I→ Episode Summary

Sepsis guidelines are constantly changing. Refer to your national guidelines or institutional protocol for most up to date treatment information.

Introduction

* Sepsis is bad and needs to be treated aggressively* Confusion around multiple conflicting guidelines and requirements* Surviving Sepsis Campaign recommendations* CMS requirements* Sepsis-3* SOFA/SIRS/qSOFA* Institutional protocols

Sepsis-3 Proposed Recommendations

* Screen for sepsis by applying qSOFA instead of SIRS criteria* qSOFA criteria* Altered mental status* Tachypnea* Hypotension* SIRS criteria* Tachycardia* Tachypnea* Leukocytosis* Hyper/hypothermia* qSOFA criteria miss cases of sepsis (too specific)* SIRS calls everything “sepsis” even if the patient is fine (too sensitive)* Change definition of “Sepsis” (no more SIRS plus source)* New definition* Source of infection* PLUS* Organ disfunction* Determined by SOFA score (different purpose than qSOFA)* Eliminate the term “severe sepsis” completely* Redefine “septic shock”* Persistent hypotension* OR * Lactic acid >4

Current Approach to Sepsis

* Step 1- If the patient has SIRS plus source* Get labs including a lactic acid* Step 2- If the patient has organ dysfunction* Diagnose sepsis* Step 3- If the patient has sepsis* Order broad spectrum antibiotics* Order blood cultures* Needs to be completed in <3 hours* Step 4- If the patient has persistent hypotension or lactate >4* Diagnose septic shock* Step 5- If they have septic shock* Give 30ml/kg crystalloid bolus* Start vasopressers if hypotension doesn’t improve with bolus

Additional Reading

* CMS Sepsis Core Measures (ACEP)* Sepsis-3 Recommendations (EMJ)* Surviving Sepsis Campaign (SCCM)

Physiology

* RBC hemoglobin breakdown -> unconjugated (indirect) bilirubin* Unconjugated (indirect) bilirubin -> liver -> conjugated (direct) bilirubin* Conjugated (direct) bilirubin -> Eliminated in stool

Causes of Hyperbilirubinemia

* Increased RBC turnover* Sepsis* Rh incompatibility* RBC disorders* Maternal diabetes* Scalp hematoma* Decreased/slow conjugation by the liver* Peaks around day 5 of life* Congenital liver disorders* Gilbert/Crigler Najjar Syndromes* Breast milk jaundice* Breast milk inhibits conjugation of bilirubin* Decreased excretion* Bowel obstruction* Breast feeding failure (dehydration)* Decreased stool output results in reabsorbed bilirubin

Kernicterus

* Brain damage from severe hyperbilirubinemia (>25 mg/dL)* Compare measured bilirubin to established nomogram* Treatment is phototherapy* (Worst case scenarios require exchange transfusion)

Additional Reading

* Approach to Neonatal Jaundice (emDOCs)

I→ Episode Summary

Good luck!!!

Clinical Presentation

* Incidental finding on routing CBC* Petechiae/purpura* Mucosal bleeding* Epistaxis* Gingival bleeding* Hematuria* Vaginal bleeding

5 Major Causes of Thrombocytopenia

* Thrombotic Thrombocytopenic Purpura (TTP)* Clinical presentation (pentad)* Thrombocytopenia* Fever* Microangiopathic hemolytic anemia* “schistocytes”* Neurologic abnormalities* Renal dysfunction* Physiology* Low ADAMTS13 results in impaired vWF breakdown* Widespread “platelet plugs”* Treatment* Plasma exchange* Hemolytic Uremic Syndrome (HUS)* Clinical presentation* Pediatric patient with bloody diarrhea* Renal dysfunction* Thrombocytopenia* Treatment* Supportive care* Heparin Induced Thrombocytopenia (HIT)* Clinical presentation* Recent heparin administration* Acute thrombocytopenia (<150) or 50% decrease in platelets* Treatment* Stop heparin and choose different anticoagulant* Disseminated Intravascular Coagulation (DIC)* Clinical presentation* Patient septic, severe trauma, or otherwise critically ill/injured* Multiple abnormal labs* Increased PT/PTT* Increased D-dimer* Increased fibrinogen degradation products* Treat underlying trigger* Immune/Idiopathic Thrombocytopenic Purpura (ITP)* Common condition* Relatively benign* Treatment* Steroids* Occasionally platelet transfusion* Other causes* HIV* Hepatitis* Heavy alcohol use

Additional Reading

* Thrombocytopenia: An ED Approach (emDOCs)

The hardest part about this chief complaint is expanding your differential beyond gastritis!!!

Step 1: Expand Your Differential Diagnosis

* Early appendicitis* Bowel obstructions* Myocardial infarction* Elevated ICP* Diabetic Ketoacidosis

Step 2: Give a Testing Plan

* High yield tests to consider* EKG – older adults* Pregnancy test – women of child bearing age* Electrolytes – most patients* Other tests to consider* CBC* LFTs/Lipase* Urinalysis

Step 3: Give a Treatment Plan

* IV fluids (1L normal saline)* Antiemetics* Ondansetron (Zofran)* Promethazine (Phenergan)* Prochlorperazine (Compazine)

Step 4: PO Challenge

* Prior to discharge patient needs to keep fluids down* Bonus points if you update your attending on this

Step 5: Repeat Abdominal Exam

* Perform this prior to discharging patient

Additional Reading

* Antiemetic Pearls (EM Cases)

Organ Failure Complications

* Hepatorenal syndrome (renal failure)* Decreased urine output* Labs show elevated creatinine* Admit to hospital (high mortality)* Hepatic encephalopathy (brain failure)* Introduction* Liver clears ammonia from body* In advanced liver failure, ammonia increases* Symptoms* Altered mental status/confusion* Asterixis* Treatment* Lactulose* Binds ammonia and is excreted* Rifaximin* Eliminates bacteria responsible for producing ammonia

Portal Hypertension Complications

* Gastric/esophageal varices* Symptoms* Altered mental status* Hepatic encephalopathy triggered by reabsorbed GI blood* Melena* Black stools from digested GI blood* Treatment* Proton pump inhibitor (PPI)* Pantoprazole* Octreotide* Antibiotics* Classic procedure* Blakemore tube (balloon tamponade)* Ascites with spontaneous bacterial peritonitis (SBP)* Symptoms* Abdominal pain/tenderness* Ascites* Fever* Testing plan* Diagnostic paracentesis* >250 neutrophils* High protein* Low glucose* Treatment* Antibiotics* Albumin

Liver Failure Complications

* Coagulopathy* Diagnose with abnormal coagulation studies* PT with INR* Patients can be BOTH hyper and hypocoagulable

Additional Reading

* How to Perform Paracentesis (Medscape)

Non-Accidental Trauma

* Estimated 10% of pediatric patients are victims of abuse* Sexual abuse* Physical abuse* Neglect* Common red flags* Changing story* Story that doesn’t make since* Delays in seeking care* Unusual bruising locations* Torso* Ears* Neck* Common tests if non-accidental trauma suspected* Skeletal survey x-rays* Head CT* Especially if altered mental status* Abdominal CT* Especially if abdominal trauma* Report to child protective services (CPS)

Tummy Ache

* Necrotizing enterocolitis* Classic presentation* Premature baby* 1st month of life* Ill appearing* Classic finding on x-ray* “Pneumatosis intestinalis”* Volvulus* Classic presentation* 1st month of life but previously healthy* Distended abdomen* Bilious vomiting* Testing* Abdominal Xray* Upper GI Series (ideal test)* Toxic megacolon* Complication of Hirchsprung Disease* Seen on x-ray* Intussusception* Telescoping bowel resulting in ischemia* Classic presentation* 2 months – 2 years old* Intermittent abdominal pain followed by lethargy* Diagnose with abdominal ultrasound* Pyloric stenosis* Classic presentation* Projectile vomiting* Normal appetite/hungry* Palpable “olive” in epigastrium * Testing* Electrolyte panel* Hypokalemia* Hypochloremia* Alkalosis* Abdominal ultraound

Additional Reading

* Pediatric Abdominal Pain (EM Clerkship)

Don’t be overwhelmed knowing/memorizing each inborn error of metabolism. The basic approach is actually quite easy!!!

Inborn Errors of Metabolism (IEM)

* Almost always result in one of the following three clinical abnormalities* Buildup of toxins* Ammonia* To test for this, obtain an ammonia level* Buildup of acids* Methylmalonic acidemia* To test for this, obtain electrolyte panel and look for decrease CO2* Shortage of glucose* Glycogen storage disorders* To test for this, obtain a blood glucose level

Congenital Adrenal Hyperplasia (CAH)

* Decreased 21-hydroxylase enzyme* Physiologic abnormalities* Decreased aldosterone* Low sodium (hyponatremia)* High potassium (hyperkalemia)* Decreased cortisol* Low glucose level* Hyperpigmentation* INCREASED sex hormone (androgens)* Fused labia* Partial male genitalia

Additional Reading

* Congenital Adrenal Hyperplasia (Wikipedia)