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.
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.
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 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 . 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 . 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 .
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].
Esophageal rupture (Boerhaave’s syndrome)
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 .
How do you insert these esophageal tamponade devices?
The following instructions are for inserting a Sengstaken-Blakemore (SB) tube [3, 6]:
Pre-measure 50 cm above the gastric balloon and esophageal balloon and mark them on the SB tube.
Fully lubricate the tube.
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.
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.
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 . However final confirmation prior to full inflation should be with a chest X-ray.
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.
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.
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.
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.
Take your manual blood pressure cuff and detach the connections so you have only a plastic tube that runs to the pressure gauge.
Connect this plastic tube end to the male Luer lock of a 3-way stopcock.
Connect the esophageal balloon to a female luer lock on the 3-way stopcock.
Place a 50 cc syringe on the final female Luer lock of the 3-way stopcock.
Turn the 3-way stopcock off towards the pressure gauge and inflate the esophageal balloon with 10 ccs of air.
Then turn the 3-way stopcock off towards the syringe and you should have a reading on the pressure gauge.
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
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.
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.
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.
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 . They can be ulcerated or necrotic with variable presence of discharge ranging from purulent to serous or serosanguinous . Sister Mary Joseph nodules typically arise late in disease and portend a poor prognosis . Most primary malignancies are adenocarcinomas (75%), and pancreatic cancers represent approximately 9% of umbilical metastases . Mean survival of patients with SMJ nodules is less than 12 months, and less than three in those with pancreatic primaries . Prognosis is slightly less bleak if the SMJ nodule is the only metastatic site . 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].
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.
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.
Palazzi DL, Brandt ML. Care of the umbilicus and management of umbilical disorders. UpToDate. Updated August 27, 2021. Accessed January 2, 2022. https://www.uptodate.com/contents/care-of-the-umbilicus-and-management-of-umbilical-disorders?search=sister%20mary%20joseph%20nodule&source=search_result&selectedTitle=2~6&usage_type=default&display_rank=2#H25.
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.
A 102-year-old female presents with intermittent epigastric abdominal pain for the last two days. Episodes have no relieving or exacerbating factors. The pain originates in the epigastrium and radiates diffusely to the abdomen and back, resolving on its own within minutes of onset. She has had one episode of nonbilious, non-bloody emesis. Her last bowel movement was two days prior and she hasn’t been able to pass gas. The pain is associated with mild shortness of breath which has been progressively worsening since the onset of symptoms. Her family was concerned and called EMS because the shortness of breath has worsened and the episodes of pain have been progressively worsening in intensity. The patient denies fever, chills, hematuria, urinary frequency, chest pain, headache, dizziness, syncope, recent traumatic events, and any other associated symptoms.
The CT demonstrates a spigellian hernia causing a small bowel obstruction. Spigellian hernias are hernias in the spigellian fascia which is located between the semilunar line and the lateral edge of the rectus abdominus muscle. These hernias constitute 0.12% of abdominal wall hernias, making them very rare and difficult to diagnose clinically. Spigellian hernias often go unnoticed until they are strangulated and require surgery. This patient not only had a rare spigellian hernia but also had a hiatal hernia causing the stomach to enter the pleural space. It’s possible that the bowel obstruction worsened the hiatal hernia with the backup of gastric contents and gas.
Spigellian hernias are rare abdominal wall hernias with a myriad of potential complications.
Shortness of breath is frequently considered a pathology involving the lungs or pulmonary vasculature, however abdominal complaints, especially in this case, can cause significant respiratory distress.
Elderly patients may have difficulty verbalizing their exact symptoms, and it is good practice to gather collateral information from families to aid in caring for these patients.
An 18-year-old male with no significant past medical history presents with diffuse abdominal pain and multiple episodes of non-bloody, non-bilious vomiting for three days. The patient was seen yesterday at another facility and states he was diagnosed with gastritis and discharged with Zofran, which provided no relief. He denies fever, diarrhea, or urinary symptoms and states his last bowel movement was two days ago and was consistent with his usual bowel movements.
Superior Mesenteric Artery (SMA) syndrome also known as Wilke’s or Cast Syndrome is a condition where the third section of the duodenum gets compressed between the superior mesenteric artery and the aorta leading to a proximal obstruction in the duodenum and stomach. The most common etiology of SMA syndrome is the loss of the mesenteric fat pad surrounding the SMA. This leads to an acute angulation between the SMA and the aorta, thus compressing the duodenum and causing a partial or complete obstruction. While the condition is rare, predisposing factors include sudden weight loss and chronic illnesses such as malabsorption syndromes, AIDS, and malignancy.
Treatment in the acute stage is conservative management including gastric decompression, IV fluids, correction of electrolyte abnormalities, and nutritional support, which may include temporary gastro-jejunostomy (GJ) tube placement. Severe refractory cases may require surgical intervention. This patient was admitted and treated conservatively, including a temporary GJ tube placement which was removed a few months later.
Hamden, A. & Scovell, S. (2020). Superior Mesenteric Artery Syndrome. In K. Collins (Ed.), UpToDate. Retrieved January 4, 2021, from https://www.uptodate.com/contents/superior-mesenteric-artery-syndrome
Niknejad, M. & Ranschaert, E. (2018). Superior Mesenteric Artery Syndrome. Radiopedia.org. Retrieved January 4, 2021, from https://radiopaedia.org/articles/superior-mesenteric-artery-syndrome?lang=us
Karrer FM. (2017). Superior Mesenteric Artery Syndrome. Medscape Reference. Retrieved December 22, 2020, from http://emedicine.medscape.com/article/932220-overview Genetic and Rare Diseases Information Center. (2018). Superior Mesenteric Artery Syndrome. [Online]. Available at: https://rarediseases.info.nih.gov/diseases/7712/superior-mesenteric-artery-syndrome#:~:text=Superior%20mesenteric%20artery%20syndrome%20(SMAS,complete%20blockage%20of%20the%20duodenum
A 2-year-old boy with a past medical history of Hirschsprung disease presents to the emergency department (ED) with vomiting, abdominal distension, and inability to tolerate PO for one day. His parents had been instructed by their pediatric surgeon to perform rectal irrigations 2-3 times daily for the few days prior to presentation.
The differential diagnosis for pediatric patients presenting with vomiting is broad and includes but is not limited to gastritis, diabetic ketoacidosis, pyloric stenosis, appendicitis, intussusception, urinary tract infection, colic, toxic ingestion, volvulus, incarcerated hernia, and bowel obstruction. However, in a child with Hirschsprung disease who presents with vomiting, an emergency medicine physician must maintain a high degree of suspicion for Hirschsprung-associated enterocolitis (HAEC).
Hirschsprung disease is a rare congenital condition affecting approximately 1-in-5,000 births that refers to a functional intestinal obstruction due to the absence of ganglionic cells in the myenteric plexus of the distal colon. Life-threatening complications of Hirschsprung disease include bowel obstruction, Hirschsprung-associated enterocolitis (HAEC), and toxic megacolon. HAEC is the leading cause of morbidity and mortality in these patients. HAEC can present with vague symptoms such as fever, diarrhea, vomiting, rectal bleeding, constipation, and lethargy. Due to these nonspecific symptoms, it is necessary for emergency medicine physicians to maintain a high index of suspicion for HAEC. Once diagnosed, immediate resuscitation should begin with the placement of a rectal tube for decompression, initiation of broad-spectrum antibiotics and fluids, as well as urgent pediatric surgery consultation.
HAEC can present with nonspecific symptoms of diarrhea, vomiting, fever, lethargy, abdominal distension, and obstipation.
HAEC must be quickly identified in patients with Hirschsprung disease due to the risk of rapid decompensation from hypovolemic shock secondary to dehydration, septic shock from HAEC, and the development of toxic megacolon.
HAEC is the leading cause of morbidity and mortality in pediatric patients with Hirschsprung disease.
Gosain A. Established and emerging concepts in Hirschsprung’s-associated enterocolitis. Pediatr Surg Int. 2016 Apr;32(4):313-20. doi: 10.1007/s00383-016-3862-9. Epub 2016 Jan 19. PMID: 26783087; PMCID: PMC5321668.
Maloney, Patrick J. “Gastrointestinal Disorders.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th Edition. Chapter 171. Page 2126-2144. 2018.