1. Case Presentations Walter Eisenhauer

3. Questions What are the two key clinical features of Neurogenic Shock? What pathophysiologic mechanism causes these unique features? Trauma to what anatomic region is the most common precipitator of Neurogenic Shock? How is the diagnosis of Neurogenic Shock Made? Describe the principles of management in a patient with neurogenic shock? Are Neurogenic shock and spinal shock the same?

4. Case You are working in a local community hospital Emergency Department when a 25 year old previously healthy male is brought in by ambulance after being involved in a mcycle accident. He is non responsive, was not wearing a helmet, and his vital signs are as follows. BP 80/40, resp-14 spontnaeous and he is noted to have on a nasal cannula, HR 60, and he is afebrile.

5. Case Secondary survey reveals no obvious external bleeding or deformities. Specifically there is no obvious evidence of a depressed skull fracture. His skin is warm and dry. The abdomen is soft without organomegaly. You systematically inspect and palpate his body and note bruising on his forehead and face but no other obvious deformities. He has an IV of crystalloid fluids is running in the right antecubital fossae at 250cc an hour

6. Case What will be your approach to further evaluating and stabilizing this patient? What condition should be ruled out before all others? Once competing diagnosis are effectively ruled out what treatment can be implemented?

7. Case A,B,Cs Rule out hypovolemia until proven otherwise Assure C/Spinal immobilization in suspected spinal injuries Bradycardia and Warm dry skin are huge clues Insertion of Central line will facilitate measurement of CVP (preload), Cardiac Output (by thermodilution), and PVR (calculated) PVR will be markedly decreased due to loss of sympathetic tone

8. Case Management ◦??Pressors ◦Atropine ◦???Steroids ◦???Spinal cord repair Spinal shock refers to loss of reflex action…these terms are not synonymous in that neurogenic shock refers to loss of sympathetic output

9. Comparison Hypovolemic shock ◦Skin cold and damp from massive sympathetic outflow ◦Tachycardia from the same ◦History consistent with rapid volume loss ◦Find source of loss and stop ◦Volume replacement/Blood replacement?

10. Comparison Cardiogenic Shock ◦“PUMP Failure” ◦Wet lungs due to Left ventricular failure ◦?? Vasculopath ◦Pulmonary Edema- ◦Management-Steve later but  Lasixfix pathology  ACE??Dig  PressorMSO4/O2/Nitrates etc Historic Concept- “MOST DAMP” Morphine Oxygen Sit up Tourniquets Digitalis Aminophylline Mercurial Diuretics Phlebotomy

11. Septic Shock Tachycardia + decreased PVR ◦Remember this toxin affects capillary networks not the loss of autonomic control ◦Rx Pressors/O2/Find and massively treat underlying sepsis

12. Ms. Smith is a 78 year old white female who presents complaining of RUQ abdominal pain. Anatomically Locate the stone based on the following constellation of findings:

13. Ms. Smith RUQ pain following fatty meal ingestion Fever, RUQ abdominal pain following meal ingestion- ???What’s different here RUQ abdominal Pain, Jaundice, no fever RUQ Pain, Fever, Jaundice, RUQ Pain…much more severe and in Mid epigastrium,

15. Ms Smith Stone in the GB ◦Ball valve on contraction causing pain ◦No infection ◦Risk low Stone in GB ◦Cholestasis in GB ◦“cesspool” infection ◦No jaundice as bile still flows through biliary system Stone in CBD ◦No infection (yet!) Stone in CBD ◦Infection- Charcot’s triad Stone at Ampulla ◦Pancreatic duct now involved

16. MS Smith Labs Cholelithiasis ◦Normal wbc ◦Alk phos ?? Increased ◦Bili normal Cholecystitis ◦Increased wbc ◦Increased alk phos ◦Bilirubin normal Choledocholithiasis ◦Wbc normal ◦Alk phos elevated ◦Bili elevated (direct bili) Choledochocystitis ◦Wbc elevated ◦Alk phos elevated ◦Bili elvated Gallstone Pancreatitis ◦Any of the above and increased amylase/lipase

17. MS Smith So Ms smith signs out AMA cause her pain is better. 2 weeks later she shows up in your ER because of abdominal distension, abdominal pain, and vomiting. ◦What happened?