Case PresentationsWalter Eisenhauer

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?

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.

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

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?

Case

A,B,CsRule out hypovolemia until proven otherwiseAssure C/Spinal immobilization in suspected

spinal injuriesBradycardia and Warm dry skin are huge cluesInsertion 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

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

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?

Comparison

Cardiogenic Shock◦ “PUMP Failure”◦ Wet lungs due to Left ventricular failure◦ ?? Vasculopath◦ Pulmonary Edema- ◦ Management-Steve later but

Lasix fix pathology ACE ??Dig Pressor MSO4/O2/Nitrates etc

Historic Concept- “MOST DAMP”Morphine Oxygen Sit up Tourniquets Digitalis Aminophylline Mercurial Diuretics

Phlebotomy

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

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:

Ms. Smith

RUQ pain following fatty meal ingestionFever, RUQ abdominal pain following meal

ingestion- ???What’s different hereRUQ abdominal Pain, Jaundice, no feverRUQ Pain, Fever, Jaundice,RUQ Pain…much more severe and in Mid

epigastrium,

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

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

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?