NG Tube for SBO

Is a nasogastric (NG) tube really needed for management of small bowel obstruction (SBO)? NG tube placement is one of my least favorite ED procedures. I therefore find myself hesitating every time surgery requests one, but what is the evidence behind it?

Surprisingly, there is little data and no randomized control trials on the use of NG tubes in SBO. A chart review in 2013 looked at 290 patients admitted with SBO. 20% of those 290 patients had a NG tube placed. They found that ⅔ of these patients were managed non-operatively, irrespective of NG tube placement. In addition, decompression with an NG tube was not found to be associated with decreased bowel ischemia or need for surgery. Use of an NG tube was actually found to be associated with worse outcomes, such as increased length of hospital stay, higher complication rate, and longer time to resolution.

Part of the reason that I dislike this procedure is the apparent discomfort we cause when placing them. Patients routinely rate it as one of the most painful procedures performed in the ED. We attempt to decrease pain with anesthetics, even though many ED physicians do not believe them to be effective. A RCT was done assessing the use of surgical lubricant versus topical lidocaine and phenylephrine for the nose with tetracaine and benzocaine spray for the throat. Patients reported a significant decrease in discomfort when providers used vasoconstrictors and topical anesthetics compared to surgical lubricant. 

However, there are some cases where NG tubes may be indicated. Patients who are vomiting after antiemetics or have a significantly distended stomach may benefit. Rather than placing them on all patients diagnosed with an SBO, we should select patients for this procedure based on their symptoms.

Thanks for reading!

Ariella 

Resources:

Fonseca AL, Schuster KM, Maung AA, Kaplan LJ, Davis KA. Routine nasogastric decompression in small bowel obstruction: is it really necessary? Am Surg. 2013 Apr;79(4):422-8. PMID: 23574854

Paradis M. Towards evidence-based emergency medicine: Best BETs from the Manchester Royal Infirmary. BET 1: Is routine nasogastric decompression indicated in small bowel occlusion? Emerg Med J. 2014 Mar;31(3):248-9. doi: 10.1136/emermed-2014-203617.1. PMID: 24532357

Singer AJ, Konia N. Comparison of topical anesthetics and vasoconstrictors vs lubricants prior to nasogastric intubation: a randomized, controlled trial. Acad Emerg Med. 1999 Mar;6(3):184-90. doi: 10.1111/j.1553-2712.1999.tb00153.x. PMID: 10192668

Witting MD. "You wanna do what?!" Modern indications for nasogastric intubation. J Emerg Med. 2007 Jul;33(1):61-4. doi: 10.1016/j.jemermed.2007.02.017. Epub 2007 May 30. PMID: 17630077

POTD: History of the Match

In celebration of everyone who successfully matched today, I wanted to talk about the fascinating history of the Match, from the crazy days of pre-Match chaos and to the unsung heroism of one medical student that changed it all!

In ye olden days...

Back at the turn of the century, residencies were only just in their nascency, and there was no strict requirement of residency in order to practice medicine. Scary thought, considering I didn't know how to order Tylenol let alone practice medicine when I graduated from medical school. In fact, residencies were once called "undergraduate repair shops" in the 1910 Flexner Report (a revolutionary-but-also-definitely-morally-grey-and-racist education reform paper). They became more popular with the rise of medical specialties, where graduates would essentially apprentice until they felt comfortable to practice on their own. However, as more specialties developed, the value of residency rose, and by the 1930s, most hospitals were requiring residency training before completing boards exams.

By the 1940s, competition for residencies grew fierce. Offers were given out increasingly earlier, so much so that they were being extended to students only in their second year of medical school. It got so bad that medical schools were embargoing recommendation letters to prevent the hospital equivalent of cradle-robbing. Soon, competition got so bad that "exploding offers" were being made that had a 12-hour expiration date, leaving many students scrambling to send off telegrams and make phone calls. No bueno STOP

Thus, the first Match system was born.

The Match that never was:

In 1951, the Mullin-Stalnaker algorithm was in works to be implemented in the first ever match process, and it was being championed by the high echelon of medicine including the Dean of Harvard Medical School. Thousands of dollars were being poured into making this event work, and it would be entirely derailed by a maverick medical student named William Hardy Hendren III. A Navy veteran with lots of chutzpah, he noticed the algorithm was flawed in several ways, and even presented his argument on the blackboard with the Dean and entire medical class present.

I won't go into the nitty-gritty of the Mullin-Stalnaker algorithm for sake of brevity, however it's actually super interesting and explained really when in this blog (https://thesheriffofsodium.com/2020/02/03/the-match-part-2-getting-under-the-hood-how-does-the-match-work/). Long story short, this match process penalized students who ranked "reach" programs, and it often produced what we call unstable matches - matches in which more favorable matches existed for both parties and were not considered or passed on. This encourages "elopement" by either party to make deals outside the matching system.

Going back to our story, Mr. Hendren realized this, and despite multiple threats from the Dean about withholding his graduation and that "[the Dean] didn't give a damn if any of [the students] get internships," he persisted in his quest for reform. In the historic frantic following weeks, Hendren led a movement and gathered over half the student leadership of medical schools across the country and created their own algorithm, "The Boston Pool Plan." This new plan assumed a "deferred acceptance" algorithm, in which a student was tentatively assigned to a hospital until or unless they match at a higher ranked place. There was, as suspected, resistance from the powers-that-be, of which Hendren replied:

"If you don't change the plan, it will be the end of it. I have votes from 95% of the students in the country...These same students have said they're going to bolt if you don't change the plan. We're not going to sacrifice our futures because of the errors you all have made in setting up this plan the way that you have."

The leadership deferred to the demands of Hendren and the students, and the following year the Boston Pool Plan was implemented for the first ever match. Hendren went on to become a renown pediatric surgeon, remaining on to serve as emeritus chief of surgery until his death just this past May at the age of 96.

POTD: Postpartum Hemorrhage

Postpartum hemorrhage (PPH) is classically defined as > 500 cc of blood loss after standard vaginal delivery or >1000 cc after a C-section. However, most recently ACOG redefined PPH as >1000 cc of blood loss OR signs and symptoms of hypovolemia in the setting of bleeding within the first 24 hours. It is an incredibly common event, occurring in almost 1 in 5 postpartum mothers and is the most frequent cause of maternal morbidity in the developed world. 

The 4 T's of Postpartum Hemorrhage

Tone: uterine atony accounts for 70-80% of PPH. Blood flow can reach up to 500-900 ml/min during delivery. Key presentation is the "soft, boggy uterus." The predisposing risk factors are

• impaired contraction from local inflammation or acidosis of uterine tissue (chorioamnionitis)

• down regulation of oxytocin receptions (prolonged labor)

• diminished actin-myosin interaction from enlarged uterus (macrosomia, multiple gestations)

Actions:

• Bimanual massage: Manually massage the uterus, with one hand internally inside the vagina and pressing against the uterus from below, while applying external pressure with the other hand above the fundus of the uterus. Avoid downward massage by the internal hand as it can cause injury to the blood vessels and potentially cause uterine inversion

• Uterotonics: there are several available medications that can increase uterine tone, of which the most important the most crucial is oxytocin. Oxytocin is endogenously excreted and induces uterine contraction. It can be given 40 mg IV in a 1 L normal saline bolus and then continued at 200 ml/hr until uterus is firm. Alternatively, it can be given as 10 mg IM x 2. Oxytocin is first-line and should be given in all patients with uterine atony. Other medications can be added as needed, see below:

  • Misoprotsol (Cytotec): a prostaglandin adjunct that stimulates uterine contraction. It can be given as 1000 mcg (usually 5 tablets) rectally or sublingually and has no contraindications in an emergent setting

  • methylergonovine (Methergine): induces smooth muscle contraction. for PPH should be given as 0.2 mg IM every 2-4 hours until max of 5 doses. This should NOT be given IV as it induces severe hypertension and can precipitate CVA and is contraindicated in patients with hypertension

  • Carboprost: a synthetic prostaglandin that induces myometrial contraction and vasoconstriction through smooth muscle contraction. It's given 250 mcg IM or injected into the myometrium, and can be in 15-90 minute intervals for a max dose of 2 mg. Similarly, this should NOT be given IV as it can induce hypertension and severe bronchospasm, and is contraindicated in patients with asthma or HTN

• Our resuscitation bay has a PPH pharmacy kit! It hands out in the fridge in room 52 and comes with a handy slip with all the dosages, route, frequency and contraindications! Go check it out!

Trauma: Genital tract trauma is the second most common cause of PPH. up to 80% of traumas are minor and occur in the vagina or perineum. However consider harder to reach areas such as cervical Any ongoing bleeding that does not stop with tamponade should be repaired via suturing. Other options include tamponade with a bark balloon, visualized below. Often we don't have these in the emergency room, so consider using a Blakemore tube (fold the distal tip back, inflate the esophageal balloon).

External aortic compression can also be used as an emergency maneuver, where you apply direct firm pressure with a closed fist over the aorta just above the umbilicus. This is obviously a temporizing maneuver and should be used as a bridge to a more permanent solution or during transport to OR, but it remains fairly effective.

Tissue: refers to retained products of conception. any retained products prevents induction of uterine contraction that occurs after disruption of the placenta. Examine the placenta to see if it's intact. If possible, attempt to retrieve products that are visible and within reach via manual or curettage. If it cannot be reached, they required OR.

Thrombin: both inherited and acquired coagulopathies should be considered. There are obviously many different ways to treat coagulopathies that are tailored to specific clinical pictures, of which I will briefly cover and not go through the mechanisms. Consider DIC and hypofibrinogenemia in placental abruptions and amniotic fluid embolism. 

• If giving MTF, you should also give FFP and platelets in a 1:1:1 ratio

• For von Willebrand, give DDAVP

• for DIC, given cryoprecipitate

• for hemophilia, give factor replacement therapy

A word on TXA: previous recommendations suggest IV TXA. However, the WOMAN trial in 2017 showed no benefit. That being said, there is much debate on the metrics of how this trial was performed, that the exclusion criteria excluded the sickest patients, there are other studies showing benefits of TXA etc. etc. Long story short, evidence is mixed, and since TXA has little adverse events, giving 1 gram IV isn't going to hurt anyone.