually unilateral)
    • Extremity changes
  • Incomplete and atypical forms more common in infants
  • Treatment (drop complications from 25% to 4-5%)
    • Aspirin 20mg/kg/dose Q6H
    • IVIG 2gm/kg over 12H


Bilious Vomiting

  • Bilious vomiting malrotation with volvulus until proven otherwise  surgical emergency
  • 1st month of life “pre-verbal child’s disease”
  • Dx: Upper GI Series (10-15%) false positive rate

Necrotizing Enterocolitis

  • 10% of cases full term
  • XR w/ pneumatosis intestinalis


  • No meconium, slightly distended abdomen
  • Less severe  later presentation, p/w constipation

Pyloric Stenosis

  • Presents around 6 wks: vomiting but very hungry
  • Diagnosis
    • US pylorus > 4mm thick, >15mm long
    • NGT aspiration 5cc is abnormal
  • Treatment
    • Resuscitate
    • Correct metabolic abnormalities
    • Consult surgery


  • Most common infant emergency
    • 3 months – 2 years
  • Abdominal pain, currant jelly, palpable mass (30% only)
  • Typical presentation
    • Lethargy (may be only sign)
    • Vomiting
    • Paroxysms of pain
    • SBO
    • PO intolerance
  • Diagnosis: US
  • Treatment: Enema (80-95% successful), 10% recurrence

Meckel’s Diverticulum

  • Around 2 years of age, boys > girls
  • Obstruction, intussusception
  • Diagnose with technetium scan


  • 1/3rd with vomiting and diarrhea (AGE-type syndrome)

Hemolytic Uremic Syndrome

  • Watery/bloody diarrhea
  • Three components
    • Acute renal failure
    • Thrombocytopenia
    • Microangiopathic hemolytic anemia (MAHA)
  • Signs
    • Pallor
    • Abdominal Pain
    • Decreased urine output
    • Low energy/AMS
    • Hypertension
    • Edema
    • Petechiae
    • Icterus
  • Treatment: Supportive vs. Dialysis (50%)

GI Bleed by Age

Age Well-Appearing Ill-Appearing
Neonate Allergic Proctocolitis Malrotation with Volvulus
Anal Fissure Necrotizing Enterocolitis
Swallowed Maternal Blood Coagulopathy
Infant/Young Child Allergic Proctocolitis Meckel’s
Gastritis Intussusception
Infectious Colitis Vascular Malformation
Older Child/Adolescent Gastritis IBD
Esophageal Bleeding Cryptic Liver Disease
Juvenile Polyps Intestinal Ulceration

Congenital Disorders

Congenital Adrenal Hyperplasia

  • Presents in first two weeks of life
  • Chief complaint may be vomiting
  • Lyte: HyperK, HypoNa, Hypoglycemia  dysrhythmias, seizures
  • Treatment
    • IVF (usual dose)
    • Glucose (usual dose)
    • Hydrocortisone: 25mg (neonate/infant), 50mg child, adolescent/adult 100mg

Inborn Errors of Metabolism

  • Possible CC: Vomiting, Lethargy, Seizures, Hepatomegaly, Metab Acidosis, Odor
  • May have normal labs and imaging
  • Life-threatening: Metabolic acidosis, Hypoglycemia, Hyperammonemia, Sepsis
  • Labs
    • VBG (acidosis),
    • CMP (liver, kidney, anion gap)
    • Ammonia, lactate, urine (ketones, reducing substance)
    • Bunch of extra tubes for labs later
  • Treatment
    • NPO
    • IVF bolus
    • D10 at 1.5x maintenance
    • Treat Sepsis
    • Control seizures PRN, correct hyperammonemia/acid/lyte (may need dialysis)



  • Toddlers (6-24 months), 5% of all children, boys > girls
    • PIV #1
    • Rhinovirus, Metapneumovirus, PIV II-IV, RSV, Flu A/B
    • Frequent co-infections with one or more viruses
  • Sx: 1-3 days of URI Sx  Abrupt cough/stridor worse for one day, then better
  • Signs: Nontoxic, if wheezing likely RSV
  • Studies: XR to r/o FB (steeple sign if positive)
  • Treatment: Racemic Epi: 0.25-0.75 cc in 3 cc Q 20 minutes, lasts < 2 hours
  • Disposition: If stridor at rest then treat if no improvement, then admit
Stridor Steroids Racemic Epi Dispo
Mild 0.15 mg/kg No Home
At rest with WOB 0.30 mg/kg Yes Admit
Severe at rest 0.60 mg/kg Yes ICU


  • Children < 2 years old, November through April (peak Jan/Feb)
    • Apnea in neonates and ex-premies < 2 months
    • Bacterial superinfection is very rare
  • Presentation: Desat, tachypnea, nasal flaring, intercostal retractions, secretions
  • Exam: Fine rales, diffuse/fine wheezing
  • Treatment: Suction, O2 (if < 90%), NPPV
  • Maybe albuterol, but no steroids/epi/abx


  • Bimodal (2-6, 20-40y), < 1% URI with stridor, boys = girls, al year
    • Non-typable H.flu, staph/strep, Moraxella
    • Candida, HSV, VZV, crack cocaine
  • Symptoms: Muffled voice, drooling rapid progression in hours
  • Signs: No pharyngeal findings with severely tender anterior neck
  • Studies: XR w/ thumb sign
  • Treatment: Laryngoscopy, airway management

Bacterial Tracheitis

  • Preschool (1-10y), boys = girls, Downs
  • Symptoms: Several days’ URI  toxic in hours, rapid progression
  • Signs: Subglottic diffuse inflammation, edema with exudates and pseudomembranes
  • Studies: CXR demonstrates narrow trachea
  • Treatment: Emergent intubation, 3rd generation cephalosporin

Portal Venous Gas

Brief HPI

Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.



CT Abdomen/Pelvis with Contrast

Inflammatory changes in the right lower quadrant concerning for ruptured appendicitis with approximately 9 cm abscess.
Gas in the liver likely representing portal venous gas which can be seen in the setting of appendicitis vs less likely secondary to bowel ischemia.

Differentiation between Portal Venous Gas and Pneumobilia

Portal venous gas vs. Pneumobilia


  1. Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia.
  2. Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia.
  3. Sebastià C, Quiroga S, Espin E, Boyé R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):1213–24–discussion1224–6. doi:10.1148/radiographics.20.5.g00se011213.
  4. Sherman SC, Tran H. Pneumobilia: benign or life-threatening. J Emerg Med. 2006;30(2):147-153. doi:10.1016/j.jemermed.2005.05.016.

Abdominal Pain

Pathophysiology of Abdominal Pain

  1. Visceral: distension of hollow organs or capsular stretch of solid organs.
  2. Somatic: parietal peritoneal irritation
  3. Referred

    • Extra-abdominopelvic

      • Epigastric: inferior MI
      • Pelvic: hip
      • Abdominal: lower lobe pneumonia/infarction
    • Abdominopelvic

      • Shoulder: diaphragmatic irritation (ex. perforated duodenal ulcer, splenic pathology)
      • Mid-back: aortopathy, pancreatitis
      • Flank: renal pathology
      • Low back: uterus, rectum

Concerning Historical Features

  • Elderly: increased probability for severe disease with poor clinical diagnostic accuracy
  • Immunocompromised: HIV/AIDS, uncontrolled diabetes, chronic liver disease, chemotherapy, other immunosuppression
  • Pain preceding nausea/vomiting: increased likelihood of surgical process
  • Abrupt onset, duration <48h, constant timing
  • Prior abdominal surgical history: consider bowel obstruction
  • No prior episodes of similar pain
  • Recent antibiotic or steroid use: may mask signs of infection
  • Cardiac risk factors (HTN, vascular disease, atrial fibrillation: increased risk for mesenteric ischemia or aortic aneurysm
  • Heavy NSAID use or anticoagulation: increase concern for gastrointestinal bleeding


  • Plain film reserved for those who would otherwise not undergo CT. XR abdomen for bowel obstruction or radiopaque foreign body.
  • CT abdomen/pelvis with IV contrast, particularly if elderly or immunocompromised.
  • Ultrasound preferred for hepatobiliary pathology
  • Bedside ultrasound for identification of IUP, free intraperitoneal fluid, cholecystitis, CBD dilation, ascites, hydronephrosis, aortopathy, volume status.

Causes of Abdominal Pain

Causes of Abdominal Pain


  1. Budhram, G., & Bengiamin, R. (2013). Abdominal Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 223-231). Elsevier Health Sciences.

Ectopic Pregnancy


32F G8P7A2 at 5 weeks by LMP presenting with abdominal pain. The patient reports acute onset of sharp left lower abdominal pain 1.5 hours prior to presentation. The pain has been constant since onset, 10/10 in severity, radiating to lower back and exacerbated with movement. She denies vaginal bleeding or discharge, passage of clots or other products. She also denies trauma, lightheadedness/dizziness/syncope, shortness of breath, nausea/vomiting or changes in bowel or urinary habits.
Her pregnancy was detected 3 weeks ago with a home pregnancy test and was confirmed at her PCP one week later. She has not had an ultrasound during this pregnancy but has a history of uterine fibroids. She has no history of sexually transmitted infections, prior ectopic pregnancy, or use of assisted fertilization.


  • HTN
  • Uterine fibroids






  • Denies tobacco, alcohol or drug use.
  • Sexually active with husband only, no history of STI.





Physical Exam:

VS: T 37.4 HR 108 RR 36 BP 148/104 O2 99% RA
Gen: Alert and oriented female, appears uncomfortable due to pain.
CV: Tachycardia, regular rhythm, no murmurs.
Lungs: CTAB, no crackles.
Abd: Normoactive bowel sounds, tenderness to palpation in LLQ and suprapubic area, with guarding but no rebound tenderness. No CVAT.
GU: No external lesions. Closed cervical os, no blood or discharge, +CMT.
Ext: Warm, well-perfused with strong peripheral pulses.


  • POC Hemoglobin: 11.8
  • POC ICON: positive


Bedside Ultrasound

  1. Transabdominal: Free fluid in hepatorenal and splenorenal recesses
  2. Transvaginal: Free fluid and debris in posterior cul-de-sac, likely pseudogestational sac in endometrial cavity, no IUP identified. Formal ultrasound revealed fetus with cardiac activity in left adnexa.
Hepatorenal free fluid

Hepatorenal free fluid

Free fluid in the hepatorenal recess (Morison's Pouch)

Splenorenal Free Fluid

Splenorenal Free Fluid

Free fluid in the splenorenal recess.

Pelvic Free Fluid

Pelvic Free Fluid

Free fluid and debris in the posterior cul-de-sac.

Pseudogestational Sac

Pseudogestational Sac

No obvious yolk sac or fetal pole.


32 year-old ICON positive female with acute-onset pelvic pain. The patient remained hemodynamically stable and absence of definitive IUP on bedside ultrasound was confirmed with presence of fetal cardiac activity in left adnexa indicative of ectopic pregnancy. OB-Gyn was consulted and the patient was taken emergently to the OR.

Differential Diagnosis of First Trimester Abdominal Pain: 1

Differential Diagnosis of 1st Trimester Abdominal Pain

Initial Evaluation of First Trimester Abdominal Pain: 1

  • 2 large-bore IV’s, begin fluid resuscitation
  • POC testing: hemoglobin, urine pregnancy
  • CBC, type and cross (Rh), serum B-hCG
  • Emergent bedside ultrasound

Features Associated with Ectopic Pregnancy: 1

  • History
    • PID
    • Tubal ligation
    • Prior ectopic
    • IUD
    • Assisted fertilization
  • Physical
    • CMT
    • Peritoneal irritation
  • Ultrasound
    • Empty uterus
    • Adnexal mass
    • Free fluid
  • Ultrasonographic Findings in the Evaluation of Ectopic Pregnancy: 2

    • Discriminatory hCG (1500-3000 mIU/mL): absence of IUP suggests ectopic or abnormal gestation
    • Normal IUP
      • 4-5wks: gestational sac (0.2-0.5cm)
      • 5wks: two echogenic rings
      • 5.5wks: yolk sac
      • 6wk: embryonic pole
      • 6.5wk: fetal cardiac activity
    • Abnormal IUP
      • >2cm gestational sac without fetal pole
      • CRL >0.5cm without cardiac activity
    • Ectopic
      • Extrauterine gestational sac with or without cardiac activity
      • Extrauterine ring sign
      • Non-homogenous adnexal mass

    Contraindications to Medical Management: 2,3

    • Absolute
      • Breast-feeding
      • Immunodeficiency
      • PUD
      • Pulmonary, hepatic or renal dysfunction
    • Relative
      • Ectopic mass > 3.5cm
      • Fetal cardiac activity


    1. Dart, R. (2003). First Trimester Emergencies A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. EB Medicine, 5(11), 1–20.
    2. Barnhart, K. T. (2009). Clinical practice. Ectopic pregnancy. The New England journal of medicine, 361(4), 379–387. doi:10.1056/NEJMcp0810384
    3. Jurkovic, D., & Wilkinson, H. (2011). Diagnosis and management of ectopic pregnancy. BMJ (Clinical research ed.), 342(jun10 1), d3397–d3397. doi:10.1136/bmj.d3397


    Swirling mesenteric vessels in mid-pelvis associated with narrowed segments of small bowel and fluid-filled proximal small bowel raises concern for volvulus and small bowel obstruction.

    Alcoholic Hepatitis


    43 year-old female with a history of alcohol abuse and alcoholic hepatitis, presenting after referral from breast clinic for abnormal labs (notable for total bilirubin 18.1). The patient was well until two weeks ago when she noted increasing fatigue associated with morning nausea/vomiting (non-bloody) as well as yellowing of skin and eyes. She also reports darkening of urine, but no dysuria, change in volume of urine, or visible blood. She also denies fevers/chills, increased abdominal girth, abdominal pain, changes in bowel habits or bloody/dark stools.

    She reports drinking 1 pint of vodka daily for the past 15 years, and perhaps more in the past 3 weeks. Her last drink was in the morning on the day of admission, she denies any history of seizures and reports withdrawal symptoms (tremor, nausea) relieved with more alcohol. She currently denies anxiety/agitation, tactile/visual/auditory hallucinations.

    The patient was in breast clinic for evaluation of a painful breast mass which developed after biopsy of a lesion which was ultimately found to be benign. The patient noted the mass was growing in size and becoming more painful over the past month.


    • EtOH abuse
    • Alcoholic hepatitis


    • None


    • No family history of breast/gynecologic malignancy.
    • Mother with history of stroke. Father with diabetes.


    • Lives alone.
    • Denies current or previous tobacco/drug use. Drinks 1 pint of whiskey daily for the past 15 years.
    • Not currently sexually active, no history of STI.


    • None



    Physical Exam:

    VS: T 98.9 HR 104 RR 19 BP 117/67 O2 99% RA
    Gen: Well-appearing obese female in no acute distress
    HEENT: PERRL, marked scleral icterus, sublingual icterus, MMM, no lesions
    CV: Tachycardia, regular rhythm, normal S1/S2, no M/R/G
    Lungs: CTAB, no crackles/wheezing
    Abd: +BS, soft, non-distended, liver edge palpated 6cm below costal margin, irregular texture slightly tender to palpation, spleen not palpated, no fluid wave or shifting dullness, no rebound/guarding.
    Ext: Warm, well-perfused, 2+ pulses (DP/PT), slight yellowing.
    Skin: Vascular spiders on anterior chest, left breast with 5x5cm ecchymosis and tender underlying mass, no erythema, warmth, skin dimpling, nipple discharge.
    Neuro: AAOx4, CN II-XII intact, no tremor noted, gait normal.


    1mo prior to admission:

    • AST/ALT/AP/TB: 444/77/234/2.5

    Day 1:

    • AST/ALT/AP/TB: 185/61/184/18.1
    • PT/PTT/INR: 14.7/37.0/1.2

    Day 4:

    • AST/ALT/AP/TB: 142/50/153/25.5
    • PT/PTT/INR: 20.1/38.9/1.7


    Abdominal US

    1. Markedly echogenic and enlarged liver with a nodular surface of cirrhosis.
    2. Markedly blunted hepatic vein waveforms commonly seen due to decreased hepatic parenchymal compliance although other etiologies causes of obstruction to hepatic venous outflow.
    3. Splenomegaly.


    44F hx EtOH abuse, alcoholic hepatitis, presenting with acute alcoholic hepatitis.
    # Alcoholic hepatitis: Rapid onset of jaundice, tender hepatomegaly, and elevation of transaminases (AST > ALTx2) in the setting of chronic alcohol use suggestive of alcoholic hepatitis. Initial Maddrey discriminant hepatic function (mDH) score 37 suggestive of severe disease with high short-term mortality. Initiated trental 400mg p.o. t.i.d.
    # EtOH withdrawal: Last drink <24h ago, monitor for signs of withdrawal, treat with Ativan per withdrawal protocol. # Cirrhosis: Newly diagnosed on abdominal ultrasound. Complicated by coagulopathy, and likely portal hypertension given splenomegaly/thrombocytopenia. Plan for outpatient screening EGD and continued GI follow-up. # Breast mass: Likely hematoma 2/2 biopsy associated given increased size associated with progression of coagulopathy/thrombocytopenia. Outpatient ultrasound and follow-up scheduled. # Anemia: Macrocytic, potentially related to vitamin deficiency vs. bone-marrow suppression associated with chronic alcohol use. Start thiamine/folate/multivitamin. # FEN/GI/PPx: Encourage p.o. intake (2g sodium restriction), continue ondansetron p.r.n. nausea/vomiting, obtain nutrition consult.

    Hospital Course

    Patient’s liver function continued to decline as evidenced by worsening coagulopathy and increased serum bilirubin. mDH had increased to 58 by day four of hospitalization and steroids were added.

    Pathophysiology of Alcoholic Hepatitis: 1

    Ethanol promotes translocation of bacterial components (lipopolysaccharide) across the intestinal wall, into the portal venous system and liver. These trigger a local and systemic inflammatory response which leads to hepatocellular injury and systemic effects such as fever, anorexia and weight loss.

    Evaluation of Alcoholic Hepatitis: 1,2

    Clinical features:

    • Rapid onset jaundice
    • Tender hepatomegaly
    • Fever
    • Ascites
    • Proximal muscle loss
    • Encephalopathy


    • AST > ALT (x2), generally < 300IU/mL
    • Leukocytosis
    • ↑Total serum bilirubin
    • ↑INR
    • ↑Creatinine associated with poor prognosis

    Other studies:

    • Screening for infection: PNA, UTI, SBP
    • Abdominal US to evaluate hepatic abscess, HCC, extrahepatic biliary obstruction

    Management of Alcoholic Hepatitis: 1,2

    Grading Severity:

    • Maddrey’s discriminant function
    • Glasgow score
    • Lille score (assess response to corticosteroids after 1wk)


    • Immediate and lifetime abstinence from alcohol
    • Trental 400mg p.o. t.i.d.
    • Prednisolone 40mg p.o. daily (controversial, some benefit in subgroup with Maddrey > 32)
    • Ascites: Sodium restriction, diuretics
    • Encephalopathy: Lactulose, rifaximin
    • Hepatorenal syndrome: albumin, vasopressors
    • Nutritional support

    Interpretation of Liver Function Tests: 3

    Disorder Bilirubin AST/ALT Albumin PT
    No bilirubinuria
    Acute hepatocellular necrosis ↑ALT > AST
    > 500IU

    (poor prognosis if elevated)
    Chronic liver disease

    < 300IU

    Alcoholic hepatitis

    AST:ALT > 2

    Intra- extra-hepatic cholestasis

    < 500IU


    (>4x normal)

    Features of Components of Liver Function Tests: 3,4

    Features of Components of Liver Function Tests


    1. Lucey, M. R., Mathurin, P., & Morgan, T. R. (2009). Alcoholic hepatitis. The New England journal of medicine, 360(26), 2758–2769. doi:10.1056/NEJMra0805786
    2. Sohail, U., & Satapathy, S. K. (2012). Diagnosis and management of alcoholic hepatitis. Clinics in liver disease, 16(4), 717–736. doi:10.1016/j.cld.2012.08.005
    3. Kaplan MM. Chapter 302. Evaluation of Liver Function. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.
    4. Johnston, D. E. (1999). Special considerations in interpreting liver function tests. American family physician, 59(8), 2223–2230.

    Elevated Hemidiaphragm

    CXR - PA
    CXR - Lateral

    Causes of an Elevated Hemidiaphragm

    Causes of an elevated hemidiaphragm


    1. Lavender, JP, Potts DG (1959). Differential diagnosis of elevated right diaphragmatic dome. The British journal of radiology, 32(373), 56–60.
    2. Nason, L. K., Walker, C. M., McNeeley, M. F., Burivong, W., Fligner, C. L., & Godwin, J. D. (2012). Imaging of the diaphragm: anatomy and function. Radiographics : a review publication of the Radiological Society of North America, 32(2), E51–70. doi:10.1148/rg.322115127
    3. Prokesch, R. W., Schima, W., & Herold, C. J. (1999). Transient elevation of the hemidiaphragm. The British journal of radiology, 72(859), 723–724.
    4. Burgener, F., Kormano, M. & Pudas, T. (2008). Differential diagnosis in conventional radiology. Stuttgart New York: Thieme.

    Nausea and Vomiting

    Neurologic pathways involved in pathogenesis of nausea and vomiting


    57yo male with a history of HTN, DM, and MI s/p stent in 2011 presenting with nausea/vomiting and hypotension. The patient had one episode of non-bloody, non-bilious emesis approximately 6 hours ago. He felt unwell so a friend checked his blood pressure which was found to be 75/50, prompting a visit to this emergency department.
    The patient’s emesis came 2 hours following a normal meal (frozen dinner), and was associated with chills/sweats but no abdominal pain. The patient had some associated shortness of breath (baselines), but no chest pain, arm or jaw pain, or palpitations.

    He states that these symptoms are unlike what he experienced during his MI. He reported no change in bowel or urinary habits.


    • HTN
    • DM
    • CAD
    • MI
    • Hyperlipidemia


    • Stent placement (2011)
    • Right knee neuroma excision (2012)


    • Non-contributory


    • No current t/e/d
    • 80 pack-year smoking history


    • carvedilol 6.25mg p.o. b.i.d.
    • metformin 1000mg p.o. b.i.d.
    • atorvastatin 20mg p.o. daily
    • aspirin 81mg p.o. daily


    • NKDA

    Physical Exam:

    VS: T 98.4 HR 65 RR 17 BP 96/56 O2 95% 2L NC
    Gen: No acute distress, speaking in complete sentences
    HEENT: PERRL, MMM no lesions, no cervical lymphadenopathy
    CV: RRR, normal S1/S2, no murmurs, no extra heart sounds, no jugular venous distension
    Lungs: CTAB, no crackles
    Abd: +BS, soft, NT/ND, no rebound/guarding, no organomegaly
    Ext: Warm, well-perfused, peripheral pulses equal b/l, no LE edema
    Neuro: AAOx3


    • EKG: normal sinus rhythm, anterior lead q-waves suggestive of old infarct, no T/ST changes
    • Troponin: <0.01
    • CBC: 7.4/15.5/47/228
    • BMP: 139/5.1/107/26/8/1.19/112 (baseline creatinine 1.06 in 2/2013)


    • CXR: no effusion, no cardiomegaly, no focal consolidation
    • Bedside US: normal cardiac wall motion, estimated EF 40-45%, retrohepatic IVC collapses with respiration


    57M hx HTN, DM, MI s/p stent presenting with nausea/vomiting x1 and hypotension. The patient’s symptoms and history were concerning for acute myocardial infarction; however, early EKG and troponins were reassuring. Additionally, the absence of characteristic physical findings that would be associated with an acute MI causing cardiogenic shock (elevated JVP, extra heart sounds, pulmonary crackles) were not present. Evidence of end-organ damage was also absent.

    Other potential causes for nausea/vomiting include SBO, however, the patient reported normal BM’s and has no history of abdominal surgery. Though occurring after a meal, a single episode of emesis without associated abdominal pain lowers suspicion for biliary disease. This patient’s emesis is most likely due to acute gastroenteritis.

    Given the evidence of hypovolemia on bedside ultrasound, the patient was bolused with a total of 1.5L NS and noted symptomatic improvement as well recovery of blood pressure.

    Differential Diagnosis of Nausea/Vomiting: 1, 2

    A System for Nausea/Vomiting

    Pathophysiology: 3, 4, 5

    • Nausea: Sensation associated with increased gastrointestinal motility (tachygastria).
    • Vomiting:
      • Chemoreceptor trigger zone (area postrema of 4th ventricle): sensitive to drugs/toxins (emetics, radiation), neurotransmitters. Located outside BBB.
      • Nucleus tractus solitaries (medulla): pattern generator for vomiting, receives vagal input from GI tract and nociceptive stimuli from peripheral nervous system – transmits to hypothalamus, limbic system and cortex. Stimulated by tickling the back of the throat, gastric distention, and vestibular input.

    Important history/physical associations: 4

    • Abdominal pain: suggests organic disease, affected organ dependent on location of pain. (See figure)
    • Abdominal distension: suggests bowel obstruction.
    • Heartburn: suggests GERD.
    • Vertigo/nystagmus: suggests vestibular etiology.
    • Positional/projectile: suggests neurogenic etiology.

    Differential Diagnosis of Abdominal Pain By Location:

    Abdominal Pain by Location


    1. Scorza, K., Williams, A., Phillips, J. D., & Shaw, J. (2007). Evaluation of nausea and vomiting. American family physician, 76(1), 76–84.
    2. Bork S, Ditkoff J, Hang BS. Chapter 75. Nausea and Vomiting. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. Accessed June 15, 2013.
    3. Koch, K. L., Stern, R. M., Vasey, M. W., Seaton, J. F., Demers, L. M., & Harrison, T. S. (1990). Neuroendocrine and gastric myoelectrical responses to illusory self-motion in humans. The American journal of physiology, 258(2 Pt 1), E304–10.
    4. Longstreth, G. F. Approach to the adult with nausea and vomiting. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.
    5. Costanzo, L. (2011). Physiology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
    6. Patanwala, A. E., Amini, R., Hays, D. P., & Rosen, P. (2010). Antiemetic therapy for nausea and vomiting in the emergency department. The Journal of emergency medicine, 39(3), 330–336. doi:10.1016/j.jemermed.2009.08.060

    Small Bowel Obstruction

    Dilated loops of small bowelCC:

    Consultation for bowel obstruction


    The patient is a 40yo male with a history of alcohol abuse, and seizure disorder secondary to traumatic brain injury who was admitted to this hospital 4d ago after an altercation with law enforcement officials. On arrival, the patient was reported to be acutely intoxicated with ecchymosis and bleeding from left lateral/posterior head and ear. No other significant injuries were found and the patient underwent CT imaging of head and c-spine, with notable findings of left occipital epidural hematoma, subarachnoid hemorrhage, but no significant midline shift. Neurosurgery was consulted and no emergent surgical intervention was required, the patient underwent serial imaging to monitor the bleed which was found to be stable and the patient slowly returned to baseline mental status.

    On HOD4, the patient developed nausea/vomiting and abdominal pain, a nasogastric tube was placed with feculent output. CT abdomen/pelvis showed high grade SBO and possible mesenteric ischemia/infarct, and general surgery was consulted for further evaluation. The patient reported experiencing some abdominal pain since the altercation, but could not recall if he was hit in the abdomen.


    • Alcohol abuse
    • Seizure disorder


    • Tibia fracture
    • No prior abdominal surgery


    • Non-contributory


    • Current alcohol, marijuana use, no tobacco use
    • History of homelessness


    • Norco PRN
    • Ativan PRN
    • LISS, SQH, Thiamine
    • NKDA

    Physical Exam:

    • VS:  T 99.5°F    HR 108    RR 16    BP 128/82    O2 99% RA
    • Gen: NAD
    • HEENT: PERRL, EOMI, sclera clear, anicteric
    • CV: RRR, normal S1/S2
    • Lungs: CTAB
    • Abd: Distended, diffuse tenderness to palpation, no rebound tenderness, no ecchymoses or signs of trauma
    • Ext: Warm, well-perfused
    • Neuro: AAOx4, appropriate


    40M w/hx alcohol abuse, TBI and seizure disorder, presented initially with evidence of head trauma which was stabilized. However, the development of abdominal pain, N/V, and finding of distension on exam associated with copious output of feculent material from NGT suggests bowel obstruction. This patient has no history of abdominal surgeries to suggest adhesions as a possible cause. Though the patient cannot recall any abdominal trauma, and there was no e/o trauma on exam, findings on CT abdomen/pelvis are suggestive of traumatic cause (hematoma causing obstruction or ischemia resulting from mesenteric injury). The patient was monitored for several days, continuing NGT to suction and with serial abdominal films. However, abdominal pain persisted, abdominal radiographs showed worsening obstruction and the patient developed leukocytosis and on HOD7 the patient was taken to the OR for exploratory laparotomy. Upon entering the peritoneal cavity, there was obvious blood and very distended small bowel which was run distally with finding of a mesenteric laceration in the distal ileum which was walled off by omentum. Additionally, a grade 2 splenic laceration was found. Ultimately, a small bowel resection with primary anastomosis along with a repair of the splenic laceration was performed.


    CT abdomen/pelvis

    CT abdomen/pelvis

    Moderate abdominal and pelvic ascites which has Hounsfield unit attenuation is greater than simple fluid suggestive of blood products.

    CT abdomen/pelvis

    CT abdomen/pelvis

    Fluid dilated small bowel

    CT abdomen/pelvis

    CT abdomen/pelvis

    Complex transition point in the central mid abdomen.
    Segment of bowel at the transition point has circumferential mural thickening and surrounding complex attenuation mesenteric fluid and mesenteric stranding.

    Abdominal X-Ray

    Abdominal X-Ray

    Small bowel distention
    Nasogastric tube is seen coiled in the gastric fundus

    CT Head

    CT Head

    Left occipital extracranial soft tissue hematoma
    Left occipital epidural hematoma subjacent to the fracture site in addition to subarachnoid hemorrhage within the sulci of the left temporal lobe and interpeduncular cistern
    Extra-axial fluid collection along the right frontal convexity, tracking down the anterior falx, compatible with a subdural hematoma

    Differential Diagnosis for bowel obstruction: 1, 2, 3

    A System for Bowel Obstruction

    Types of Abdominal Pain: 4

    Types of Abdominal Pain


    1. Kulaylat MN, Doerr RJ. Small bowel obstruction. In: Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001. Available from:
    2. Jackson, P. G., & Raiji, M. T. (2011). Evaluation and management of intestinal obstruction. American family physician, 83(2), 159–165.
    3. Maung, A. A., Johnson, D. C., Piper, G. L., Barbosa, R. R., Rowell, S. E., Bokhari, F., Collins, J. N., et al. (2012). Evaluation and management of small-bowel obstruction. Journal of Trauma and Acute Care Surgery, 73, S362–S369. doi:10.1097/TA.0b013e31827019de
    4. Stabile, Bruce. “The Acute Abdomen.” Chairman’s Hour. Harbor UCLA Department of Surgery Student Lecture Series. 5/17/13. Lecture.

    Abdominal Wall Hernias

    Inguinal hernia CTHPI:

    23M w/no known medical history presenting with abdominal “ball” x10d. Patient denies pain, and is tolerating regular diet w/o N/V. Reports lifting weights.


    None, non-contributory, no t/e/d.


    Acetaminophen, NKDA


    • VS:     T N/A      HR 86     RR 18       BP 116/64      O2 N/A
    • Gen: Well-appearing young male, no acute distress
    • HEENT: PERRL, MMM no lesions
    • CV: RRR, normal S1/S2, no murmurs
    • Lungs: CTAB, no crackles/wheezes
    • Abd: +BS, soft, NT/ND, 3cm bulge in right inguinal region with valsalva, above inguinal ligament, ~7cm lateral to symphysis, non-tender, reduces spontaneously after valsalva GU: uncircumcised penis, testes descended b/l, normal size, non-tender, no herniation through inguinal canal palpated with valsalva
    • Ext: Warm, well-perfused, 2+ peripheral pulses
    • Neuro: Alert and oriented, appropriate


    23M ċ inguinal hernia, currently asymptomatic with no evidence of incarceration/strangulation. Recommend follow-up at city hospital for evaluation and possible surgical repair. Advised to refrain from strenuous activity, heavy lifting.

    Physical Examination Techniques: 1

    Physical Examination Techniques

    • Observation: Best performed with patient standing and physician seated on a stool facing the patient
    • Palpation: place hand over patient’s groin (see figure), with two fingers each superior and inferior to the inguinal ligament. Have the patient cough and feel for a palpable bulge or impulse.
    • GU: With a finger in the inguinal canal, bulges felt against the side of the examining finger are direct hernias, while those felt at the tip of the finger are indirect.

    Types of Abdominal Wall Hernias: 2

    Types of abdominal wall hernias

    Name Location Etiology/Epidemiology
    1. Umbilical Linea alba through weakened umbilical ring.Paraumbilical hernias through linea alba in the region of the umbilicus. Congenital or acquired due to increased intra-abdominal pressure (obesity, pregnancy, ascites, PD)
    2. Epigastric Linea alba between umbilicus and xiphoid process Congenital weakness of linea alba (lack of decussating fibers)
    3. Spigelian Semilunar line: along the lateral borders of rectus abdominus. Herniation typically occurs caudally (below arcuate line) due to absence of posterior rectus sheath.
    4. Incisional Site of prior incision Poor fascial healing possibly due to: infection (increased risk in wound dehiscence), obesity, smoking, immunosuppression excess wound tension, CT disorders.
    5. Inguinal Indirect: internal (deep) inguinal ring, lateral to inferior epigastric vessels.Direct: external (superficial) inguinal ring, medial to inferior epigastric vessels. Indirect > direct.
    6. Femoral Inferior to the inguinal ligament, through empty space medial to femoral sheath. F > M, increased likelihood of incarceration/strangulation (40%)
    7. Lumbar 3 Arise in two anatomical triangles:Superior lumbar triangle – lateral border internal oblique, medial border erector spinae, superior border 12thrib.Inferior lumbar triangle – lateral border external oblique, medial border latissimus dorsi, inferior border iliac crest. (See figure) Associated with surgery (incisional), typically urologic.
    8. Obturator Protrusion of peritoneal sac through obturator foramen. Rare, occur primarily in elderly women (high predisposition for incarceration).

    Locations of Abdominal Wall Hernias:

    Locations of abdominal wall hernias

    Layers of the Anterior Abdominal Wall:


    Differential diagnosis for groin masses: 4

    Category Inguinal 5 Scrotal 6 Vulvar 7 Perineal 8
    Vascular Varicocele extension Varicocele Vulvar varicocity

    Infectious, Inflammatory Lymphadenopathy
    Inflammatory joint process (hip, related bursae)
    Bartholin’s cyst
    Neoplastic Benign (lipoma)
    Lymph node metastatsis
    Testicular malignancy Malignant skin lesions Soft-tissue malignancy
    Anal SCC
    Rectal GIST
    Metastasis (commonly anorectal, prostatic)
    Congenital, Anatomic Hernia
    Testis (undescended, retracted)
    Epididymal cyst
    Embryological remnants (mucocele)
    Traumatic Hematoma
    Aneurysm (complication of catheterization)
    Hematoma Hematoma

    Locations of Groin Masses: 9

    Locations of groin masses


    1. Amerson JR. Inguinal Canal and Hernia Examination. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 96. Available from:
    2. Aguirre, D. A., Casola, G., & Sirlin, C. (2004). Abdominal Wall Hernias: MDCT Findings. American Journal of Roentgenology, 183(3), 681–690. doi:10.2214/ajr.183.3.1830681
    3. Guillem, P., Czarnecki, E., Duval, G., Bounoua, F., & Fontaine, C. (2002). Lumbar hernia: anatomical route assessed by computed tomography. Surgical and radiologic anatomy : SRA, 24(1), 53–56.
    4. Roberts, J. R., & Hedges, J. R. (2010). Clinical procedures in emergency medicine. (5th ed., Vol. section 7, p. Ch. 44). W B Saunders Co. Retrieved from
    5. Shadbolt, C. L., Heinze, S. B., & Dietrich, R. B. (2001). Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics : a review publication of the Radiological Society of North America, Inc, 21 Spec No, S261–71.
    6. Eyre, RC. Evaluation of nonacute scrotal pathology in adult men. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, MA, 2013.
    7. Foster, D. C. (2002). Vulvar disease. Obstetrics and gynecology, 100(1), 145–163.
    8. Tappouni, R. F., Sarwani, N. I., Tice, J. G., & Chamarthi, S. (2011). Imaging of unusual perineal masses. American Journal of Roentgenology, 196(4), W412–20. doi:10.2214/AJR.10.4728
    9. Collins, R. (2008). Differential diagnosis in primary care. Philadelphia: Lippincott Williams & Wilkins.