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2 Range Why Generalists Triumph in a Specialized World - Early expertise and overspecialization do not equate to success. Having a breadth of knowledge is key to solving issues that cross different disciplines. - An extensive explanation of the benefit of the breadth of knowledge and the risks of super sub-specialization. Loss of cross-communication between silos of isolated components. - Wicked problems- issues that require outside-the-box thinking, can't be solved by relying on specialization but needs interaction between various contexts. - Capitalize on the varied backgrounds when trying to solve a problem. Gathering 10 specialists who all share the same knowledge and experience to focus on one issue can easily lead to a dead-end- without the benefit of new and fresh ideas, the team ends up in a loop. Diversity can exponentially increase problem-solving by drawing from different perspectives, viewpoints, and thought processes. - Contrasts to the 10,000-hour rule, which asserts the benefits of focused training and specialization. Previous Next

< Back Anorectal Disease Anorectal pain is an incredibly common condition . Thanks to our low-fiber Western diet and often inadequate hydration, constipation is a frequent occurrence. People also often spend long periods on the toilet. We used to read books, but now many play games or text on their smartphone. Constipation and prolonged sitting on the toilet can lead to several different problems. While discussing these symptoms can be awkard or uncomfortable, please talk to your doctor if your symptoms don't go away on their own. So what is anorectal pain? Although "butt pain" may be a common complaint, I want to be clear with my explanations. In reality, “butt” more accurately refers to the gluteal region, which is also known colloquially as derriere, buttock, backside, or fanny. It may be simplest to describe the butt as the area that rests on the surface of a chair when you sit. Anorectal refers to a more specific location, the anus and rectum, where stool passes through when you have a bowel movement. Please see the anatomically correct depiction below. What are the common causes of anorectal pain? Fissures Hemorrhoids Pruritis Ani Abscesses Less common- pelvic floor dysfunction, cancer Anatomy of the anus and rectum Two sphincter complexes encircle the rectal vault. The internal sphincter provides 85% of the resting tone. It is under involuntary control- this is how your body controls when you have a bowel movement. The external sphincter provides 15% of resting tone- it is under voluntary control, which means this is how you consciously control holding in a bowel movement. The internal hemorrhoids are veins that line the inside of the rectum, while the external hemorrhoid plexus is on the anal verge. These means that hemorrhoids are a NORMAL part of anatomy! They fill with blood to aid in incontinence, helping you control when you have a bowel movement. Anything that increases pressure in the abdomen, including prolonged straining, coughing, pregnancy, and enlarged prostate requiring straining to urinate, can lead to abnormally large venous plexuses, which are what most people know as hemorrhoids. See “Hemorrhoids” below for more details. Glands line the inside of the rectum and help lubricate stool. When the glands become obstructed, they can lead to abscesses. What are the common symptoms of anorectal disease? Pain Bleeding- either blood dripping in the toilet, blood on the toilet paper with wiping, and blood mixed with or on the stool's surface. Mucus drainage (constant moisture), which can cause challenges with perianal hygiene Pruritis (itching) Palpable mass Constipation/ diarrhea, incomplete voiding What causes anorectal disease? Prolonged straining or prolonged time sitting on the toilet, often due to constipation (hemorrhoids) Constipation and passing a hard stool can lead to tears in the skin (fissure) Underlying gastrointestinal disease (inflammatory bowel disease, etc.) How do I prevent anorectal disease? The goal is to improve bowel habits and minimize constipation. High fiber diet. Most Americans have a low-fiber diet, consuming way less than the recommended 20-35 grams of fiber per day. Fiber can come from dietary intake (the foods you eat) as well as supplements. Take the time to read labels. The foods we commonly think of as “high-fiber,” including lettuce, are not as fiber-rich as we think. A word of warning If you quickly add a significant amount of fiber to your diet, this can lead to gastrointestinal distress (gas, diarrhea, cramping, etc.). Add fiber slowly until you reach your goal! Stay hydrated! Fiber without adequate hydration will create hard stools (rabbit pellets), making constipation worse. The recommendation is a minimize of 64 ounces of water per day. Plain water is best, but flavoring with Crystal Light, lemon, or lime can make it more palatable. Listen to your body regarding bowel movements. Hold it until socially acceptable, but don’t hold for longer than necessary. But just as important, don’t force a bowel movement if you don’t feel the urge. Some people may be trained to try to have a bowel movement before leaving for work- if this works for you, that’s fine. But don’t let the clock dictate when you have to use the bathroom. Minimize the amount of time sitting on a toilet. Prolonged sitting increases pressure, which predisposes to pathology. If you are still having challenges, consider investing in a device to facilitate improving your posture. We are accustomed to using toilets…unfortunately, sitting creates an angle that makes it difficult to have a bowel movement. Squatting, with knees elevated closer to the chest, creates a straighter path leading to more optimal conditions to have a bowel movement. Consider a squatty potty! Specific Anorectal Pathology Hemorrhoids Anal Fissures Pruritis Ani Patient Info- Fiber Guide .pdf Download PDF • 68KB Patient Info- Hemorrhoids .pdf Download PDF • 58KB Patient Info- Anal Fissure .pdf Download PDF • 59KB Patient Info- Pruritis Ani .pdf Download PDF • 58KB Patient Info- Constipation .pdf Download PDF • 54KB Previous Next

< Back Pruritis Ani What is Pruritis Ani? Patient information: Pruritis Ani [American College of Colon and Rectal Surgeons] Pruritis ani is an unpleasant itching of the perianal skin (around the anus). Scratching can lead to further irritation and sets up a vicious cycle. Caused by other anorectal diseases, primary dermatology conditions, hygiene issues (sweat, stool, mucus on the skin), foods, soaps, clothing, or over-vigorous hygiene (aggressive wiping with rough material, use of topical cleaning agents). Diagnosis- detailed history, thorough exam to rule out underlying anorectal pathology What is conservative management for pruritis ani? Try not to scratch/ wipe/ scrub. It will just itch more, and things will get worse. Clean the anal area after bowel movements with hypoallergenic personal wipes. Do NOT over clean, as this may worsen your condition. Dry with a hairdryer on the cool setting instead of wiping the area dry. Use unscented Dove soap or dilute white vinegar for cleansing. AVOID potential contributing factors Citrus foods, caffeine-containing foods/ beverages- coffee, tea, cola, chocolate. Scented soaps, lotions, creams, powders, medicated wipes, witch hazel. Keep the area dry (can use cotton ball or a gauze pad). Avoid tight synthetic clothing that doesn’t breathe. Wear cotton undergarments. Maintain regular bowel movement with normal consistency (minimize stool leakage). Increase stool bulk by increasing fiber intake. Maintain adequate hydration- you MUST drink at least 64 ounces of fluid per day, in addition to increasing fiber intake. Medication Capsaicin- causes a low-grade burning sensation and decreases the perception of itching Zinc oxide- Apply a small amount of a barrier cream to the perianal skin in a thin layer. This will protect the skin from irritants. Mix Benadryl cream with the zinc oxide cream and apply it to the affected area. Benadryl- 25 mg by mouth at night for itching Patient Info- Pruritis Ani .pdf Download PDF • 58KB Patient Info- Fiber Guide .pdf Download PDF • 68KB Previous Next

< Back Nutrition...pending Nutrition Previous Next

< Back Abdominal Pain- Mesenteric Ischemia A 65-year-old male with 1 week of progressive abdominal pain presented to a small hospital. His medical history is significant for a myelofibrosis with chronic portal vein thrombosis. He underwent CT scan and was urgently transferred to the surgical ICU at the nearby tertiary hospital. CT abdomen and pelvis (coronal) https://video.wixstatic.com/video/3b6ff6_3a044f13731447f68a338b2b814e0d65/480p/mp4/file.mp4 CT abdomen and pelvis (axial) https://video.wixstatic.com/video/3b6ff6_102334b9eba6428f8c132cdcc0aa175e/360p/mp4/file.mp4 The abdomen pelvis CT showed chronic portal vein thrombosis with cavernous transformation as well as distal SMV thrombosis with inflammatory changes of the distal small bowel. There is a moderate amount of intra-abdominal fluid, including around the spleen and liver as well as in the pelvis. There is thickening of the small bowel wall as well as stranding and edema in the mesentery. There was also evidence of a splenorenal shunt. Representative slice from CT, axial Representative slice from CT, axial- labels Representative slice from CT, axial Representative slice from CT, axial- labels Differential diagnosis? Splenic injury secondary to splenomegaly (minor trauma can lead to splenic injury in the setting of splenomegaly). Bowel ischemia. Hollow viscus perforation. On arrival to the ICU, his abdominal exam revealed diffuse rebound tenderness. He became disoriented during our interview. Concurrent with our evaluation, the images with reviewed with radiology who reported that the fluid was not consistent with hemoperitoneum from a splenic injury. Based on our concern for bowel ischemia, he was taken to the operating room for abdominal exploration. He was noted to have a significant length of ischemic and necrotic bowel. This was resected and his bowel was left in discontinuity. He was returned to the ICU with an open abdomen and plan for second look laparotomy within 24 hours. Evaluation and Management of Acute Mesenteric Ischemia Causes Arterial Embolism- from the left atria (atrial fibrillation), left ventricle (decreased function following cardiac ischemia) or heart valves. Arterial Thrombosis- progression of underlying atherosclerotic disease leading to critical stenosis at the takeoff of the celiac or SMA from the aorta. Venous Thrombosis- hypercoagulable states, acute inflammatory process around the SMV (pancreatitis), post-operative following splenectomy or bariatric surgery. Non-occlusive mesenteria ischemia (NOMI)- low-flow through the SMA with vasoconstriction. Often having underying illness or cardiac failure, which is exacerbated by vasoconstrictive medications and hypovolemia. Presentation Severe abdominal pain, "pain out of proportion to exam" (report severe pain but abdominal exam doesn't elicit tenderness). Arterial thrombosis may be acute on chronic, if there is underlying chronic mesenteric ischemia. Diagnosis Etiology can be suspected based on symptoms and medical/ surgical history. Sudden onset is suggestive of arterial embolism. Known hypercoagulable state is suggestive of venous thrombosis. Chronic abdominal symptoms including pain with eating (food fear) and weight loss are suggestive of arterial thrombosis. Imaging Plain films may be non-specific, but may show free air or portal venous gas later in the course. Angiography Arterial thrombosis- often seen right at the takeoff of the celiac or SMA from the aorta. Arterial embolism- typically an occlusion of the celiac or SMA at a branch (versus right at the takeoff). Treatment Volume resuscitation, antibiotics Anticoagulation Surgery consultation for assessment of bowel viability and treatment of vessel occlusion Previous Next

< Back Anal Fissure What is an anal fissure? Patient information: Anal fissure [American College of Colon and Rectal Surgeons] Patient education: Anal fissure (Beyond the Basics) [UpToDate] Trauma from hard stool (constipation) creates a tear in the anoderm distal to the dentate line. Pain leads to internal sphincter spasm, setting up a vicious cycle! Symptoms- severe pain during and immediately following a bowel movement ("like pooping glass", "passing a razor blade"), blood on toilet paper with wiping. This often leads to fear of having bowel movements. Pain leads to muscle spasm→ higher pressure→ vicious cycle. Diagnosis- classic history is almost enough, but pain with effacement of the buttocks and visualization of a tear in the anoderm confirms. Don’t torture them with a digital rectal exam! On exam, typically seen in the posterior midline. If a fissure is seen in a different location, consider IBD, trauma, infection (Tuberculosis, sexually transmitted diseases), cancer. Source: UpToDate Images: Anal Fissure Anatomy What is conservative management for an anal fissure? See “ Anorectal Disease: How do I prevent anorectal disease? ” Improving bowel habits is the first-line treatment for an anal fissure. See patient handouts below. The majority of patients with an acute fissure heal with conservative management. If a fissure has been present for a long time, it is less likely to heal with conservative therapy. Sitz baths- fill a tube with water as warm as you can tolerate, and soak your bottom after every bowel movement and at least 3 times per day. Topical compounds- nitrates, calcium channel blockers→ relax muscle→ improved blood flow→ allows healing. Local anesthetics can also improve symptoms during the healing process. Avoid suppositories, Tucks pads, and Preparation H. These would be painful and won’t treat the disease. This is why diagnosis is vital. Patient Info- Anal Fissure .pdf Download PDF • 59KB Patient Info- Fiber Guide .pdf Download PDF • 68KB What is the operative management for an anal fissure? For the few patients who fail a trial of conservative therapy, surgical intervention can provide relief. Botulinum toxin (Botox) blocks neuromuscular function leading to muscle relaxation. Yes, this is the same Botox that is used to treat wrinkles. Low risk of complications. Lateral internal sphincterotomy is the treatment of choice for chronic fissures that have failed to resolve with other interventions. More successful healing compared to other interventions. Risk of incontinence (inability to control the passage of gas and stool). If incontinence occurs, the inability to control gas is more common than the inability to control liquid stool, which is more common than the inability to control solid stool. Previous Next

< Back Don't mess with the Pancreas A 47-year-old female with epigastric abdominal pain and nausea presents to the ER for evaluation. She is an otherwise healthy female, with no prior surgical history. On further questioning, her pain started 3 days ago and radiates toward her back. It has persisted and wasn't relieved with over-the-counter Tums, Gas-X, and Pepcid. She has had nausea but no vomiting. She has had minimal appetite over the past few days. Her history is otherwise unremarkable with no prior similar symptoms. On exam, she is uncomfortable but not in acute distress. HR 112, BP 112/63, T 99.1, O2 sat 99% on room air. Her abdominal exam is notable for focal tenderness in the epigastrium. What is on your differential and what is your initial workup? Peptic ulcer disease, esophagitis, hepatobiliary pathology (cholecystitis, hepatitis), pancreatitis, bowel obstruction, GERD, and bowel perforation. Labs- CBC, amylase, lipase, lactate. Imaging- acute abdominal series, possibly CT scan. Her labs are notable for a WBC of 11K, markedly elevated lipase, normal bilirubin and normal renal function. Her acute abdominal series shows non-specific bowel gas pattern with minimally dilated loops of small bowel. Right upper quadrant ultrasound revealed gallstones without evidence of acute cholecystitis. Based on the patients clinical presentation and lab findings, she is diagnosed with acute gallstone pancreatitis and was admitted to the surgical service. What are your initial goals of management? Pain control, IV fluid resuscitation. NPO until pain is improving. NGT if nauseated/ vomiting. Monitor vitals and organ function (urine output, labs). On her second hospital day, she developed worsening nausea/ vomiting, so an NGT was placed to decompress her stomach. Over the next few days, she has ongoing low grade sinus tachycardia, and then she developed intermittent low grade fever and mild leukocytosis. At that point, a CT scan is obtained. CT abdomen and pelvis https://video.wixstatic.com/video/3b6ff6_7d78015ba7b5430bb996145d60f8b0d6/360p/mp4/file.mp4 The scan reveals peripancreatic inflammation with peripancreatic stranding, gland edema and hypoperfusion. There is also simple appearing peripancreatic fluid. Over the next few days, the patient developed worsening pain and an uptrend in her leukocytosis. She is mildly hypotensive and she is urinating less frequently. When a Foley catheter is placed, she has a small volume of concentrated urine in the collection bag. She is transferred to the ICU and a Dobhoff tube was placed for post-pyloric enteral feeding. Over the next two days, she develops fevers, an increasingly oxygen requirement and persistent pain. A repeat CT scan was obtained. Follow-up CT abdomen and pelvis https://video.wixstatic.com/video/3b6ff6_e3134e03b3f242a291efd6dbc2e187e2/360p/mp4/file.mp4 There is evidence of progression of her pancreatitis. There are bilateral pleural effusions as well as worsening intra-abdominal free fluid. There is evidence of non-perfusion of the midportion of her pancreas, consistent with pancreatic necrosis. She remained in the ICU over the next several days. She did not clinically deteriorate and her pain slowly resolved. She had persistent high-volume output from her NGT. Why would she have high volume output in her NGT? Gastric outlet obstruction from peripancreatic fluid collection or necrosis. Ileus from ongoing intra-abdominal inflammation. Her distension improved with NGT decompression, and she continued to have bowel function. She was started on post-pyloric enteral feeds via a nasojejunal tube, and this was continued for the next month, awaiting for the acute necrosis to wall-off and develop a rind. Management of Acute Pancreatitis Etiology Gallstones and alcohol account for the vast majority of cases of pancreatitis. Other causes include hypertriglyceridemia, medication, ERCP, and hypercalcemia. Diagnosis Clinical presentation- epigastric pain, sometimes radiating to the back or shoulder. Nausea/ vomiting. Labs- elevated amylase/ lipase at least 3x normal Radiology- peripancreatic inflammation on contrast CT of abdomen. CT scan is not always mandatory on admission, but its commonly obtained for patients who have significant enough disease that they warrant a surgical consult. CT is also useful to rule out other pathology if the diagnosis is unclear. Clinical Course Most patients (about 80%) with acute pancreatitis suffer only mild disease and have resolution of symptoms without sequalae. The remaining 20% progress to moderate or severe pancreatitis, which is defined by the development of peri-pancreatic fluid collections or necrosis (sterile= moderate, infected= severe), or organ failure (transient= moderate, persistent= severe). Patients with organ dysfunction require ICU admission. Initial management Fluid resuscitation and ensuring adequate pain control. Nutritional support is also important, and patients are allowed to eat. Enteral nutrition should be initiated if the patient doesn't have adequate intake over the first few days. Close monitoring for development of sequalae. Patients are at risk for ARDS, abdominal compartment syndrome and infection. Assessment of Disease Severity Ranson's Criteria: Classic criteria for estimating pancreatitis severity[1] Admit data: WBC >16K, age >55, glucose >200, AST >250, LDH >250 48 hours: ↓Hct >10%, ↑BUN >5, Ca <8, PaO2 <60, Base deficit >4, >6L IVF. CT Severity has also been used to grade pancreatitis- inflammation, fluid collections and necrosis.[2] Management of Complicated Pancreatitis- Fluids Collections, Necrosis, Infection Diagnosis and Classification of peri-pancreatic fluid collections and necrosis [3] Acute interstitial edematous pancreatitis Less than 4 weeks, the fluid collection is an acute peripancreatic fluid collection . After 4 weeks, it becomes walled-off/ encapsulated and is a pancreatic pseudocyst . Acute necrotizing pancreatitis [non-enhancing pancreatic parenchyma] Less than 4 weeks, the fluid collection is an acute necrotic collection . After 4 weeks, it becomes walled-off/ encapsulated and is walled-off necrosis . Infected pancreatic necrosis- diagnosed by air in the necrosis, clinical symptoms consistent with infection and confirmed by aspiration and culture. A negative culture does not definitely rule out infection, so in the appropriate setting of clinical deterioration, there must be a high index of suspicion for infection. Indication for Antibiotics Antibiotics are NOT indicated for severe pancreatitis or pancreatic necrosis as a prophylaxis for infection.[4, 5] They are only indicated in known or highly-suspected infected necrosis. The antibiotics chosen must penetrate pancreatic tissue to be effective- quinolones and carbapenems are both broad-spectrum antibiotics (cover gram positive and gram negative) that penetrate pancreatic tissue. Carbapenems also cover anaerobes. Metronidazole covers gram negatives. Regimen: carbapenem or quinolone + metronidazole. Also consider antifungal coverage in severely ill patients.[6] Diagnosis of Infected Necrotizing Pancreatitis Infected pancreatic necrosis can be a challenging clinical diagnosis because the inflammatory state associated with pancreatitis can present with similar signs and symptoms, including fever, tachycardia, leukocytosis and ileus. CT evidence of air in the pancreatic necrosis is highly suggestive of infection, although absence of air does NOT definitively rule out infection. Fine-needle aspiration (FNA) can be used to obtain a sample for culture. There is a risk of infecting a sterile necrotic collection by performing an FNA, so this requires careful clinical decision-making. Management of Infected Necrotizing Pancreatitis These patients need broad spectrum antibiotics. Some patients may improve with antibiotics alone, but a drainage procedure is often needed. Percutaneous IR drain placement has a low rate of complications, but frequently fails to fully resolve the infection. Upsizing the drain or proceeding to more invasive intervention (see below) is required if that patient deteriorates despite drain placement and antibiotics. Previously, open necrosectomy was the standard. This is a highly morbid procedure, that requires maintaining an open abdomen, repeat washouts, and a prolonged ICU stay. Now, the step up approach is being increasingly utilized to manage these patients less invasively with similar or better outcomes (percutaneous retroperitoneal drainage or endoscopic transgastric drainage, endoscopic necrosectomy, followed by retroperitoneal necrosectomy).[7-10] Management of peri-pancreatic fluid collections [11-13] Enteral nutrition and pain control. A trial of a regular diet is appropriate, but if the patient is able to tolerate a regular diet, supplemental nutrition is required. Enteral nutrition is ideal, as it is associated with improved outcomes compared to TPN. Enteral access distal to the 3rd portion of the duodenum may theoretically avoid stimulation of the pancreas, but there is no evidence that jejunal feeds are superior to gastric feeds. However, depending on the location of the fluid collection, gastric outlet obstruction is a potential complication. Ideally, post-pyloric access would be obtained prior to obstruction, and can be used for long-term feeding while the fluid collection is allowed to resolve/ mature. Most resolve without intervention. As long as the patient is not systemically ill, drainage of pancreatic necrosis should be delayed as long as possible, ideally 6-8 weeks. Goal is to avoid procedural intervention until the fluid/ necrosis have become walled off, and then only intervene if the patient remains symptoms (pain, early satiety). However, if the patient clinically worsens, earlier intervention is necessary. Open pancreatic necrosectomy is associated with significant morbidity and mortality. An algorithm starting with least invasive (percutaneous or endoscopic drainage) and progressing to more invasive if the patient continues to do poorly is associated with decreased morbidity and mortality. References Ranson JH et al. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynecol Obstet. 1974 Jul;139(1):69-81. Balthazar EJ et al. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331-336. Banks PA et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan;62(1):102-11. Dellinger EP et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double-blind, placebo-controlled study. Ann Surg. 2007 May;245(5):674-83. Leppanieme A et al. Executive summary: WSES Guidelines for the management of severe acute pancreatitis. J Trauma Acute Care Surg. 2020 Jun;88(6):888-890. Howard TJ. The role of antimicrobial therapy in severe acute pancreatitis. Surg Clin North Am. 2013 Jun;93(3):585-93. van Santvoort HC et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010 Apr 22;362(16):1491-502. van Brunschot S et al. Endoscopic or surgical step-up approach for infected necrotising pancreatitis: a multicentre randomised trial. Lancet. 2018 Jan 6;391(10115):51-58. Luckhurst CM et al. Improved Mortality in Necrotizing Pancreatitis with a Multidisciplinary Minimally Invasive Step-Up Approach: Comparison with a Modern Open Necrosectomy Cohort. J Am Coll Surg. 2020 Jun;230(6):873-883. Boxhoorn L et al. Immediate versus Postponed Intervention for Infected Necrotizing Pancreatitis. N Engl J Med. 2021;385(15):1372-1381. Tyberg A et al. Management of pancreatic fluid collections: A comprehensive review of the literature. World J Gastroenterol. 2016 Feb 21;22(7):2256-70. van Dijk SM et al. Acute pancreatitis: recent advances through randomised trials. Gut. 2017 Nov;66(11):2024-2032. Maurer LR et al. Contemporary Surgical Management of Pancreatic Necrosis. JAMA Surg. 2023;158(1):81. Previous Next

< Back Stomach Ulcers UpToDate Patient Information Patient education: Peptic ulcer disease (Beyond the Basics) Patient education: Helicobacter pylori infection and treatment (Beyond the Basics) Patient education: Upper endoscopy (Beyond the Basics) Patient Information from Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) Upper Endoscopy Previous Next

< Back What happens during Surgical ICU (SICU) Rounds? This does NOT reflect the practice pattern of every SICU. All the components must be addressed, but there are many variations on how they are incorporated into the daily routine. Flash Rounds A multi-disciplinary process that includes the charge nurse, respiratory therapist, clinical nutritionist, physical therapists/ occupational therapists, clinical case manager, and a senior member of the team (attending, fellow, APP). Focused on ensuring that each patient has daily goals and a plan from each of the team members, ensuring that key issues are addressed early instead of waiting until after rounds (nutrition, plans for ventilator weaning, disposition planning, etc.). Working Rounds A multi-professional process that includes the bedside nurse, "learners" (broad term to include students, residents, advanced practice provider (APP) fellows), as well as the APPs (nurse practitioners (NP) and physicians assistants (PA)) and a clinical pharmacist. The team is led by the attending physician or critical care fellow. Engagement and communication by all team members are encouraged. After reviewing overnight events, a system-based approach is used to methodically evaluate the patient's current clinical status and then develop a management plan. 1. Systems-Based Rounds- presented by resident or APP - Neurologic- assessment of mental status, including the Glasgow Coma Scale (GCS), Richmond Agitation-Sedation Scale (RASS), etc. Current sedation and analgesia regimen. Review relevant radiologic imaging. - Cardiovascular- relevant vital signs and hemodynamic monitoring parameters, including trends and ranges. Review current cardioactive medication. - Pulmonary- current ventilator settings, relevant laboratory values (arterial blood gas), relevant radiologic imaging (chest radiograph). - Gastrointestinal- physical exam. Assess nutritional status (tolerating enteral nutrition, contraindication for enteral feeds, plan for parenteral nutrition). Review relevant radiologic imaging (abdominal radiograph). - Genitourinary/ Renal- review intake/ output (I/Os). The total volume of fluid intake (intravenous fluids, nutrition, blood, antibiotics, etc.) and fluid output (urine, stool, drains, etc.). Relevant laboratory values (basic metabolic panel). - Endocrine- review glycemic control. - Hematology- assessment of coagulation status or abnormal blood counts (hemoglobin, platelets). - Infectious Disease- physical exam- fever and evaluation of all possible infection sources (catheters, wounds, respiratory secretions). Review relevant laboratory values (white blood cell count, culture results), review current antibiotic therapy. - Prophylaxis- review needs for venous thromboembolism and stress ulcer prophylaxis. 2. A-F Bundle presentation by bedside nurse [SCCM ICU Liberation Bundle] - Assess, prevent, and manage pain - Breathing (Spontaneous awakening and breathing trials) - Choice of analgesia and sedation - Delirium assessment, prevention, and management - Early mobility and exercise - Family engagement 3. Develop a management plan based on comprehensive patient assessment. Previous Next

Advanced Practice Nurses to begin coming to Code Blues and supervising residents Code Blue: Who's in Charge? < Back Advanced Practice Nurses to begin coming to Code Blues and supervising residents I recently came across this article on Twitter and wrote my reply as soon as I read it. But as I was preparing to post this, I did a little more background research on the article. Let's start with the source- the website is called "MidlevelWTF ". The tagline is- "Exposing midlevel incompetence in the fight to ensure patient safety and preserve physician-led, physician-supervised medicine." The author's user name/ Twitter handle is MidlevelWTF; motto: "an actual doctor, with an actual MD." In light of this, the tone of the article makes much more sense. I'm disgusted to discover that a physician has dedicated their time/ energy to specifically target and defame APPs. Reply I disagree with a policy that formally designates a nurse practitioner to supervise any resident who runs a code. It's not appropriate to assign anyone else the authority to unilaterally overrule the decisions of the code leader. Codes need 1 leader- this is typically not the most junior person in the room, but someone in the middle or upper level of their training- a midlevel or senior resident. This doesn’t mean leaders can’t get recommendations from others. The more senior personnel in the room are welcome to provide advice- if there is egregious incompetence, which I would guess is the exception far more than the rule, someone, such as an attending or fellow or senior resident, can take over the role as leader. Working with the premise that the leader is competent, correcting a mistaken dose, helping develop a differential and general troubleshooting are all in the patient's best interest. These are also integral to closed-loop communication, and shouldn't be considered undermining or met with resistance. Team members should be able to speak up freely without having to worry about being yelled at for correcting another provider who is potentially more senior. The problem with this policy lies in the disruption of the team dynamics- adding another layer of "leadership" by formally assigning someone to have authority over the team leader creates confusion. If there is a contradiction, does the team listen to the leader or the "assigned" supervisor, who could reasonably have less experience than the resident? I've gladly welcomed advice from those with more experience than me during a difficult situation, and I trust them to speak up if they see something amiss. I trust all the non-physicians who care for our patients in my absence, and I trust them to call me if there is any concern; I hope they will feel empowered to do this in a code situation as well. So I support the author's general stance that the policy is inappropriate. However...I take great offense at this article. Implying that nurse practitioners (NPs) are minimally qualified and poorly educated is insulting and severely erroneous. Worst of all, the writer implied that a midlevel might decide to call it quits on a code “because they didn't feel like doing it anymore.” Absolutely inflammatory. Implying that any healthcare professional would be lazy or bored and just give up is preposterous. I have worked with many APPs (advanced practice providers), which includes NPs and PAs (physicians assistants) in the ER, on the inpatient wards, in the operating room, in the ICU, and in clinic. I have found them to be phenomenal teammates, motivated and eager to continually learn about how to best care for patients. Yes, some are less competent than others. But this is equally true of all healthcare professionals. I would gladly have a competent NP run a code if they were at the bedside at felt comfortable/ empowered to do so. While I would never designate a non-physician to oversee a resident running a code, I would similarly never expect a resident to take over the role of team leader from a competent NP or PA. As a fellow, during my time in the ICU, I would gladly let either an APP or a resident run the code, depending on availability and comfort level. I would be readily available and provide input when needed such as when the decision-making process extends past the algorithm of ACLS and into specific patient scenarios. In addition, if the patient needed an emergent/ urgent procedure, I was free to perform or assist while those procedures were being performed, as the NP/PA or resident continued to manage the overall code situation (meds, compressions, US to examine for cardiac activity, calling for MTP, etc). So I disagree with the policy, but I am deeply disappointed in the way the author chose to make petty accusations to undermine APPs and justify their disagreement with the policy. It's disappointing that a professional would stoop low enough to attack the character of our teammates. Previous Next

< Back Vent Mgmt #2: Modes Mandatory Breaths Volume control (volume limited)- set TV and flow, pressure and inspiratory time are the dependent variables. Pressure control (pressure limited)- set inspiratory pressure and inspiratory time, volume and flow are the dependent variables. What is the downside of VC and PC? You can only control one parameter, and the dependent variable varies based on the patient's lung mechanics. For a patient on VC, if their lungs become less compliant, delivering the same tidal volume will generate higher pressure, increasing the risk of barotrauma. For a patient on PC, if their lungs become less compliant, the target pressure will be reached at a lower volume, so there is a risk of decreased ventilation (↑PaCO2). Pressure-regulated volume control (PRVC) is a hybrid mode that attempts to overcome this limitation. The target volume is delivered at the lowest possible inspiratory pressure by assessing the delivered tidal volume at the inspiratory pressure during each breath. What about inverse ratio (IR, IRV-PC) ? Increasing the inspiratory time relative to expiratory time increases mean airway pressure. This can be accomplished with pressure-controlled modes, where inspiratory time can be prolonged (normal ratio 1:2, IRV is when inspiratory time is greater than expiratory time). As discussed, MAP affects the surface available for oxygen exchange. This is why IR can be used to optimize oxygenation. Mandatory and Spontaneous Breaths Synchronized intermittent mandatory ventilation (SIMV)- a variation on VC or PC. The machine delivers mandatory breaths, but the patient can also control spontaneous breaths in between the mandatory breaths. Spontaneous Breaths Pressure support- spontaneous mode, the patient initiates breath, the ventilator provides support to overcome the resistance of breathing through the endotracheal tube, flow is adjusted to maintain the inspiratory pressure. The support is terminated when the flow decreases to <25% of peak flow. The patient controls duration and volume. *This is also a setting that can be adjusted in SIMV for assisting spontaneous breaths between ventilator breaths. Airway Pressure Release Ventilation (APRV)- invasive form of ventilation with BiPAP. The patient breaths spontaneously, alternating between a sustained time (time-high) at a set pressure (pressure-high) with a very brief release (time-low) of pressure (pressure low) to allow expiration. The goal is to maintain a higher MAP to optimize oxygenation. Previous Next

< Back Intracranial Hypertension A 32-year-old male was an unhelmeted motorcyclist who was struck by a car and throw 20 feet. He had decreased alertness on the scene and was urgently transported to the hospital. On arrival to the ED, his GCS was 7 (E2V2M3). He was hemodynamically normal and secondary survey was only remarkable for diffuse road rash and a large scalp laceration. He was intubated for concern for inadequate airway protection. Chest x-ray revealed multiple left sided rib fractures, FAST was positive in the right upper quadrant and the pelvis x-ray was unremarkable. He was taken to the CT scanner for head, c-spine, chest, abdomen and pelvis imaging. He was transported to the trauma ICU as his images were reviewed. Head CT Case courtesy of Derek Smith. From the case rID: 169704. Imaging revealed a large right sided subdural hematoma. He has left lower rib fractures and a grade 3 splenic injury. Neurosurgery evaluated him upon arrival to the ICU. How is intracranial pressure monitored? The preferred method for ICP monitoring is with an external ventricular drain. This allows the dual function of monitoring ICP as well as allowing to treatment of elevated ICP via drainage of cerebrospinal fluid (CSF). What is a normal value for ICP? Normal ICP is <20 mmHg and treatment is recommended for sustained ICP >22 mmHg. Neurosurgery places an external ventricular drain. His opening pressure was 32, and his ICP ranges from 25-32 over the next few hours. He was in reverse Trendelenburg, and he was adequately sedated. His repeat head CT was unchanged. He had CSF drainage via his EVD. He was given 2 boluses of hypertonic saline. His ICPs improved, and were sustained at 18-20 mmHg. He develops hypotension, with systolic pressures in the 80s. What are some of the possible etiologies for hypotension, and how would you evaluate/ treat the various etiologies? Bleeding from his spleen→ urgent splenectomy. Hypotension is detrimental to TBI. Side effects from sedation medication→ decrease dosages or switch therapeutic agents, implement other treatment strategies Evaluation and Management of Traumatic Brain Injury The goal of the initial management of TBI is the prevention of secondary brain injury. Avoid hypotension and hypoxemia Target normal pulse oximetry, normal PaCO2 (35-45 mmHg) and PaO2 (≥100 mmHg), normal blood pressure (SBP ≥100), normal electrolytes, normal temperature, platelets >75K, hemoglobin >7 g/dL.[1] Treat pain and provide sedation as appropriate. Optimize patient positioning to promote cerebral venous drainage- elevate the head of the bed and ensure the cervical collar or endotracheal tube support is not too tight. Monro-Kellie Doctrine[2] Inside the bony skull, there is brain tissue, blood and cerebrospinal fluid. Increase in any one of these (tumor, hemorrhage, edema) requires a compensatory decrease in one of the other substances in order to maintain normal intracranial pressure (ICP). ICP rises when compensatory mechanisms fail. Elevated ICP leads to decreased cerebral perfusion pressure (CPP). CPP is the difference between mean arterial pressure and intracranial pressure, and serves as an additional measure of adequacy of cerebral perfusion [CPP= MAP – ICP]. This is similar to the concept of abdominal compartment syndrome- when intraabdominal pressure increases above a threshold, there is decreased organ perfusion. Initially, the brain is able to autoregulate and maintain cerebral blood flow (CBF) across a narrow range of CPP, but this compensation is also limited, and CBF decreases as CPP falls. The general target for CPP is ≥60 mmHg, but note that this may vary if cerebral blood flow autoregulation is impaired. Monitoring intracranial pressure (ICP) is not independently associated with improved outcomes. It does not replace serial neurologic exams. Clinical decision making based on the neurologic exam, the ICP, CT imaging and any other relevant information is the key to improving outcomes. There are several patient scenarios that should prompt consideration of ICP monitoring.[1,3] GCS ≤8 + structural brain injury on head CT GCS >8 + structural brain injury on head CT + high risk for progression (large/ multiple contusions, coagulopathy Severe TBI with a normal CT scan + at least 2 of the following- age >40 years, unilateral or bilateral motor posturing, or SBP <90 mm Hg. Progression of brain injury on repeat CT imaging Patients who require urgent surgery for extracranial injuries Clinical deterioration There is a tiered approach to treating elevated ICP.[1] At each tier, patients should continue to have close neurologic exams as well as interval repeat CT imaging of the head to rule-out the progression of hemorrhage. Tier 1- ensure optimization of analgesia and sedation, elevate head of bed, intermittent drainage of CSF. Tier 2- hyperosmolar therapy- mannitol or hypertonic saline. Consider advanced monitoring, including assessment of cerebral autoregulation and other markers of cerebral oxygenation. If utilizing advanced monitoring, consider hyperventilation to PaCO2 30-35 as long as cerebral oxygenation is maintained. Paralysis with neuromuscular blockade. Tier 3- decompressive craniectomy is a potential salvage therapy- may be associated with decreased mortality, but no improvement in neurologic outcomes.[4,5] Continuous infusion of neuromuscular blockade if there is a response to the test dose in Tier 2. Consider Barbiturate coma. Hypothermia and hyperventilation are no longer routinely recommended. Hyperventilation therapy can be used as a bridge to additional interventions. A study of hypothermia in severe TBI has shown no improvement in early neurologic outcome.[6] References ACS Committee on Trauma. American College of Surgeons Trauma Quality Improvement Program. Best Practices in the Management of Traumatic Brain Injury. 2015 Jan. Wells AJ et al. The management of traumatic brain injury. Surgery (Oxford). 2021;39(8):470-478. Carney N et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017 Jan 1;80(1):6-15. Cooper DJ et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011 Apr 21;364(16):1493-502. Cooper JD et al. Effect of Early Sustained Prophylactic Hypothermia on Neurologic Outcomes Among Patients With Severe Traumatic Brain Injury: The POLAR Randomized Clinical Trial. JAMA. 2018;320(21):2211-2220 Sahuquillo J, Dennis JA. Decompressive craniectomy for the treatment of high intracranial pressure in closed traumatic brain injury. Cochrane Database Syst Rev. 2019 Dec 31;12(12):CD003983 Previous Next