Internal Medicine Residency Program

Boot Camp 2015 Introduction Welcome to Boot Camp 2015! Copyright laws prohibit us from copying articles and “republishing” them in a Boot Camp book. Therefore, what you will find in this book are the cases and occasional summaries of the topics provided by some of our residents. At the end of each section there is a list of references that will be covered. Some topics have multiple references and, in general, the first and/or second references are to be considered the “primary” references. All articles with Internet addresses are accessible utilizing the KUMC web server. If the article is not available electronically, the article may be obtained from the library. We have made every attempt to ensure that all primary references are available electronically. To obtain a reference you must either be on campus, logged in through KU Remote Access (dialup Internet) or be using the KUMC proxy server (if you have a high-speed connection). Once you have located the appropriate Internet site, you will need to locate the article by using the listed reference. Searching by citation is usually the quickest and easiest method. If you have trouble locating the appropriate Internet site, go to the Dykes Library Online Journals site for a link. (Web address below) http://mt8fd2he2v.search.serialssolutions.com/ You need to be logged on through KU to maximize the links through the library site. All cases and direct links to the articles are published on the KU Internal Medicine Intranet site. https://share.kumc.edu/SOM/wichita/IM/default.aspx We look forward to a new and exciting year of Morning Teaching Conference beginning with Boot Camp. If you have suggestions or find any errors, please contact the Internal Medicine Chief residents so that changes can be incorporated for next year.

Table of Contents Topic Acute Coronary Syndromes

Date JUL – 7

Acute Respiratory Distress Syndrome

JUL – 8

Sepsis Case/SIRS Overview

JUL - 9

Congestive Heart Failure

JUL - 14

Pancreatitis

JUL - 15

Neutropenic Fever

JUL - 16

Atrial Fibrillation

JUL - 21

GI Bleeding

JUL – 22

Acute Kidney Injury

JUL – 23

Hypertensive Emergencies

JUL – 28

Status Epilepticus

JUL – 29

Chronic Obstructive Pulmonary Disease + Asthma

JUL – 30

Aortic Dissection

AUG – 4

Acid-Base Analysis

AUG – 5

Pleural Effusions + Pulmonary Embolism

AUG – 6

Syncope

AUG – 11

Stroke

AUG – 12

Community Acquired Pneumonia

AUG – 13

Acute Infective Endocarditis

AUG – 18

Hyponatremia + Hypernatremia

AUG – 19

Meningitis

AUG – 20

Hyperkalemia

AUG – 25

Delirium

AUG – 26

Diabetic Ketoacidosis

AUG – 27

Alcohol Withdrawal

SEPT - 8

Pain Management + Leaving Against Medical Advice

SEPT – 9

Morning Teaching Conference Tutorial

SEPT –10

Acute Coronary Syndromes Part I: ST Elevation Myocardial Infarction Objectives 1. Risk factors for myocardial infarction 2. Diagnosis of ST elevation MI 3. Treatment of ST elevation MI

CC:

Chest Pain/Pressure

HPI: 73 yo white male presents to the ED with two hours of severe, pressure-like discomfort in the center of his chest associated with nausea, vomiting, and diaphoresis. The discomfort does not radiate. The pressure is rated at 8 on a 1-10 point scale but decreased to a 4 when given sublingual nitroglycerin by EMS. The patient complains of SOA that started with the chest discomfort PMH: Benign prostatic hyperplasia, Hypertension PSH: TURP Meds: HCTZ 25mg qd, tamsulosin 0.4mg qd Allergies: NKDA FMH: Mother – HTN, Father – deceased MVA, age 50, Sister 78 with “heart problems” SOC: Smoked 1 ppd for 30 years. Quit 13 years ago. Denies alcohol or drug use. Married with four children. ROS: No weight change, recent decreased exercise tolerance. No SOA until acute episode. No prior cardiac events. PE Vitals: GEN: NECK: CV: Lungs: Abd: Ext:

T 98.8 RR 30 P 110 BP 150/90 Well-developed, well-nourished, in moderate distress secondary to pain and SOA. JVD to 15cm normal S1, S2. S3 is present. No murmur; pulses equal bilaterally Bilateral crackles over the lower lobes benign No edema

Labs CBC: BMP: Cardiac: CXR EKG

WBC 10.5, Hgb 15.2, Plts 226 Na 135, K 4.2, Cl 113, Bicarb 23, BUN 13, Cr 0.8, Glu 157 Troponin = 2.0 bilateral congestion see attached

Differential Diagnosis of chest pain - Cardiac: ACS, pericarditis, myocarditis - Vascular: Aortic dissection, pulmonary embolism - Pulmonary: Pneumonia, tension pneumothorax, pleuritis - Chest wall: Costochondritis, sternoclavicular arthritis, zoster, muscle strain, rib fracture or contusion, neuropathic pain… - GI: esophagitis, esophageal spasm, PUD, gastritis, biliary pain, pancreatitis - Psych: Anxiety, somatiform disorders

Differential Diagnosis of ST segment elevation o Myocardial ischemia/infarction o Acute pericarditis o Early repolarization (normal variant) o LVH or LBBB o Trauma, tumor, myocarditis, hyperkalemia, hypothermia, Brugada syndrome DEFINITIONS Acute coronary syndrome (ACS) — Applied to patients where myocardial ischemia is suspected. Classified into three types: 1. ST Elevation myocardial infarction (STEMI) 2. non-ST elevation myocardial infarction (NSTEMI) 3. Unstable angina The first two (the infarctions) are characterized by a typical rise in markers of myocyte injury (i.e. cardiac enzymes). These biomarkers do not rise in unstable angina.

Myocardial Infarction (MI) - Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Health Federation (ESC/ACCF/AHA/WHF) defined acute MI as: - clinical (or pathologic) event caused by myocardial ischemia in which there is evidence of myocardial injury or necrosis Generally, change in cardiac biomarker values (preferably troponin) with at least one of the following are needed to meet criteria for an MI: • • • • •

Symptoms of ischemia Development of pathologic Q waves in the ECG New or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle branch block (LBBB) Identification of an intracoronary thrombus by angiography or autopsy Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality.

Clinical Classification of MI: o Type 1: Pathologic process in the wall of the coronary artery (eg: plaque rupture) o Type 2: Increased oxygen demand or decreased oxygen supply (eg: coronary artery spasm, anemia, arrhythmias, hypotension/sepsis) o Type 3: Sudden unexpected cardiac death before blood samples could be taken o Type 4a: Associated with PCI (i.e. after PCI) o Type 4b: Stent Thrombosis o Type 5: Associated with CABG (i.e. after CABG)

Localizing Area of Ischemia on EKG (Figure from ACP Smart Medicine)

Clinical Classification of MI: o Type 1: Pathologic process in the wall of the coronary artery (eg: plaque rupture) o Type 2: Increased oxygen demand or decreased oxygen supply (eg: coronary artery spasm, anemia, arrhythmias, hypotension/sepsis) o Type 3: Sudden unexpected cardiac death before blood samples could be taken o Type 4a: Associated with PCI (i.e. after PCI) o Type 4b: Stent Thrombosis o Type 5: Associated with CABG (i.e. after CABG)

Risk Factors: o Non-modifiable Family history - (only first degree relatives, male< 55, female 40, female>50) Race (Black>Caucasian) o Modifiable HTN/CAD Obesity/Sedentary lifestyle Tobacco Diabetes mellitus Hyperlipidemia o Past Procedures Previous heart catheterization/CABG

Initial evaluation of patients presenting with possible ACS: o Remember, women, the elderly, and diabetics may have atypical presentations o within 10 minutes: triage for rapid care and start MONA-Morphine, oxygen, nitroglycerin and aspirin o IV access, focused H&P, continuous cardiac monitor, and initial ECG (first ECG should ideally be done by EMS) o Basic labs (CBC, INR, aPTT, BMP, magnesium, lipids, cardiac markers) o Repeat ECG at 5-10 min intervals if initial ECG is non-diagnostic o Aspirin chewed (160 to 325 mg) o Supplemental oxygen for patients who are hyperemic (SaO2 increased neutrophils -> toxic mediators -> alveolar damage and capillary endothelial damage -> increased leak of protein rich material -> pulmonary edema and hyaline membrane formation 2) Proliferative stage – 7-10 days later, resolution of edema, proliferation of type II alveolar cells and interstitial inflammation 3) Fibrotic stage – some progress to this stage- obliteration of normal lung architecture, diffuse fibrosis, cyst formation c) Important to remember: Epithelial cells (pneumocytes) i. Type I – 90% - barrier ii. Type II – 10% - make surfactant, ion transport, replenish type I iii. Dysfunction of type II cells can occur in ARDS resulting in: 1. Increased permeability and alveolar flooding 2. Decreased ion transport and impairment of edema removal 3. Decreased production of surfactant with alveolar collapse 4. Loss of barrier and increased risk of septic shock 5. Reorganization of epithelial cells can lead to fibrosis (scar)

IV.

Risk factors Direct Lung Injury

Indirect Lung Injury

Pneumonia Aspiration

Sepsis Severe trauma with shock

Pulmonary contusion Fat emboli Near-drowning Inhalation injury Reperfusion after lung transplant

Cardiopulmonary bypass Drug overdose Acute Pancreatitis Blood product transfusion

Common

Less Common

V.

Outcomes a. Mortality of 26-58%% b. Increased mortality: increased age, failure of oxygenation to improve, sepsis, chronic liver disease, non-pulmonary organ dysfunction c. Failure to improve in first week is poor prognostic indicator

VI.

Treatment a. Treat the cause – pneumonia, sepsis b. Decrease oxygen consumption: treat fever, pain, and anxiety which can all increase O2 consumption with antipyretics/sedation/analgesia c. Nutrition/Fluids i. Enteral preferred over parenteral if possible – Increased risk of nosocomial infections when using parenteral nutrition ii. Conservative fluid management- aim to minimize or eliminate positive fluid balance d. Prevention i. GI prophylaxis ii. DVT prophylaxis e. Mechanical Ventilationi. Goal is to maintain adequate gas exchange until inflammation subsides w/o causing ventilator—induced lung injury ii. Reduced tidal volume (TV) ventilation-> helps prevent alveolar overdistension and improves mortality – 6-8 mL/kg IBW iii. PLATEAU pressure goal ≤ 30 cmH2O, if >30 then gradually decrease the TV and can even go down to 4ml/kg for TV iv. Permissive hypercapnia (as a result of low TV) 1. Maintain oxygenation even if CO2 rises 2. Maintain physiologic pH 7.2-7.5, can increase RR to compensate while trying to keep TV low v. PEEP 1. Used to maintain oxygenation because keeps alveoli open 2. May have very high levels 10-20 cm H2O 3. Refer to table for correlation of PEEP to FiO2

vi. Oxygen 1. Try to titrate to 100.4˚F or 90 bpm o Resp. rate >20 bpm or PaCO2 12,000 cells/mm3, 10% bands Sepsis is the systemic response to infection, SIRS + evidence of infection. Severe Sepsis is associated with end organ dysfunction, hypoperfusion, or hypotension. Septic Shock is sepsis with hypotension despite adequate fluid resuscitation with perfusion abnormalities such as lactic acidosis, oliguria, or acute altered mental status. Epidemiology • >650,000 cases annually with >100,000 deaths. • Mortality o SIRS-7% o Sepsis- 16% o Severe Sepsis 20% o Septic Shock 46% Risk Factors • Positive blood cultures • Middle-aged and elderly • Cancer • Pre-existing Renal Failure • Pre-existing Hepatic Failure • AIDS • Community acquired pneumonia Natural History • SIRS to sepsis to severe sepsis to septic shock is a continuum of severity o 48% pts with SIRS progressed to a form of sepsis o Incidence of positive blood cultures increased along the continuum o Increasing mortality from SIRS → Septic shock o Complications include severe organ dysfunction manifested as ARDS, ARF, DIC Factors associated with Poor Prognosis • Afebrile or hypothermia • Leukopenia • Age >40 • Comorbid condition- AIDS, Cirrhosis, Hematologic Malignancy, Mets Cancer, Immunosuppression

• • • • •

Malnutrition Nursing home/care home resident Indwelling catheters/central line GI or Lung source of infection Nosocomial infection

Management: A. Initial Resuscitation • Protocolized, quantitative resuscitation of patients with sepsis-induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmol/L). • Goals during the first 6 hrs of resuscitation:  Central venous pressure 8–12 mm Hg  Mean arterial pressure (MAP) ≥ 65 mm Hg c) Urine output ≥ 0.5 mL/kg/hr d) Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively (grade 1C). • In patients with elevated lactate levels targeting resuscitation to normalize lactate (grade 2C). B. Screening for Sepsis and Performance Improvement • Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C). • Hospital–based performance improvement efforts in severe sepsis (UG). C. Diagnosis o Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (38.3ºC (101ºF), or a sustained temperature >38ºC (100.4ºF) for more than one hour •The definition of neutropenia varies from institution to institution but is usually defined as an absolute neutrophil count (ANC) oral treatment -Antibiotics should be given within 60 minutes of presentation. If outpatient, low risk: Fluoroquinolone like cipro 750 mg BID plus beta-lactam like amoxicillin-clavulanic acid (500/125 mg TID). If inpatient, high risk: • Cefepime or ceftazidime (meropenem, imipenem, piperacillin-tazobactam can also be used) • Additional antibiotics (fluoroquinolones, vancomycin, azithromycin) may be used if specific infections more likely • Addition of antifungal therapy recommended after 4-7 days of continued fevers, in patients who are expected to have neutropenia >7 days, or in patients becoming more clinically unstable with ermpiric antibiotic therapy Vancomycin criteria: • pneumonia • skin/soft tissue infections • severe mucositis in patients who were receiving prophylaxis with fluroquinolone • hemodynamic instability/severe sepsis • positive blood cultures for gram positive bacteria • suspected central line infection • history of resistant organisms like MRSA Stop vancomycin after 48 hours if negative blood cultures At 48 hours if fever persists: • D/C cefepime or ceftazidime • Start imipenem/cilastatin or meropenem to cover for anaerobes At 96 hours (after 4 days) if fever persists:

• Add amphotericin B, caspofungin, or voriconazole for Candidemia/Aspergillosis At 7 days if fever persists: • CT scan of sinuses: • Look for any sign of sinusitis, especially fungal sinusitis. • Aspergillus will require 1 – 1.5 mg/kg of amphotericin B for treatment Hematopoietic Colony-Stimulating Factors – ASCO Guidelines • Primary Prophylaxis (before Febrile Neutropenia) • Not Recommended routinely • May use if expected incidence of neutropenic fever >20% or if 65, poor performance status • Secondary Prophylaxis (to avoid febrile neutropenia from occurring in next cycle) • Not recommended routinely and usually recommend to just decrease dose of next cycle of chemo • Should use it however if dose-reduction not recommended especially for potentially curable malignancies (i.e. germ cell tumor) • Adjunctive Therapy for Febrile Neutropenic Patients: not routinely used but in patients that remain neutropenic and febrile after initiation of antibiotics. Also, consider for those with poor prognostic factors (ANC < 100/ul, age >65, uncontrolled primary disease, pneumonia, hypotension, multiorgan dysfunction of invasive fungal infection) Duration of therapy: -In patient with documented infection secondary to specific organism then duration is dictated by the organism but should be continued at least until ANC greater than or equal to 500 -If unidentified source of fever, then continue empiric therapy until marrow recovers, ie ANC is greater than or equal to 500 References: 1. Freifeld, A, et al. Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the IDSA. www.idsasociety.org 2014. 2. Hughes WT, Armstrong D, Bodey GP, Bow EJ, Brown AE, Calandra T, et al. 2002 Guidelines for the use of antimicrobial agents in neutropenic patients with cancer. Clin Inf Dis 2002;34:730-51. 3. http://www.journals.uchicago.edu/CID/journal/home.html 4. Up to Date 2014, “Fever in the Neutropenic Adult Patient with Cancer”

Atrial Fibrillation Objectives 1. Recognize atrial fibrillation (AF) 2. Understand the common causes for new onset AF 3. Understand the approach to the patient with AF 4. Review the indications for anticoagulation in patients with AF CC: Burning sensation in chest HPI: 67 y/o male who has a sudden onset of a burning sensation in his chest. He was doing well until the morning of admission. Shortly after taking his medications, he began to develop a burning sensation in his chest that radiated to his neck and left jaw. He reports having similar discomfort three years ago at which time he underwent coronary angiography with percutaneous transluminal angioplasty and stent placement. He denies ever having suffered an acute myocardial infarction. He denies any dyspnea, nausea or vomiting. He denies any palpitations. PMH: DM – II, non-insulin requiring HTN CAD Hypercholesterolemia PSH: PTCA/Stent placement in RCA three years ago PTCA RCA two years ago Meds: Metoprolol 25 mg twice daily Simvastatin m40g daily Omeprazole 20 mg daily Multivitamin All: NKDA FMH: Brother with CAD/CABG at age 54. Several first degree relatives with diabetes and HTN SOC: Remote tobacco use with estimated 20 pack year history. Occasional alcohol use which is quantified as 1 – 2 drinks per week. ROS: Unremarkable PE Vitals: T: 98.6, BP: 136/82, P: 110, RR: 24 GEN: WD/WN in moderate distress secondary to discomfort and dyspnea. HEENT: PERRLA, EOMI CV: Normal S1, S2. No audible murmur. No JVD. Distal pulses 2/4. Rhythm is irregularly irregular Lungs: Minimal bilateral crackles lower lobes Abd: Benign Ext: No edema Labs CBC: BMP:

WBC: 6.8, Hg: 11.6, Plt: 185 Na: 135, K: 4.2, Cl: 109, Bicarb: 23, BUN: 13, Cr: 0.8, Glu: 157

EKG:

shown

Atrial Fibrillation • •

Most common cardiac arrhyhmia Identified by irregularly irregular rhythm on ECG with absence of distinct p waves

Risk factors o hypertension and ischemic heart disease o age, rheumatic heart disease, CHF, congenital heart disease, sick sinus syndrome, WPW o pericarditis, PE, COPD, thyrotoxicosis, post-operatively, DM, ethanol, sympathomimetic drugs o caffeine, hypoxia, hypokalemia, hypoglycemia, systemic infection Consequences o Thromboembolism / stroke o CHF / Cardiomyopathy Classification o Paroxysmal AF —recurrent AF (≥2 episodes) that terminates spontaneously in ≤ 7 days, usually < 24 hours. o Persistent AF — AF that fails to self-terminate within seven days. Usually need pharmacologic or electrical cardioversion to revert to sinus rhythm. progression to persistent and permanent AF occurs in >50 % of patients despite therapy o Long-standing persistent AF--persistent AF that lasts for ≥ 1 year o Permanent AF — patients with persistent AF where a decision has been made to no longer pursue a rhythm control strategy Signs/Symptoms o Often asymptomatic o When symptomatic, symptoms can include palpitations, tachycardia, fatigue, weakness, dizziness, lightheadedness, reduced exercise capacity, increased urination, or mild dyspnea. More severe symptoms include dyspnea at rest, angina, presyncope, or infrequently, syncope Diagnosis o EKG, thyroid, electrolytes, 2D Echo (ventricular function, atrial size, valve disease) o Eval for CAD in pt with risk factors Therapy: ***If hemodynamically unstable, perform immediate Synchronized Direct Current Cardioversion 100-200J Acute treatment: A-Fib with RVR (rapid ventricular response) •

Rate control o Goal < 110 bpm o 1st line: beta blockers, calcium channel blockers  Diltiazem, verapamil, metoprolol, esmolol

•

o 2nd line: digoxin  Can be preferred agent in CHF or hypotension Rhythm control o Can use electrical cardioversion or chemical cardioversion o Anticoagulation needed first if symptoms >48 hts  3 weeks prior and 4 weeks after cardioversion  Other option is TEE and proceed with cardioversion if no thrombus

Chronic treatment o RATE VS. RHYTHM CONTROL--AFFIRM TRIAL 1. Showed no mortality benefit in rhythm vs. rate control in long term management, but trend toward better survival with rate control arm of study 2. No decrease seen in CVA’s in rhythm control; therefore continued anticoagulation needed after A.fib converted to NSR (eg pt probably still going in and out of A.fib after conversion) o Rate Control 1. Meds: Beta blocker, Ca channel blocker, Digoxin o Rhythm Control: most effective if a.fib duration short 1. Amiodarone, Procainamide, Propafenone (contraindication in CAD), Sotalol 2. Efficacy rate approx 50-70% in maintaining NSR at 6 months 3. Proarrhythmia risk o Other treatment options 1. Ablation o Consider if on meds and still symptomatic o Higher success rate in atrial flutter Stroke prevention o Warfarin still most commonly used, though there are several newer alternatives (dabigatran, apixaban, rivaroxaban) o Indications • Valvular heart disease, especially mitral valve o CHADS2 score: • 0 → aspirin alone • 1 → aspirin or anticoagulation • ≥ 2 → anticoagulation Some recommend use of CHA2DS2-VASc score rather than CHADS2

References: 1. Fuster et al., ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation J Am Coll Cardiol 2001;38:1266i-1xx 2. Cheng and Kumar. Overview of atrial fibrillation. UpToDate, Waltham, MA, 2013 3. www.utdol.com 4. MKSAP 16

GI Bleeding Objectives 1. Identify causes of GI bleeds. 2. Identify the best way to make a diagnosis and treat a patient. HPI: A 58 yo white female visiting from Texas woke up around 1 am feeling nauseated and began vomiting. She said that she vomited dark blood. She denies having syncope or abdominal pains. The patient called 911 and was brought to the hospital. The patient is a recovering alcoholic. She was still drinking approximately eight months ago. PMH: liver cirrhosis with ascites, breast cancer PSH: Bilateral mastectomies 20 years ago with partial reconstruction of the breasts for cancer. She did not have radiation or chemotherapy. All: No known drug allergies Meds: Furosemide Spironolactone PE: Vitals: P 120 BP 124/68 (lying), 108/52 (sitting), 86/46 (standing) Gen: 58 yo female who looks older than her stated age; no acute distress HEENT: Icteric sclerae. NG tube present with suctioned coffee-ground material Chest: Spider angiomas over anterior chest CV: Regular rate and rhythm with tachycardia Lungs: Clear bilaterally. Decreased at the bases Abd: Non-distended. Slightly tender in the epigastric area. Bowel sounds positive though decreased. No rebound. Rectal: Normal sphincter tone. Black tarry stool, heme positive Ext: Revealed no clubbing, cyanosis, or edema. Vasc: Pulses slightly decreased, but symmetrical in the lower extremities. Skin: Pale with a yellow tinge. Neuro: There were no neurological deficits. Cranial nerves were grossly intact. Lab: CBC: Admission WBC 15.5 Hgb 7.5 Hct 26.7 MCV 105 Plts 96 Coags: PT 16.5 PTT 46.3INR 1.6 BMP: Na 132 K 4.7 Cl 99 CO2 27 BUN 39 Cr 0.9 Glucose 168 LFT: ALT 27 AST 71 AP89 Albumin = 2.8 BiliT 5.8Direct 1.7 Indirect 4.1

GI Bleeding Upper GI bleeding Bleeding that occurs from mouth to upper part of small intestine (ligament of treitz) Lower GI bleeding Bleeding that occurs distal to the ligament of treitz (small intestine, colon, rectum) Both can range from microscopic to massive and life-threatening Etiologies: Upper bleeds: • Peptic ulcer disease (H. pylori, NSAIDs, stress, gastric acid) — 55% • Esophageal/gastric varices — 14% • Arteriovenous malformations (AVMs) (angiodysplasia, vascular ectasia) — 6% • Mallory-Weiss tears — 5% • Tumors and erosions — 4% each • Other (include GAVE [gastric antral vascular ectasia], portal hypertensive gastropathy, aortoenteric fistula, Dieulafoy’s lesion, plus others) — 11 % Lower Bleeds: • Diverticular — 5 to 42% • Ischemia — 6 to 18% • Anorectal (hemorrhoids, anal fissures, rectal ulcers) — 6 to 16% • Neoplasia (polyps and cancers) —3 to 11% • Angiodysplasia (AVM) — 0 to 3% • Postpolypectomy — 0 to 13% • Inflammatory bowel disease — 2 to 4% • Radiation colitis — 1 to 3% • Other colitis (infectious, antibiotic associated, colitis of unclear etiology) — 3 to 29% • Small bowel/massive upper GI bleed — 3 to 13% • Other causes — 1 to 9% • Unknown cause — 6 to 23% History of melena, melena on rectal exam, blood or coffee grounds seen during nasogastric lavage, and BUN/Cr ratio > 30 predictive of upper GI bleed Presence of blood clots in stool or BRBPR predictive of lower GI bleed

Initial Evaluation and Management (any GI bleed - upper or lower) • Stabilize. • ICU admission • ABC’s • IV (2 large bore) • Targeted history (NSAIDS, antiplatelets, anticoagulants, steroids, smoking, ETOH, wt loss, prior hx of gi bleeding, liver disease, history of AAA or aortic graft)

• • • •

Exam (vital signs, petechiae, spider angiomas, abdominal tenderness, organomegaly, rectal exam) Labs: CBC, CMP, coagulation panel, type and crossmatch, Serial blood testing H/H. Admitting H/H is not necessarily indicative of current circulating volume. Vital signs are more accurate (ORTHOSTATIC VITALS IMPORTANT) Volume resuscitation (isotonic fluids)

Estimating fluid status using vital signs: • • •

resting tachycardia = mild to moderate hypovolemia Orthostatic hypotension = blood volume loss of at least 15% Supine hypotension = blood volume loss of at least 40%

Transfusions:  Transfuse for: o Hemodynamic instability despite crystalloid resuscitation o Hemoglobin 1.5); plts for (platelets 20; urine sodium 1% (except contrastinduced AKI), Most common cause after prerenal state.

5. AIN: Allergic (nearly all drugs: PCN, rifampin, NSAIDS..), infection (severe PNitis, legionella…), infiltration (lymphoma, leukemia), inflammatory (sjogren…) UA: Pyruria, WBC casts, urinary eo’s Intrarenal tubular obstruction: rhabdomyolysis, tumor lysis syndrome, crystalluria, or multiple myeloma. UA: Coarse tubular casts (granular of muddy brown), crystalluria, urinary light chains. Renal vein obstruction: Nephrotic syndrome (membranous neph), clotting d/o, malignancy, trauma, compression. UA: Hematuria, nephritic range proteinuria 3. Postrenal (urinary tract obstruction) Nephrolithiasis, tumors, granuloma, pregnancy, hematomas, radiation, neurogenic bladder BPH, retroperitoneal fibrosis UA: hematuria (micro or macro), bacteria, pyuria, crystals. UA can be nl. Approach to the patient: 1. Define acute kidney injury (versus risk or acute renal failure) investigate the cause. (Distinction between AKI and CKD if no baseline Scr is suggested by small/shrinked kidneys on U/S, renal osteodystrophy, normocytic anemia or secondary hyperpara with hyperphos and hypoca). 2. History: --Clues: (nausea, vomiting, diarrhea, light-headedness upon standing, decreased urine volume, dark urine, recent illness) --Is there a history of heart failure, liver disease, diabetes, known kidney disease, recent abdominal surgery, BPH, pelvic malignancy, renal stones, difficulty passing urine, recent contrast studies? --When did they last see their doctor? Have they had any lab done recently? --Medication list  look for NSAIDS, diuretics, ACE, ARB, renin inhibitors 3. Physical exam: Assess volume status!! --vital signs (tachycardia, hypotension, febrile?) --postural hypotension --mucous membranes -- neck veins/JVD/hepatojugular reflex -- S3 on cardiac exam -- crackles in lungs -- spider angiomata, jaundice, ascites, abdominal fullness (stigmata of liver disease) --prostate enlargement --purpura, petechiae, joint swelling, skin rash -- neuro changes. 4. Laboratory: CBC, CMP, Mg, Phos, uric acid

UA with micro (look at the urine yourself if suspicious of glomerulonephritis or other infrarenal issues; techs will usually not call dysmorphic RBCs) urine sodium and creatinine (urine protein) 5. Imaging: Renal ultrasound, non-contrast CT, renal nuclear scan, renal artery Doppler 6. Therapy: --Non drug therapy is used to increase renal perfusion and relieve obstruction Foley Treat volume depletion with normal saline Treat severe anemia with transfusion Discontinue all nephrotoxic drugs Manage electrolyte abnormalities Albumin for patient with HRS (contact your friendly nephrologist if you suspect this diagnosis) Consider renal replacement therapy  see indications below for RRT Indications for acute dialysis: A = acidosis (severe metabolic acidosis resistant to tx). pH220/120 or if BP >185/110 and having tPA o Aortic dissection: SBP should be rapidly lowered to 100-120mmHg within 20 minutes. Specific treatment guidelines for each type of hypertensive emergency is detailed below: Neurological emergencies: Hypertensive encephalopathy • Preferred medications • Labetalol • Nicardipine • Esmolol • Medications to avoid • Nitroprusside • Hydralazine • Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours. Acute ischemic stroke • Preferred medications • Labetalol • Nicardipine • Treatment guidelines: Withhold antihypertensive medications unless the systolic blood pressure (SBP) is >220 mm Hg or the diastolic blood pressure (DBP) is >120 mm Hg UNLESS patient is receiving IV or IA fibrinolysis, then goal BP: SBP 40mmHg from baseline, not associated with other causes 20 year retrospective study showed >500,000 diagnosed PE’s with 200,000 deaths. Greater than ½ of all PE remain un-diagnosed Prognosis: Untreated pulmonary embolism have 30 % mortality d/t recurrent embolism Adequate diagnosis and anticoagulant trt decreases mortality to 2-8% Risk factors: 1. Immobilization 2. Surgery in last 3 months 3. Stroke 4. Hx of venous thromboembolism 5. Malignancy 6. Preexisting respiratory dz 7. Chronic heart failure 8. Congenital hypercoagulability syndromes 9. Obesity, hypertension, and cigarette smoking in women Diagnosis: PE is easy to miss. Must maintain high level of suspicion 1. ABG: limited role (hypoxemia, hypocapnia, resp alkalosis, Aa gradient not specific or sensitive). 2. BNP insensitive and nonspecific 3. Troponin elevated in 30-50 % with moderate to large PE 4. EKG: 70 % have abnormality a. Sinus tachycardia with nonspecific st-t change is most common b. S1Q3T3 is infrequent unless massive PE with cor pulmonale c. Poor prognosis i. Atrial arrhythmia, rbbb, inferior Q waves 5. Modified Wells a. Clinical symptom of DVT (3pts) b. Other diagnosis less likely than PE (3 pts)

c. Heart rate > 100 ( 1.5 pts) d. Immobilization or surgery in prior 4 wks (1.5 pts) e. Prior DVT/PE (1.5 pts) f. Hemoptysis (1 pt) g. Malignancy (1 pt) h. 4 or less = PE unlikely 6. Imaging a. CXR: usually abnormal i. Atelectasis, pleural effusion, cardiomegaly, infiltrates ii. Westermark sign: rare finding 2% 1. Dilation of pulmonary arteries proximal to embolus and collapse of distal vasculature creating appearance of a sharp cut off on CXR iii. Hampton’s hump: wedge shaped, pleural based consolidation associated with pulmonary infarction. Low sens 11% and high specificity 92% for PE b. Spiral CT (CT angio): most common diagnostic modality. Venous phase imaging improved sensitivity to 90% and specificity to 95%. Still best to correlate with clinical probability c. V/Q scan: accuracy greatest when combined with clinical probability. i. High clinical probability with high probability v/q, had 95% likelihood of PE. Low clinical probability with low probability v/q had 4% likelihood of PE. ( normal V/Q virtually excluded PE) ii. Usually reserved for contraindication to CTA iii. Inaccurate if underlying lung disease d. D dimer: Sens (abnormal in 50% of pt with sub segmental PE), Spec (normal in only 25% of pts without PE. Negative predictive value Pts with normal d dimer have a 95% likelihood of not having a PE e. Angiography: Gold standard. High morbidity and mortality of procedure itself. Rarely done f. LE dopplers: Be aware that there is 3% false positive

Treatment: • Support if hemodynamically unstable o Oxygen o Pressors o Fluids • Thrombolytics o Use if hemodynamically unstable • Acute anticoagulation o LMWH preferred if not contraindicated o Heparin preferred in renal failure or persistent hypotension o Warfarin  Should be started on day 1 and continued for at least 5 days and until INR is therapeutic for 24 hours • Long term anticoagulation o Continued for at least 3-6 months o Extension of therapy based on underlying risk of recurrent VTE vs. bleeding risk o Usually therapy continues with warfarin, except LMWH preferred with malignancy

• Newer anticoagulants o Dabigatrin, rivaroxiban & apixiban are alternatives to warfarin • IVC filter indictions o Contraindiction to anticoagulation o Recurrent PE with adequate anticoagulation o Complication of anticoagulation • Embolectomy o surgical or catheter based if contraindications for thrombolysis or failed thrombolysis, provided surgical expertise and resources available. REFERENCES 1UpToDate. Approach to the adult with metabolic acidosis simple and mixed acid-base disorders 2Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. NEJM 1998;338:26-34 and 107-111. 3Dalen JE. Pulmonary embolism: what have we learned since Virchow? Natural history, pathophysiology and diagnosis. Chest 2002;122:1440-1456. 4Dalen JE. Pulmonary embolism: what have we learned since Virchow? Treatment and prevention. Chest 2002;122:1801-1817. 5Langan CJ, Weingart S. New diagnostic and treatment modalities for pulmonary embolism: one path through the confusion. Mt Sinai J Med. 2006 Mar;73(2):528-41. 6www.utdol.com. UpToDate 7MKSAP 16

Syncope Objectives: 1. Discuss the different etiologies of syncope 2. Discuss the approach to a patient presenting with syncope IIPI: 85 yo white male who woke up at 2 am in the morning of the admission to urinate. He has been feeling well except for some nausea, vomiting , and diarrhea. These symptoms have been ongoing for the last three days but had recently stopped the day prior to the admission. At the time he started voiding, he felt dizzy and the next thing he knew, his wife found him lying on the bathroom floor. The patient seemed moderately alert; did not seem confused and denied any symptoms of palpitations or dizziness prior to this episode. EMS was called and the patient was transported to the ED for further evaluation. The patient states that he did have a similar episode six months earlier for which he did not seek medical attention. PMH: Non-contributory. The patient has no known coronary disease, no known hypertension, no history of stroke. History of nephrolithiasis approximately 30 years earlier. Meds: PRN OTC anti-inflammatory ALL: NKDA Soc: The patient is retired; lives with wife. No alcohol use for greater than 30 years and no history of tobacco ingestion. FMH: Non-contributory ROS: Occasional headaches for which he uses over the counter antiinflammatories. Mild to moderate shortness of breath on exertion which started approximately a year prior to this evaluation. Occasional chest discomfort with severe exertion. No syncope or pre-syncopal symptoms except one episode six months earlier. The patient does have difficulty voiding and uses the bathroom 2-3 times a night. PE: Vitals: Gen: Neck: CV: Lungs: Abd: Ext: Neuro: Labs: BMP: EKG: Lumbar

T97.2 P93 BP128/83, not orthostatic Mild distress secondary to back discomfort Supple, no thyromegaly. No lymphadenopathy RRR, no murmurs, rubs or gallops Decreased breath sounds in both bases and diffuse basilar crackles Soft, non-tender with positive bowel sounds No c/c/c A&Ox3, CNII-XII intact, strength and sensation intact, no cerebellar signs

Na 138, K 3.9, C1 98, CO2 17, BUN 29, Cr 0.9, Glu 89 NSR with right bundle branch block. No ST abnormalities L2, L3 compression fractures

Syncope Overview Syncope: The abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and rapid spontaneous recovery. Distribution of causes of syncope    

Reflex (neutrally-mediated; this includes vasovagal) - 58% Cardiac disease (often a bradyarrhythmia or tachyarrhythmia) — 23% Neurologic or psychiatric disease — 1% Unexplained syncope — 18%

The term "syncope" should be reserved LOC secondary to transient global cerebral hypoperfusion. Not all LOC = syncope (i.e. seizures causes LOC, but not due to cerebral hypoperfusion, therefore technically not syncope)

Identification of the underlying etiology for syncope can often be made from just the history, physical examination (including orthostatic vitals), and an ECG. Physician findings and clinical presentation

• • • •

Blood pressure: if low, consider orthostatic hypertension: if unequal in both arms (difference >20 mm Hg), consider subclavian steal or dissecting aneurysm. Pulse: if tachycardia, bradycardia, or irregular rhythm, consider arrhythmia. Mental status: if confused after the “syncopal episode,” consider postictal state. Heart: if there are murmurs present suggestive of AS or HOCM, consider syncope secondary to left ventricular outflow obstruction; if there are JVD and distal heart sounds, consider cardiac tamponade.

Clues for etiology •

Vasovagal (vasodepressor) Neurally Mediated Syncope 1. 2. 3. 4. 5.

•

Syncope due to Orthostatic hypotension 1. 2. 3. 4.

•

Psychophysiologic (panic disorders, hysteria) Visceral reflex Carotid sinus hypersensitivity Glossopharyngeal neuralgia Reduction of venous return caused by Valsalva maneuver, cough, defecation, or micturition

Hypovolemia Antihypertensive drugs Neurogenic (autonomic neuropathy) Idiopathic

Cardiovascular 1. Reduced cardiac output 2. Arrhythmias or asystole a. Extreme tachycardia (>160 to 180 bpm) b. Severe bradycardia (