SAEM Clinical Images Series: An Ultrasonographic Rabbit Hole


An 86-year-old man with a past medical history of coronary artery disease, hypertension, hyperlipidemia, chronic kidney disease, COPD, choledocholithiasis requiring ERCP and sphincterotomy 2 years ago presented with five days of feeling unwell. History was limited due to cognitive impairment. His daughter had reported to staff he had been feeling unwell for five days, intermittently having nausea and generalized abdominal pain, subjective fevers, chest pain, and shortness of breath. His daughter also reported a history of intermittent lower abdominal cramping which was chronic for him. He denied changes to urination or bowel movements.

Vitals: BP 106/67, Temp 36.2°C, Pulse 115, Resp 20, SpO2 95%

General: Nontoxic appearing, no distress

Heart: Regular, no murmurs

Lungs: Clear bilaterally, normal work of breathing

Abdomen: Diffusely tender, greatest in left upper quadrant

CBC with differential: WBC 14.1, Neutrophil 12% (high)

Comprehensive metabolic panel (CMP): Total bilirubin 2.7 (high), AlkP 328 (high), AST/ALT normal

Lipase: Normal

Troponin x2: Negative

Chest x-ray: No acute abnormality

This patient has sonographic evidence of perforated gangrenous cholecystitis which was confirmed on subsequent CT scan. Gallbladder perforation is a complication of cholecystitis and has a reported incidence of 5-10%. It has been reported as early as two days after the onset of symptoms to as late as several weeks afterward. The most common site of perforation is the fundus due to relatively poor blood supply. In this case, the culprit perforation was in the proximal body adjacent to the stone which is suspected to have eroded through the wall.

Figure 1 depicts a minimally thickened gallbladder wall measured at 3.5 mm with a large shadowing stone-in-neck and associated perihepatic fluid collection (arrow) with a subtle intraluminal membrane and wall irregularity consistent with gangrenous cholecystitis. Figure 2 doppler images show no flow within the fluid collection and a suspiciously thin gallbladder wall (arrow). Figure 3 again highlights an irregular wall with small “hole sign” (arrow) signifying perforation of the gallbladder into the adjacent fluid collection. This patient was admitted to the hospital’s general surgical service and treated with IV broad-spectrum antibiotics and a percutaneous cholecystostomy tube placed by interventional radiology.

Take-Home Points

  • Look out for “hole signs” with adjacent fluid collection on your gallbladder ultrasounds which would suggest perforation.
  • Intraluminal membranes or wall irregularities suggest gangrenous cholecystitis.
  • Initial treatment includes broad-spectrum antibiotics and cholecystostomy tube decompression.

  • Indiran, V., Prabakaran, N. & Kannan, K. “Hole sign” of the gallbladder. Indian J Gastroenterol 36, 66–67 (2017).
  • Jeffrey RB, Laing FC, Wong W, Callen PW. Gangrenous cholecystitis: diagnosis by ultrasound. Radiology. 1983 Jul;148(1):219-21. doi: 10.1148/radiology.148.1.6856839. PMID: 6856839.
  • Sood, B.P., Kalra, N., Gupta, S., Sidhu, R., Gulati, M., Khandelwal, N. and Suri, S. (2002), Role of sonography in the diagnosis of gallbladder perforation. J. Clin. Ultrasound, 30: 270-274.

SAEM Clinical Images Series: Bulge in the Belly


A 45-year-old male status-post right nephrectomy secondary to a renal mass presented to the emergency department with right-sided flank pain. He endorsed low-grade intermittent right-sided flank pain since the nephrectomy one year prior, associated with an increasingly enlarging mass extending laterally from his right abdomen. Over the course of the past several days, the mass had become larger and more painful. He denied any fevers, chills, or signs of systemic illness, and reported no urinary symptoms.

Vitals: T 98°F; HR 88; RR 17; BP 121/67; SpO2 97% on RA

Respiratory: Clear to auscultation in all lung fields. No diminished breath sounds in the right lower lobe.

Abdomen: Soft, non-tender to palpation. 10 cm mobile, non-erythematous mass protruding from the right flank.

White Blood Cell (WBC) Count: 5.5 K/uL

BUN: 10 mg/dL

Creatinine: 0.88 mg/dL

Lactate: 1.1 mmol/L

Urinalysis (UA): WBC 0-5, Neg Bacteria, Neg Nitrites, Neg Leukocyte Esterase, Neg Ketones

The major risk factor that predisposes patients to the development of abdominal wall hernias is a decrease in the strength of the abdominal wall musculature. Additionally, cardiovascular co-morbidities, such as obesity, hypertension, and diabetes, can increase the risk. Urologic procedures predispose patients to flank hernias in particular due to the postoperative weakening of the muscular wall. The patient in question had a right-sided nephrectomy, which likely predisposed him to the development of this hernia (Figure 1).

The critical complications that can develop secondary to a hernia are incarceration and strangulation (which can result in subsequent necrosis). Initial management focuses on a rapid assessment to evaluate for these complications, while also providing pain control. Incarcerated hernias are erythematous, edematous, tender to palpation, and unable to be reduced. If strangulated, patients will additionally have signs of peritonitis. Ancillary laboratory tests, such as an elevated lactate, may also suggest ischemia secondary to strangulation. CT imaging should be acquired in cases of suspected incarceration or strangulation (Figure 2: CT showing right-sided abdominal wall hernia containing fat and non-obstructed bowel loops without evidence of strangulation). Patients without evidence of emergent hernia complications can be managed with outpatient surgical follow-up.

Take-Home Points

  • Abdominal wall hernias are classified by their location: ventral, groin, pelvic, and flank.
  • Major risk factors for their development include prior abdominal surgeries that weaken the musculature as well as cardiovascular co-morbidities.
  • Evaluation should include a physical exam, laboratory work (particularly a complete blood count, comprehensive metabolic panel, and lactate), and CT Abdomen/Pelvis.
  • If an incarcerated or strangulated hernia is suspected, surgery should be consulted emergently.
  • Hernias that can be reduced at the bedside can be managed with outpatient surgical follow-up.
  • Pastorino A, Alshuqayfi AA. Strangulated Hernia. 2022 Dec 19. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32310432.
  • Zhou DJ, Carlson MA. Incidence, etiology, management, and outcomes of flank hernia: review of published data. Hernia. 2018 Apr;22(2):353-361. doi: 10.1007/s10029-018-1740-1. Epub 2018 Jan 27. PMID: 29380158.

By |2023-12-05T20:31:20-08:00Dec 8, 2023|Gastrointestinal, SAEM Clinical Images|

SAEM Clinical Images Series: Utility of Bedside Ultrasonography


A 24-year-old G1P0010 female with a PMHx of ovarian cyst (unknown laterality) and emergency contraceptive use 3 months prior presented with sudden onset abdominal pain (upper > lower) that awoke her from sleep four hours prior to presentation with associated nausea and mild lower back pain. The pain is 10/10, sharp, stabbing, and diffuse. Additionally, she reported trace white vaginal discharge at baseline. No acute increase. She had intermittent vaginal bleeding since contraception use over the past two months, which has now resolved. She denied fever, chills, vomiting, chest pain, shortness of breath, diarrhea, or constipation. No pertinent surgical history.

Constitutional: Uncomfortable. Appearing to be in acute pain.

Cardiovascular: Tachycardia. Regular rhythm and normal heart sounds.

Pulmonary: No respiratory distress. Breath sounds normal.

Abdominal: Diffusely tender abdomen with voluntary guarding, otherwise soft. Normoactive bowel sounds. Negative Murphy’s sign.

Pelvic: Scant white vaginal discharge and CMT. No vaginal bleeding, lacerations, or external lesions.

Neurologic: A&O x 3

WBC: 18.9 k/uL

Hgb: 10.5 g/dL

BMP, lipase, Alk phos/Bili/ALT/AST, PT/PTT, and lactate: Unremarkable

Serum HCG: Negative

Urinalysis (UA): Unremarkable

COVID: Negative

An ideal RUQ ultrasound visualizes the liver, Morrison’s pouch, superior and inferior poles of the right kidney, and diaphragm in the coronal plane. Here, we see a thickened hepatic capsule, septations, and trace ascites.

Fitz-Hugh-Curtis syndrome (FHCS) is characterized by perihepatitis in the setting of pelvic inflammatory disease (PID). It traditionally presents with right upper abdominal pain with associated nausea, vomiting, and fever in women of childbearing age. While overall considered a rare manifestation of PID, the true incidence of FHCS is poorly defined in the literature [1]. The pathophysiology of spread is also poorly understood. It is speculated that bacteria (N. gonorrhoeae, C. trachomatis) travel to the liver via blood, lymphatics or peritoneal fluid, causing perihepatitis [1]. Diagnosing FHCS poses a diagnostic challenge to clinicians. Traditionally, the diagnosis is made via laparoscopic exploration of the abdomen with visualization of the characteristic “violin-string” adhesions, with growing evidence also supporting the use of contrast-enhanced CT [1]. Limited evidence exists to support the use of ultrasonography in diagnosing FHCS. One case report published in 1993 used RUQ abdominal ultrasound to identify septations (violin-string adhesions) and ascites to ultimately diagnose FHCS, later confirmed by serologic and operative evidence [2]. Another case report from 2018 used ultrasonography to identify a thickened hepatic capsule in an 18-year-old female with RUQ pain, later confirming FHCS by CT without the need for laparotomy [3]. While more research is needed, identification of FHCS via bedside ultrasonography in the emergency setting followed by appropriate antibiotic therapy can be an effective approach to FHCS, ideally reserving laparoscopy only for lysis of adhesions in refractory cases.

Take-Home Points

  • RUQ abdominal ultrasound findings of a thickened hepatic capsule, ascites, and septations should raise suspicion for Fitz-Hugh-Curtis syndrome in the emergency setting.

  • Moon, Y.H., Kim, J.H., Jeong W.J., Park, S.Y. Ultrasonographic findings in Fitz-Hugh-Curtis syndrome: a thickened or three-layer hepatic capsule. Yeungnam Univ J Med 35(1), 127-129 (2018).
  • Theofanakis, C.P., Kyriakidis, A.V. Fitz-Hugh–Curtis syndrome. Gynecol Surg 8, 129–134 (2011).
  • van Dongen PW. Diagnosis of Fitz-Hugh-Curtis syndrome by ultrasound. Eur J Obstet Gynecol Reprod Biol. 1993 Jul;50(2):159-62. doi: 10.1016/0028-2243(93)90181-b. PMID: 8405645.

SAEM Clinical Images Series: A Dangerous Cause of Abdominal Pain

liver abscess

A 65-year-old male presented with chest and abdominal pain for three weeks. He endorsed a poor appetite and a weight loss of 16 kilograms in the last month. He denied fever, vomiting, diarrhea, and tarry stools and described having his usual bowel movements.

Vitals: BP 172/71; HR 127; T 35.9°C; O2 Sat 100%

General: In acute distress

Cardiovascular: Regular rate and rhythm; no murmur; bilateral upper extremity and lower extremity pulses palpable

Gastrointestinal: Soft; generalized tenderness, no abdominal masses, palpable subcutaneous emphysema

Complete blood count (CBC): WBC 31 x 10^3/mcl; Hgb 15 g/dl; Hct 49.1%; Plt 477 x 10^3/mcl

Basic metabolic panel (BMP): Na 130 mmol/L; K 5.6 mmol/L; Glucose 538 mg/dL

CRP: 42.6 mg/dL

Ketone body: 5.9 mmol/L

Venous blood gas (VBG): pH 6.967; pCO2 27.9 mmHg; pO2 45.8 mmHg; BE -24.7 mmol/L

Rupture of gas-forming pyogenic liver abscess complicated by necrotizing fasciitis. The most common pathogen is Klebsiella pneumoniae, and diabetes mellitus is the most common risk factor.

Treatment includes drainage, systemic antibiotic therapy, and emergent surgical intervention.

Take-Home Points

  • Gas-forming pyogenic liver abscess is a rare but life-threatening disease. Consider it especially in the patient with abdominal pain with diabetes mellitus.
  • Treatment includes not only drainage and systemic antibiotic therapy, but also emergent surgical intervention if complicated by necrotizing fasciitis.

  • Chen CE, Shih YC. Monomicrobial Klebsiella pneumoniae Necrotizing Fasciitis With Liver Abscess: A Case Report and Literature Review. Ann Plast Surg. 2017 Mar;78(3 Suppl 2):S28-S31. doi: 10.1097/SAP.0000000000001001. PMID: 28177973.
  • Cheng NC, Yu YC, Tai HC, Hsueh PR, Chang SC, Lai SY, Yi WC, Fang CT. Recent trend of necrotizing fasciitis in Taiwan: focus on monomicrobial Klebsiella pneumoniae necrotizing fasciitis. Clin Infect Dis. 2012 Oct;55(7):930-9. doi: 10.1093/cid/cis565. Epub 2012 Jun 19. PMID: 22715175.

By |2023-08-27T21:58:28-07:00Sep 1, 2023|Gastrointestinal, SAEM Clinical Images|

Trick of Trade: Inflating the Esophageal Balloon of a Blakemore/Minnesota Tube without a Manometer 

esophageal balloon manometer trick minnesota blackmore tube

A heavy alcohol drinker, who is well known to your Emergency Department, presents with altered mental status, except that he looks different this time. He looks really bad, stating that he has been vomiting blood. He is hypotensive. He then vomits a copious amount of blood right in front of you. You intubate the patient and initiate the massive transfusion protocol, but everything you pour into him seemingly comes right back out. The gastroenterologist on-call states that he is too unstable for endoscopy. It is time for a balloon tamponade device. You’ve trained for this and set up everything. You call the respiratory therapists (RT) for this mystical “manometer” that you have seen in instructional videos, except that they look puzzled by your request. It is time to MacGyver a method that allows you to know the esophageal balloon pressure that you are generating to avoid an esophageal rupture.

esophageal balloon devices linton sengstaken blakemore minnesota tube

Esophageal Balloon Tamponade Devices – Linton-Nachlas, Sengstaken-Blakemore, Minnesota Tubes (image courtesy of Dr. Mark Ramzy at REBEL EM)

What are esophageal balloon tamponade devices?

There are 2 commonly used devices for tamponading the esophagus during a variceal bleed, the Sengstaken-Blakemore (SB) tube and the Minnesota tube. There is also the Linton-Nachlas tube, but that only has a gastric balloon. The SB tube was created in 1950 in order to help tamponade variceal bleeds [1]. It is a 3-lumen device that has ports to inflate the gastric balloon, aspirate gastric contents, and inflate an esophageal balloon. The Minnesota tube was developed later as a variation to the SB tube and contains an additional port and lumen for aspirating esophageal contents [2]. Another minor difference is that the gastric balloon in the Minnesota tube holds 450-500 ccs of air, while the SB gastric balloon holds 250 ccs of air [2].

Indication: The uncontrolled hemorrhage from esophageal or gastric variceal bleeding after medical or endoscopic treatment fails, is not available, or is not technically possible [3, 4].

Contraindications [4]:

  • Unprotected airway
  • Esophageal rupture (Boerhaave’s syndrome)
  • Esophageal stricture
  • Uncertainty of bleeding site
  • Well-controlled variceal bleeding

Esophageal balloon tamponade devices achieve hemostasis in 60-90% of cases; however, they are only a temporary measure of hemorrhage control because over 50% of variceal bleeds rebleed after deflation [5].

How do you insert these esophageal tamponade devices?

The following instructions are for inserting a Sengstaken-Blakemore (SB) tube [3, 6]:

  1. Pre-measure 50 cm above the gastric balloon and esophageal balloon and mark them on the SB tube.
  2. Fully lubricate the tube.
  3. Insert the tube similar to an orogastric tube until you have reached the 50 cm mark for the gastric balloon
    • Additional trick: You can insert it with a nasogastric tube to have more rigidity and make inserting the tube easier.
  4. Use a slip syringe at the gastric aspiration site and auscultate to confirm that you are in the stomach. Then fill the gastric balloon with 50 cc of air.
  5. Verify the placement of the gastric balloon with a chest x-ray.
    • Additional trick: If the x-ray is delayed, you can pre-check with ultrasound [7]. However final confirmation prior to full inflation should be with a chest X-ray.
  6. Fully inflate the gastric balloon with 200 more ccs of air for a total of 250 ccs.
    • The Minnesota tubes should have the gastric balloon inflated to 450-500 ccs.
  7. Apply traction to the tube by tying a roller bandage to the end of it and then the other end to a 1 L bag of IV fluids. Then hang the roller bandage over an IV pole.
  8. Place the nasogastric tube down to the pre-measured level above the gastric balloon and suction the esophageal space. If there is continued bleeding coming from the nasogastric tube then you will need to inflate the esophageal balloon.
    • Note that Minnesota tubes already have their own esophageal suction port and will NOT need this NG tube placement to suction the esophagus.
  9. Use a “manometer” to inflate the esophageal balloon to 30 mmHg. If bleeding persists, you can go to a maximum of 45 mmHg.

What is this “manometer” typically used for the esophageal balloon?

The manometer referenced in numerous videos [6, 8] is actually a cuff manometer, or pressure gauge, to measure endotracheal cuff pressures. Hence, the RT’s are supposed to have them. In our emergency department, the RTs do not spend a lot of time going around measuring cuff pressures and usually save that until the patient reaches the ICU. It is convenient to use for the inflation of the esophageal balloon because it can inflate and measure pressure at the same time.

Pearl 1: Check the units of pressure being used. Manometers often use cmH2O, while esophageal balloons use mmHg.

  • The conversion rate is: 1 cmH2O = 0.74 mmHg
  • The esophageal balloon goal of 30-45 mmHg is approximately 40-60 cm H2O.

Pearl 2: While the gastric balloon sets a target VOLUME, the esophageal balloon sets a target PRESSURE.

Trick of the Trade: Use a sphygmomanometer as the manometer

Once the inflated gastric balloon is confirmed to be in place, it is time to inflate the esophageal balloon. A manual blood pressure instrument can be repurposed to inflate and measure the esophageal balloon pressure.

  1. Take your manual blood pressure cuff and detach the connections so you have only a plastic tube that runs to the pressure gauge.
  2. Connect this plastic tube end to the male Luer lock of a 3-way stopcock.
  3. Connect the esophageal balloon to a female luer lock on the 3-way stopcock.
  4. Place a 50 cc syringe on the final female Luer lock of the 3-way stopcock.
  5. Turn the 3-way stopcock off towards the pressure gauge and inflate the esophageal balloon with 10 ccs of air.
  6. Then turn the 3-way stopcock off towards the syringe and you should have a reading on the pressure gauge.
  7. Repeat this using small increments (we chose 10 ccs) until you have a pressure reading of 30 mmHg on the pressure gauge. If bleeding continues, you can increase to 45 mmHg.

Video Demonstration: Esophageal Balloon Inflation


  1. Sengstaken RW, Blakemore AH. Balloon tamponage for the control of hemorrhage from esophageal varices. Ann Surg. 1950 May;131(5):781-9. doi: 10.1097/00000658-195005000-00017. PMID: 15411151; PMCID: PMC1616705.
  2. Nickson C. Sengstaken–Blakemore and Minnesota Tubes. Life in the Fast Lane • LITFL. Published January 30, 2019.
  3. Powell M, Journey JD. Sengstaken-Blakemore Tube. [Updated 2022 Jun 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
  4. Yartsev A. Sengstaken-Blakemore, Minnesotta and Linton-Nachlas tubes. Deranged Physiology. Published July 13, 2015. Accessed April 6, 2023.
  5. García-Pagán JC, Reverter E, Abraldes JG, Bosch J. Acute variceal bleeding. Semin Respir Crit Care Med. 2012 Feb;33(1):46-54.
  6. Mason J. Placement of a Blakemore Tube for Bleeding Varices. EM:RAP HD Videos. Accessed December 17, 2021.
  7. Farkas J. PulmCrit Wee: Ultrasound-guided blakemore tube placement. EMCrit Project. Published May 4, 2016. Accessed April 6, 2023.
  8. Roohollahi A, Suleiman Bilal Rana H, Hadique S. Blakemore Tube Insertion – BAVLS. American Thoracic Society. Published June 1, 2020. Accessed April 7, 2023.

SAEM Clinical Images Series: An Ominous Umbilical Lesion


A 54-year-old male with a past medical history of atrial flutter and alcohol use disorder presents with an umbilical wound that has been bothering him for approximately six months. There is no history of trauma, prior infection, or umbilical surgery. There is intermittent mild pain and irritation that occurs randomly. No drainage or bleeding. He admits to picking at the wound regularly. He denies fever, chills, nausea, generalized abdominal pain, diarrhea, constipation, dysuria, and hematuria. The patient drinks four or more alcoholic beverages daily and has a long-standing history of tobacco use.


Vitals: BP 105/73; HR 70; RR 16; SpO2 97% on room air; Temp 36.1°C

Constitutional: Appears stated age, resting comfortably, well-appearing.

Abdominal: Soft, flat, non-tender.

Skin: Umbilical wound characterized by a peripheral eschar and a central area of hyperpigmented and crusted tissue overlying an area of whiteish moist tissue that was uncovered by gentle cleansing. No surrounding erythema and no areas of fluctuance. No active drainage or malodor.

None available.

Sister Mary Joseph (SMJ) nodule is a rare cutaneous metastasis of gastrointestinal or genitourinary primary malignancies to the umbilicus [1,3]. They are typically firm, painful, indurated, and irregularly shaped, with sizes typically less than 2 cm [1]. They can be ulcerated or necrotic with variable presence of discharge ranging from purulent to serous or serosanguinous [1]. Sister Mary Joseph nodules typically arise late in disease and portend a poor prognosis [1]. Most primary malignancies are adenocarcinomas (75%), and pancreatic cancers represent approximately 9% of umbilical metastases [1]. Mean survival of patients with SMJ nodules is less than 12 months, and less than three in those with pancreatic primaries [1]. Prognosis is slightly less bleak if the SMJ nodule is the only metastatic site [1]. Sister May Joseph Dempsey was a nun and surgical assistant to Dr. William Mayo, the surgeon who developed the approach to umbilical hernia repair and the first to identify the connection between abdominopelvic cancers and umbilical nodules [2,3].

Abdominal CT imaging.

Our patient was discharged on the initial visit with wound care instructions. He returned to the Emergency Department two months later and was admitted for atrial flutter with rapid ventricular response and acute on chronic congestive heart failure. During that visit, the patient had a CT chest/abdomen/pelvis that demonstrated likely a pancreatic tail adenocarcinoma with metastasis to the peritoneal and abdominal walls. The patient declined any further intervention.

Take-Home Points

  • Sister Mary Joseph nodules are umbilical metastases from abdominopelvic primary malignancies.
  • Recognition of their features on clinical exam can lead to a more rapid diagnosis.
  • Prognosis is grim with an average survival of less than one year.

  1. Vekariya P, Daneti DB, Senthamizh Selvan K, Verma SK, Hamide A, Mohan P. Sister Mary Joseph Nodule as an Initial Presentation of Pancreatic Adenocarcinoma. ACG Case Rep J. 2020 Aug 25;7(8):e00453. doi: 10.14309/crj.0000000000000453. PMID: 32903972; PMCID: PMC7447472.
  2. Palazzi DL, Brandt ML. Care of the umbilicus and management of umbilical disorders. UpToDate. Updated August 27, 2021. Accessed January 2, 2022.
  3. Tso S, Brockley J, Recica H, Ilchyshyn A. Sister Mary Joseph’s nodule: an unusual but important physical finding characteristic of widespread internal malignancy. Br J Gen Pract. 2013 Oct;63(615):551-2. doi: 10.3399/bjgp13X673900. PMID: 24152477; PMCID: PMC3782795.

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