Brace yourselves: Thyroid Storm is coming


Thyroid storm is rare, but has a high mortality ranging from 10-30%. It is more commonly precipitated by an acute stress event such as surgery, trauma, infection, etc. Less commonly it is from untreated hyperthyroidism.

This guide reviews the common causes, presentation, and diagnosis of thyroid storm, as well as the life-saving treatment needed in the ED.


Pathophysiology and Presentation

Remember the simplified approach to hyperthyroidism and the 2 B’s:

Increased Beta-adrenergic activity: tachycardia, palpitations, tremor, diaphoresis, heat intolerance, oligomenorrhea.

Increased Basal metabolic activity: weight loss with high appetite, diarrhea, polyuria, hyperglycemia, hypocholesterolemia, increased lipolysis.


Common physical exam findings:

Hyperpyrexia: temperature is often >102 F.

Skin: erythematous, warm skin to touch, thinning of hair.

Eyes: only Grave’s has ophthalmopathy causing exophthalmos. Inflammation of extraocular muscles and connective tissue results in proptosis and impaired eye function due to edema. Lid lag on exam.

Neck: goiter only in Grave’s.

Cardio: tachycardia with wide pulse pressure. Heart rate often exceeds 140 in >60% of patients. Atrial fibrillation can be found in ~20% of patients.

Pulm: tachypnea.

Neuro/Psych: agitation, restlessness, emotional lability, sometimes if severe enough, psychosis. High association with mortality (very similar to excited delirium).


Major causes include:

1)     Grave’s Disease: most common cause worldwide. Autoimmune disease in which thyroid-stimulating immunoglobulin binds to the TSH receptor and stimulates it, leading to excess thyroid hormone production.

2)     Toxic Multinodular Goiter: hyperactive nodules within the gland that release thyroid hormone.

3)     Iodine-induced hyperthyroidism: rare. Iodine load from iodine-rich drugs like amiodarone or iodinated contrast.



Note: these sick patients required a large differential and generous workup. See our handout on delirium for mnemonic and diagnostic approach!


All patients with overt hyperthyroidism will have some clinical constellation of symptoms and low TSH.

Serum TSH cannot determine the cause or degree of hyperthyroidism.

High free T4 and/or T3, however they are no higher than in patients with just simple hyperthyroidism.


There are no validated, clinical tools available to assist in diagnosis. A high index of suspicion in patients is needed in those with fever, tachycardia, and psychological symptoms, especially in those with a history of other endocrine/autoimmune disorders.


Determining cause will likely not occur in the ED, although most commonly the cause is Grave’s. Radioiodine uptake and/or thyrotropin receptor antibody measurement should be performed but this will occur in the ICU. This should never delay treatment.



Should be without delay and in a distinct order as outlined below.

1)     Control unstable beta-adrenergic symptoms                                       Beta-blockers

2)     Stop hormone release                                                                                   Thionamides

3)     Stop new hormone production                                                                 Iodine

4)     Reduce inflammatory burden                                                                   Glucocorticoids


Step 1 Beta-blockade

Propranolol 60-80 mg orally every 6 hours or IV 1 mg every 1-2 hours as needed

Propranolol has added benefit of reducing T3 levels by inhibiting Type 1 deiodinase.

Why propranolol? It is for sure the correct answer on boards, but it doesn’t have to be in real life. In cardiac patients or those with asthma/COPD, B1-selectivity and titratability would be more preferred. Esmolol, metoprolol, diltiazem can be used. In fact, esmolol is best suited for IV form due to rapid titration and minimizing adverse effects from quick on/offset.


Step 2 Thionamides

-Propylthiouracil 200 mg every 4 hours

-Methimazole 20 mg every 6 hours

PTU is favored as it has peripheral blockage of conversion from T4 to T3. However, there is no difference in mortality or morbidity in patients receiving either drug.

Thionamides start working in ~1-2 hours.

Methimazole is preferred for less severe hyperthyroidism due to less frequent dosing and overall it is less hepatotoxic. Methimazole should be used once discharge approaches because it is less dosing.


Unfortunately, both thionamides are only in PO form. So, either the patient is able to tolerate oral intake (debatable if it’s true Thyroid Storm), or intubated with an NG/OG tube.


Side effects: agranulocytosis, hepatotoxicity, but these are complications that occur much later in the patient’s care and are not typically observed in the ED.


Step 3 Iodine

KI 5 drops PO every six hours or Lugol's solution, 10 drops every eight hours

It should be given 1 HOUR after thionamide dose to prevent it from being used as substrate.

A large bolus of iodine inhibits further T4 and T3 production in the thyroid (Wolff-Chaikoff effect), preventing the production of new hormone for ~5-7 days. Works within a few hours.


Step 4 Glucocorticoids

IV Hydrocortisone 100 mg every 8 hours.

Glucocorticoids reduce T4-to-T3 conversion and possibly reduce the autoimmune process in Graves' disease.

They should not be given in hyperthyroidism absent of storm.


Other critical supportive care  measures

-APAP for fever

-Aggressively look for infection, empiric antibiotic coverage is not a bad call.

-Early intubation for control of airway and proper administration of medications.

-In those with Grave’s disease, radioactive iodine or thyroidectomy should be performed when clinically stable, within 5-7 days.

-Rate control for A fib (via B-blockers). A fib automatically converts in 60% patients if hyperthyroid is treated. These patients still need anticoagulation.





1.       Akamizu T, Satoh T, Isozaki O, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid 2012; 22:661.

2.       Swee du S, Chng CL, Lim A. Clinical characteristics and outcome of thyroid storm: a case series and review of neuropsychiatric derangements in thyrotoxicosis. Endocr Pract 2015; 21:182.

3.       Angell TE, Lechner MG, Nguyen CT, et al. Clinical features and hospital outcomes in thyroid storm: a retrospective cohort study. J Clin Endocrinol Metab 2015; 100:451.

4.       Ono Y, Ono S, Yasunaga H, et al. Factors Associated With Mortality of Thyroid Storm: Analysis Using a National Inpatient Database in Japan. Medicine (Baltimore) 2016; 95:e2848.

5.       Ngo SY, Chew HC. When the storm passes unnoticed--a case series of thyroid storm. Resuscitation 2007; 73:485.

6.       Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am 2006; 35:663.

7.       Chiha M, Samarasinghe S, Kabaker AS. Thyroid storm: an updated review. J Intensive Care Med 2015; 30:131.

8.       Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid 2016; 26:1343.

9.       Cooper DS, Daniels GH, Ladenson PW, Ridgway EC. Hyperthyroxinemia in patients treated with high-dose propranolol. Am J Med 1982; 73:867.

10.     Cooper DS, Saxe VC, Meskell M, et al. Acute effects of propylthiouracil (PTU) on thyroidal iodide organification and peripheral iodothyronine deiodination: correlation with serum PTU levels measured by radioimmunoassay. J Clin Endocrinol Metab 1982; 54:101.

11.     Mazzaferri EL, Skillman TG. Thyroid storm. A review of 22 episodes with special emphasis on the use of guanethidine. Arch Intern Med 1969; 124:684.

The Trolling Stones: Cholecystitis

Check out our podcasts on cholecystitis (Episode 26) and choledocholithiasis (Episode 43), also check out other cool study guides at



Gallstone disease, most commonly manifesting as cholecystitis, is seen in up to 10% of patients who have symptomatic gallstones. This guide will serve as a succinct outline to approaching patients with RUQ pain suspected of having gallstone pathology. One of the trickiest parts of these pathologies is keeping all these “C names” straight.

In this document we will focus on biliary colic and cholecystitis, we will also touch on emphysematous cholecystitis.

Cholelithiasis: stone in the gallbladder. Simple as that. It does not indicate if the patient is symptomatic or not. In fact, ~6% of Westerners walk around with gallstones, and only about 10% of them end up having cholecystitis.

Biliary colic: RUQ pain due to gallbladder contraction. It typically comes in phases after eating and lasts a total of a few hours (always <6). Fever and peritoneal signs are always absent, but the RUQ pain can mimic cholecystitis. 70% of patients develop recurrent symptoms in 2 years. Furthermore, biliary colic usually does not present with fever or leukocytosis (no inflammatory component).


Acute cholecystitis: obstruction of the cystic duct with subsequent inflammation of the gallbladder. Although it is most commonly due to cholesterol or bilirubin stones obstructing the cystic duct, in 5-10% of cases acalculus cholecystitis is the cause. Look for acalculous cholecystitis as the cause in ICU patients or those usually patients on TPN (outside the scope of this review).


Presentation: RUQ or epigastric pain lasting > 4 hours, often has referral pain to shoulder or back. Patients may experience fever, nausea/vomiting, and anorexia, however these are not seen in the majority of patients. The episode is most likely post-fatty food ingestion.

On exam, patients can often be ill-appearing, with voluntary and involuntary guarding of the RUQ.

Murphy’s sign can be elicited when palpating the RUQ and asking the patient to take a deep breath there is cessation of inspiration. On inspiration the gallbladder is displaced from beneath the liver to be against the examiner’s fingers. Murphy’s Sign is NOT simply palpable tenderness of the RUQ (this is a common misconception). Murphy’s Sign is very sensitive but poorly specific (97% and 48% respectively).

Rarely, if the patient has another form of gallbladder pathology, they can look very sick (think fever and jaundice for choledocholithiasis, generalized peritonitis and sepsis for emphysematous cholecystitis, etc).


In fact, those with emphysematous cholecystitis are by far the most critical biliary pathology patients that roll into the ED. Gas-forming organisms (classically, clostridium welchii) invade the gallbladder wall, causing fever, RUQ pain, and early markers for sepsis. Classically more in males with diabetes, these patients have a high risk of perforation and necrosis, with rapid progression to perforation.


Diagnosis: Labs are not sensitive or specific, usually CBC, CMP, lipase. Leukocytosis with left shift is expected but pretty much every major pathology on the planet. Very rarely there is a mild elevation in bilirubin, also nonspecific.

Alkaline phosphatase and LFT elevation are NOT expected, and their elevated presence should raise suspicion for choledocholithiasis or other hepatic pathology.


Ultrasound: the best, initial test. Findings that diagnose cholecystitis:

-wall thickening >5mm, pericholecystic edema (double wall sign)

-presence of gallstones,

-sonographic Murphy sign elicited during visualization with a probe

RUQ US truly is the best “bang for your buck” in terms of ED tests. It is hands down the best initial step test and “next step” test. For its ability to quickly acquire images and not requiring much technician skill, it is the most specific test for identification of gallstone disease, with sensitivity about 84% and 99% specificity.


In emphysematous cholecystitis, the US can be false negative because of air in the wall of the gallbladder. The report could falsely report “overlying bowel gas blocks view” or something like that. This is due to gas-forming organisms.


HIDA (cholescintigraphy): if ultrasound is equivocal (if gallstones seen without wall thickening or pericholecytic edema, or if peri-wall edema is appreciated without stone visualization) HIDA scan can be performed. This is when IV tracer (technetium) is given and taken up by bile secreting hepatocytes. The tracer is able to track bile flow from the liver to the gallbladder and also into the common bile duct. Inability to see the tracer fill the gall bladder lumen in 30 minutes to 1 hour is diagnostic of cholecystitis.

Its sensitive and specificity approach 90-97% and 70-90%, some pretty wide ranges.


This test should never be ordered first line. It should also never be ordered in the ED (huge workflow killer). Patients that undergo this test likely need admission for observation and further investigation.


CT: there has been an increase in CT detecting cholecystitis only because the number of patients receiving CT in the ED has increased as well. CT can detect wall edema, pericholecystic fluid, and large gallstones, and its sensitivity approaches 94%, BUT its specificity is extremely poor, 59%. Therefore, we do not recommend its routine usage for biliary pathology. Ultrasound first!



Besides calling your friendly general surgeon for cholecystectomy, remember your job doesn’t just end there in the ED…

Supportive therapy: IV hydration, electrolyte correction, keep NPO

Pain control: Opioids have long been thought of causing sphincter of oddi spasm, whether or not this translates into actual clinical                                    medicine is unclear (we think it’s mostly hogwash). Opioids should be used for pain control as indicated.

Empiric antibiotics: The goal is to prevent secondary infection such as: gallbladder necrosis with subsequent perforation or                                                                 pericholecystic abscess. Coverage needs to include gram negative rods and anaerobes.

    Options: piperacillin/tazobactam, or ciprofloxacin/ceftriaxone and metronidazole


Who needs an emergent cholecystectomy?

-Anyone with suspected perforation or gangrenous necrosis (the latter is nearly impossible to diagnose until in the OR)

-Those with emphysematous cholecystitis


In those with emphysematous cholecystitis or gangrenous necrosis/perforation, resuscitation needs to be rapid and aggressive, with full sepsis workup and early antibiotics. Very often these are started empirically before US (sometimes they are too sick for US and this is where CT comes into play). Work with the surgery team and get them on board early. They will hesitate to take an incredibly sick patient to the OR who appears to have a “medical problem” (sepsis), but the imaging should the gallbladder as a cause. If the patient has obvious evidence of perforation (e.g. air under the diaphragm), it’s an easier discussion: antibiotics and OR.



If untreated, acute cholecystitis often resolves in 7-10 days. However, complications are frequent and have great potential to be life threatening. This is the driving reason for why we operate on gallbladders.

·       Gall bladder gangrene/necrosis: most common complication, seen in 20% of cases. Patients present septic. The elderly and diabetics are especially prone to this.

·       Perforation: seen in 10% of cases. Usually local but can expand into generalized peritonitis.

·       Cholecystoenteric fistula: a perforated gall bladder can lead to cholecystoduodenal or cholecystocolonic fistulas. This is rare and more typically seen in chronic gallbladder necrosis, <2% of all gallstone disease cases total. Symptoms include bile acid diarrhea and gallstone ileus.

o    Gall stone ileus: cholecystoenetric fistula leading to stone obstructing the ileocecal valve (gall stone size usually >2.5cm). Rare. Patient will have symptoms of small bowel obstruction.



1.       Williams, D. Gallbladder. Retrieved September 16, 2018, from

2.       Zakko, SF, Afdhal, NH. Acute Cholecystitis: Pathogenesis, clinical features, and diagnosis. UpToDate.Waltham, MA: UpToDate Inc. (Accessed on September 17, 2018.) 

3.       Zakko, SF. Overview of gallstone disease in adults. UpToDate.Waltham, MA: UpToDate Inc. (Accessed on September 17, 2018.

4.       Abboud PA, Malet PF, Berlin JA, et al. Predictors of common bile duct stones prior to cholecystectomy: a meta-analysis. Gastrointest Endosc 1996; 44:450.

5.       ASGE Standards of Practice Committee, Maple JT, Ben-Menachem T, et al. The role of endoscopy in the evaluation of suspected choledocholithiasis. Gastrointest Endosc 2010; 71:1.

6.       Einstein DM, Lapin SA, Ralls PW, Halls JM. The insensitivity of sonography in the detection of choledocholithiasis. AJR Am J Roentgenol 1984; 142:725.

7.       Fitzgerald JE, White MJ, Lobo DN. Courvoisier's gallbladder: law or sign? World J Surg 2009; 33:886.

8.       Tse F, Barkun JS, Barkun AN. The elective evaluation of patients with suspected choledocholithiasis undergoing laparoscopic cholecystectomy. Gastrointest Endosc 2004; 60:437

9.       Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Cochrane Database Syst Rev 2012; :CD009779.

10.     Teefey SA, Dahiya N, Middleton WD, et al. Acute cholecystitis: do sonographic findings and WBC count predict gangrenous changes? AJR Am J Roentgenol 2013; 200:363.

11.     Wu B, Buddensick TJ, Ferdosi H, et al. Predicting gangrenous cholecystitis. HPB (Oxford) 2014; 16:801.

All that wheezes... - Approach to management of Asthma and COPD in the ED

Objectives: identify similarities and differences in asthma and COPD presentations as well as their causes, relevant history and physical exam findings, diagnosis and complications, treatment, and disposition.


Asthma: reversible bronchoconstriction of the upper airways. Type 1 hypersensitivity response with immediate and late (“delayed”) phase.

Common precipitants: environmental (most common cause- worsened by poor compliance and includes cold temperature, pollution, airborne allergens, exercise), infection less common.

Presentation: acute dyspnea over hours to days with wheezing and/or poor air movement on exam.

Assessment: ABC’s as always. Are they protecting their airway? How alert are they? Are they in respiratory distress or able to speak in clear, complete sentences? Are they using accessory muscles to breathe? What is heard on their lung exam? Relevant history: ever intubated? How many exacerbations and hospitalizations per year? ICU admission?

From these questions you must decide what type of asthmatic you are dealing with and from here on out we detail these separately in either column: stable vs unstable (see pdf).

 Always the wrong answer on tests and in real life: theophylline, Heliox. We do not give these medications in the ED as they are no longer indicated (as for Theo.), or they are often controversial with limited data (Heliox).

-Leukotriene modifiers/antagonists, LABAs, and Omalizumab should never be given.


Bonus time: NIPPV à BiPAP and CPAP             

NIPPV is a form of noninvasive respiratory support delivered via face mask that has a tight seal. Oxygen, inhaled medications, and other gases can be given with higher airway pressures. NIPPV helps “stent” airways open and allow for better oxygenation, ventilation, and relief from obstructive lung disease.

-BiPAP: 2 pressure settings, inspiratory (IPAP) and expiratory (EPAP). Bigger the IPAP = bigger the “push” of air coming in. EPAP is essentially PEEP.

-CPAP: same thing as PEEP à positive end expiratory pressure. This mode keeps a steady stream of pressurized air in the airways throughout the respiratory cycle, allowing for alveoli to remain open and be recruited.


Last resort: Intubation

-Endotracheal intubation does NOT help fix the underlying problem in asthma and COPD. It should only be used if the patient can no longer tolerate the work of breathing and ventilation/airway protection are the concern.

-Delayed sequence intubation:

-Once intubatedà continue efforts to maximize airway obstruction (Albuterol through ETT, Mag, steroids, etc.)

-Vent settings: “permissive hypercapnia”. We want to avoid barotrauma which includes pneumothorax, so we do the following… low tidal volumes, low minute ventilation (6-8 breaths/min), <5 PEEP, Oxygen >88% is fine, and pH does not need full normalization. I:E ratio 1:4.

-In a critical scenario when the patient appears to be arresting or the ventilator states there is high peak pressure, disconnect the vent and compressing the chest to release trapped air. Also, these patients should be heavily sedated and consider short term paralysis so that the patient does not interfere with the ventilator.



Overview: COPD is just a name. It is divided into emphysema and chronic bronchitis, but for ED purposes these patients receive the same therapy. The good news is the algorithm for COPD workup is almost the same as asthma, except for 2 critical differences: 1) COPD is a destructive pathology of the lung, 2) COPD patients are generally older, have more medical problems, and therefore need a more established workup.

Assessment: same as asthma patients (see above!). In addition, Gold Criteria is used for COPD patients.

Gold Criteria for COPD exacerbation: increased cough, increased sputum production/change in color, increased dyspnea

Causes: unlike asthma, the most common cause of COPD exacerbation is infection (70%). Greatest predictor of COPD exacerbations is prior exacerbations (duh). >2 exacerbations/year or >1 hospitalization/year = high risk COPD patient! (see pdf for stable vs unstable).

*Fluoroquinolones should be used with caution or avoided altogether in many older patients (>65) as they have been shown to cause multiple concerning side effects (neuropathy, delirium, QT prolongation, tendinopathy and arthropathy, hepatic toxicity).

Other quick facts from studies (not for the test but good to know!):

MDI equals Nebulizer delivery for efficacy, however nebulizer preferred in acute setting due to patient tolerance and reliable delivery.

PO equals IV steroids for efficacy and time of onset but it’s the same story as above. We want to optimize patient breathing and tolerance. No swallowing pills.

Steroids can be considered the most important part of treatment so these need to be given as early as possible if able: multiple studies have shown decreased hospital stay, improved lung function and symptoms, reduced treatment failure risk by 50%, and even reduced relapse risk at 1 month.

Nearly all patients should be discharged home with steroids unless contraindicated or if they were recently given a course and are still on that prior course.

Critically, the 5 day “burst” course of 50-60mg daily prednisone found to be the same as tapered prednisone. Burst preferred due to easier dosing and less complications from patient’s mis-dosing.

Not just gas: appendicitis in adults in kids


Inflammation of the vermiform appendix is one of the most common causes of acute abdomen worldwide. It occurs most commonly in ages 10-30. In children <5 years old, appendicitis is <5% incidence.

Forget what you learned in medical school. This condition can be very difficult to diagnose in patients without CT imaging. The presentation is extremely variable, especially children.

This guide will discuss clinical features, presentation, and diagnosis of appendicitis in adults and kids


Initial inflammation (due to obstruction from fecalith, calculi, lymphoid hyperplasia, infection, tumors) -> Increase in intraluminal pressure along with bacterial overgrowth  —> necrosis and perforation

20% of patients have perforation in <24 hours of initial symptoms. 65% had perforation after 48 hours of symptoms.

 Presentation in adults

RLQ abdominal pain with anorexia. The case of periumbilical pain that migrates to the RLQ only occurs about 50-60% of the time.

The location of the appendiceal tip is also important. The tip can be located anterior, retrocecal, or even RUQ (pregnancy). Atypical abdominal pain is not uncommon.

Fever is often late in presentation. A strong differential of other causes of fever should be present.

McBurney’s Sign: point tenderness 2 inches from the ASIS on a straight line to the umbilicus. Sens and Spec range considerably (50-94%; 75-85% respectively).

Rovsing’s Sign: tenderness with palpation of LLQ which can reflect peritoneal irritation. Once again, Sens and Spec vary (20-70%; 60-96% respectively).

Psoas Sign: RLQ pain with passive right hip extension. The sensitivity <40% is quite awful, the specificity is 80-97% when done correctly.

Obturator Sign: flexion of the patient’s right hip and knee along with internal rotation of the right hip causes RLQ pain. Sens is 8% (not a typo), and Spec is 94%.


Labs are not very helpful. Typically, CBC, CMP, pregnancy test and urine studies are ordered.

80% of patients have leukocytosis, but leukocytosis is nonspecific in most cases of disease as well. Sens and Spec of leukocytosis: 80 and 55% respectively.

Its presence does not necessarily suggest appendicitis, but its absence might help.

Best diagnostic test: CT abdomen and pelvis with contrast. It is most accurate than the other modalities and the fastest to acquire. Findings that suggest appendicitis:

-enlarged >6mm diameter with occluded lumen

-wall thickening >2 mm

-fat stranding along periappendix or wall enhancement

-Appendicolith (~25% of patients)

One of the biggest concerns is nonvisualization of the appendix (10-20% of cases). This decreases the likelihood of appendicitis but does not eliminate it. Overall, Sens and Spec 95% and 96%, respectively.

US: preferred in children and pregnancy. Most accurate finding: appendiceal diameter >6 mm

Advantages: no radiation, no contrast. Unfortunately, the test is strongly dependent on patient body habitus, and operator experience. Overall, Sens 85% and Spec 90%.

This test effectively rules in/out appendicitis if the appendix is visualized.

MRI: most often used in pregnancy. Not well tolerated by patients as they are often in pain and have to lie on the table for >10 minutes for testing.

Plain radiographs have no role in diagnosis.


Modified Alvarado Score: Used to identify patients with low likelihood of appendicitis.

-Migratory RLQ pain (1 pt)      -Anorexia (1 pt)

-Nausea or vomiting (1 pt)       -RLQ tenderness (1 pt)

-Fever >99.5 (1 pt)                      -Rebound tenderness in RLQ (1 pt)

-Leukocytosis (2 pts)

Physician gestalt has been found in multiple studies to be equal in performance to the Alvarado score.

Analgesia: there is often concern that analgesia will limit the surgeon’s physical exam findings. Although there are no studies on the impact of analgesia on diagnosis, pain control has not been found to negatively impact overall care. Multiple studies where patients received IV morphine in the ED. Morphine was not associated with increased risk of perforation, negative appendectomy, or missed appendicitis.


What about the kids?!

Children have some of the same clinical features as noted above, however at much different rates. The absence of classic clinical features as noted above in the adult section is not sensitive or specific for excluding appendicitis.

-Lack of migration to RLQ (50%of patients), Absence of anorexia in 40%, no rebound tenderness in 50%. Wow, got to make it difficult don’t you, pediatrics? 

Neonates: appendicitis is rare. High mortality at 30%. Abdominal distention, vomiting, sepsis, anorexia. Huge overlap with necrotizing enterocolitis. These children typically look sick.

Children <5: uncommon. RLQ <50% of patients. Diffuse pain, fever, irritability, vomiting, grunting respirations, refusal to ambulate are all more common.

Children 5-12: frequent. Anorexia, vomiting, fever. RLQ pain and migration from periumbilical region is common. In most children they lie still, with one or both hips flexed. Not too uncomfortable unless they are disturbed. Abdominal pain can be elicited if child is asked to hop on one foot.

Children >12: mirrors adult findings as noted above.

CBC, CMP, urine studies, pregnancy test (in appropriate age and setting).

Leukocytosis: 96% of patients have it but has Sens and Spec of 70% and 80%, respectively.

Urine studies: pyuria can be seen up to 25% of patients. Its presence or absence alone should never be used to diagnose appendicitis.

Ultimately, patients with a clear alternative diagnosis present (pneumonia, UTI, pharyngitis) should undergo treatment for that condition first. For those whom it is difficult to exclude appendicitis, we divide patients into low, moderate, high risk groups.

Low risk: few clinical features, negative lab studies, no RLQ pain or RLQ pain but none with walking/jumping. Discharge with generous return precautions. If RLQ pain is present and distressing, reeval by PCP in 24 hours is warranted.

Moderate risk: decent exam findings and some symptoms, often leukocytosis. US evaluation +/- surgery eval. +/- admission with repeat abdominal exams.

High risk: strong exam findings, +/- concern for perforation, leukocytosis. Call surgery.

Many clinical scoring systems have been developed, all are beyond the scope of this handout and all have limited ability to identify patients. No studies have evaluated their ability to improve diagnosis compared to gestalt. We do not routinely use them.

Management with antibiotics?

There is a lot of ongoing talk about using a nonoperative approach to appendicitis with antibiotic therapy and close follow up. Its all the rage in Europe apparently. This discussion is outside the scope of the review, and to date there are 6 trials have been published.

Its definitely worth investigating further, but in general this decision will be made in concert with a surgeon’s evaluation. Surgery should always be called on cases of suspected or confirmed appendicitis.

Saddle up: All about Pulmonary Emboli

Sometimes in the ED you just need to saddle up and face adversity... John Wayne said something once to the effect of “Saddling up requires one to always think of PE”. We cannot find the reference but read it on Buzzfeed so it must be true. PE always seems to be on the differential. Its ever-elusive, dropping people dead at will, and we’re left rolling the dice with D-dimer. Let's review PE, its classic presentations, how to diagnose, treat, and disposition.

Airway Superiority: ED RSI

Wish to be an Airway ace? King of the glottis? This guide defines RSI, why we do it in the ED, when to do it/not do it, and a step by step overview with paralytics and induction agent details. ALL IN 2 PAGES. NO BS. It’s time to rule the airway.