Sample Lecture – Compartment Syndrome, Glasgow Coma Scale and Rhabdomyolysis

Next Step: Make Cards on the Automatic Key Concepts, and Vignettes

Remember, the more you automatically know what each sentence means on your test, the better you will do. There are 4 stages in making interpretation more automatic:

  • Stage 1: Unable to Make Pathophysiologic Chronologies in Either Timed or Untimed setting
  • Stage 2: Basic Pathophysiologic Chronologies, but with Significant Gaps
  • Stage 3: Detailed Pathophysiologic Chronology Without Time, but Unable to Consistently Generate PC During Timed Setting
  • Stage 4: Consistent Pathophysiologic Chronologies in Timed Setting

My goal with these vignettes is to help you reach Stage 4. How do you do so?

  • With the Automatic Key Concept cards, you can master the underlying information to move past Stages 1 + 2.
  • Then, with the Vignette/Pathophysiologic Chronology cards, you can teach yourself to make these connections on your exam.

Automatic Key Concepts:

Copy + paste these into your cards, to make these key concepts more automatic.

 

Compartment syndrome – what is it? What is the mechanism of pain/tissue damage?

Contents of an enclosed space  ↑ (e.g. tissue swelling, bleeding) and/or volume of a space ↓ (e.g. tight cast) → pressure ↑ → ischemia

 

What are the classic ”P’s” associated with compartment syndrome? 

Pain, paresthesia, paralysis/paresis, pulselessness, and pallor

 

Why do the classic symptoms of compartment syndrome occur? 

Tissue ischemia → pain

Arterial flow ↓ → pallor / pulselessness

Nerve ischemia/compression → paresthesia/paralysis

 

Compartment syndrome: based on the relative pressures, where would you see blood flow decrease first? Why?

Venous flow/return would decrease first, since its pressures are the lowest. Capillary flow would be next, followed by arterial flow

 

Abdominal compartment syndrome: one early complication may be thrombosis in the IVC/portal system. Why?

Abdominal compartment syndrome: intraabdominal pressures ↑ → venous flow ↓ → venous stasis → risk of thrombosis ↑ 

 

How would ischemia lead to CELL swelling?

Ischemia → ATP ↓ → Na/K ATPase activity ↓ → net accumulation of ions inside of cells. Recall that Na/K ATPase moves 3 Na+ out, and 2 K+ in the cell, for a net movement of 1 ion out of the cell for each ATP consumed. If the Na/K ATPase activity ↓ → net outflow of ions ↓ → accumulation of ions/water inside cell ↑ → cell swelling

 

Compartment syndrome: what effect would tissue ischemia have on interstitial pressure? How would this affect the progression of compartment syndrome? Why?

Ischemia → O2 delivery ↓ → anaerobic glycolysis → lactate / adenosine ↑ → vasodilation leakage of fluid into interstitium → interstitial pressure ↑ → compartment pressure ↑ → worsening of cycle

 

Impending compartment syndrome – what is the most important symptom? What might you suspect is the pathophysiology?

Pain out of proportion to the injury. Presumably from tissue (not necessarily nerve) ischemia. Nerve ischemia is typically associated paresthesias/hypoesthesia

Ischemia – classic presentation of ischemia = pain out of proportion to exam (~pain without a lot of tenderness)

Reminder: what are the classic ”P’s” associated with compartment syndrome? 

Pain, paresthesia, paralysis/paresis, pulselessness, and pallor

 

Compartment syndrome – what are late findings? Why might this might make sense?

Paralysis and pulselessness. Paralysis would likely result from prolonged nerve ischemia, so would be expected to be late. Similarly, for pulselessness, compartment pressure > arterial pressure, which would likely happen very late.

 

Compartment syndrome – using the pathophysiology, explain the treatment

Must relieve pressure of the compartment. Typically this means fasciotomy. Fascia is tough/non-distensible, so to allow the contents of the compartment to expand, you would have to cut it.

 

Glasgow Coma Scale 4,5,6 motor score-correspond to what?

4 – Withdrawal from pain (absence of abnormal posturing; unable to lift hand past chin with supraorbital pain but does pull away when nailbed is pinched)

5 – Localizes to pain (purposeful movements towards painful stimuli; e.g., brings hand up beyond chin when supraorbital pressure applied)

6 – Obeys commands (the person does simple things as asked)

 

 

 

 

 

 

Vignette/Pathophysiologic Chronologies:

Copy + paste these into your cards, to make the connections behind these vignettes more automatic.

 

A 36-year-old male patient is admitted to the hospital following a crush injury. The patient was working in construction, and had a large metal beam fall on his left leg. CT demonstrates a tibial fracture. Two days following surgical repair of his fracture, the patient complains of severe pain in the left leg over the past eight hours, with urine output decreasing over this time. Over the past two hours, he also reports feeling paresthesias. On exam, his left leg appears swollen. Sensation is diminished to light touch, and his left dorsalis pedis pulse is diminished.​

What is the pathophysiologic chronology?​

Paresthesias: what’s the significance?​

How can you make sense of the degree of tenderness?​

 

Summary:

Fracture/crush injury → swelling → compartment pressure ↑ → capillary flow / venous flow ↓ → tissue ischemia (pain) ↑ + nerve ischemia (paresthesia/hypesthesia)

 

Detailed:

Fracture/crush injury → direct damage to leg tissue → swelling → compartment pressure ↑ → capillary flow / venous flow ↓ → ischemia ↑ → anaerobic glycolysis + Na/K ATPase ↓ → vasodilation/capillary leakage ↑ + tissue swelling ↑ → vascular engorgement + compartment pressure ↑ → even more ischemia → pain + nerve ischemia (paresthesia/ hypesthesia)

 

 

An unconscious 25-year-old woman is brought to the emergency department after being found on the beach. On arrival, her temperature is 36ºC, pulse is 95/min, respirations are 22/min, and blood pressure is 100/70. She does not withdraw to painful stimulus. Her serum creatinine is 2.5 mg/dL, and blood alcohol concentration is 230 mg/dL. Urine toxicology is otherwise negative.​

What is the pathophysiologic chronology? Specifically:​

What is the significance of her neurologic exam findings?​

Why is her creatinine elevated?

 

Summary:

EtOH intoxication → unconscious + unable to withdraw from painful stimuli → pressure ischemia of muscles → rhabdomyolysis → myoglobinuria → kidney failure

Detailed:

EtOH intoxication → unconscious + unable to withdraw from painful stimuli → external compression of capillaries → pressure ischemia of muscles → rhabdomyolysis → myoglobinuria → glomerular damage/blockage → kidney failure

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