Conference Notes 9-18-2012

Conference Notes 9-18-2012

Kutka/Urumov  Oral Boards

Case 1: Crytpococcal meningitis in a man with AIDs. Critical actions include ordering cryptococcal antigen and/or india ink test (usual csf studies won’t pick up crytpococcal infection), giving antifungal medication (amphotericin B), rewarming for hypothermia, get a head ct prior to LP.

Andrej’s comments: cryptococcal meningitis is rare if CD4 count is greater than 100.  Opening pressure can be high.  High opening pressure portends a worse prognosis.  Routine CSF studies can be completely normal so cryptococcal antigen and/or india ink studies are essential to making the diagnosis.  

Case2:  Intracranial hemorrhage.    Critical actions include airway management, treat BP, elevate head of bed, treat intracranial hypertension with mannitol.

Andrej’s comments: Treat BP if over 180 systolic with a iv drip antihypertensive medication.   Anti-seizure meds not routinely indicated.  Some weak data showing worsened outcome with seizure prophylaxis.  

Case 3:  7yo with BB gunshot to eye with a retro-orbital hematoma.  Critical actions include lateral canthotomy, consult optho, pain management and prophylactic antibiotics.

 Elise comment: Think about doing ct scan brain with iv contrast in patients with hx of cancer and immunocompromised patients.

Chastain    7-UP Scan for Hypotension

Non-invasive study to augment clinical evaluation in the hypotensive patient.

7 UP scan includes FAST plus lungs, aorta, parasternal echo views.

When in the sucostal window you should look at the heart for pericardial fluid, RV dilatation, and overall contractility.   Paradoxical movement of ventricular septum is also an indication of PE.  The septum should move from LV toward RV.  If it is moving from RV to LV think PE.  Also look at the cava to see if it collapses.  More than 50% collapse indicates a CVP less than 10.  You should take this measurement as close to the heart as possible.  A crude indicator of location is that you should be looking at the ivc right by the liver.

In PSL window if aortic root is more than 4cm think about dissection.    Be sure to image this window with enough depth to see the descending aorta.  Frequently pericardial fluid will collect in the pericardium anterior to the descending aorta.  

Lung windows can help with causes of dyspnea.   Use the linear probe in the 2nd and  3rd intercostal spaces bilat.  No sliding of pleura means pneumothorax.   Increased vertical comet tails (B lines) indicates chf.  Increase horizontal A lines indicates COPD or Asthma.

Apical view of heart can also show RV dilation and bowing of the septum to the the left.

LUQ view usually needs the probe to be “closer to the bed and closer to the head” than when viewing the RUQ.   The spleen/liver tends to be more superior/posterior than the liver/kidney. 

Wise   Deadly Triad in Trauma

Hypothermia/acidosis/coagulopathy comprise the deadly triad.

Damage control surgery is temporizing procedures to obtain hemostasis. 

Hypothermia: trauma causes loss of thermoregulation.  Hypothermia exacerbates coagulopathy by decreasing platelet activation and altering enzyme kinetics. It also alters fibrinolysis. 

Acidosis: Causes decreased contractility, vasodilation, an worsened coagulopathy.   Base deficit >6 and elevated lactate  correlates with increased mortality.

Fluids can cause dilutional coagulopathy and hypothermia.

2002 study with sick trauma patients:  coagulopthy required BOTH tissue injury and hypotension.  Protein C is over-activated in severe trauma that may be the mechanism of the coagulopathy.

Tranexamic Acid:  CRASH-2 trial showed all-cause mortality benefit.   Benefit in bleeding patients depended on time of administration.  First hour had most benefit.   After 3 hours may increase mortality.  

Elise comment:  ACMC does not have tranexemic acid currently.

Permissive hypotension: goal is to maintain BP only to the point of maintaining minimal adequate perfusion.   Resuscitation fluids/blood products are restricted.   Goal BP is 70-90 systolic.   Generally accepted that patients with penetrating trauma should not be resuscitated to normal BP prior to gaining hemostasis.

Damage control resuscitation: permissive hypotension  plus damage control surgery plus resuscitation volume is predominantly blood products rather than crystalloid.

Factor 7 was discredited as a resuscitation drug.   Erik and Elise pounded  Factor 7 into the ground during the discussion.     Erik said there is new data supporting further tranexemic acid. 

Recommendations: shoot for a lower BP goal, avoid large volumes of crystalloids, use the massive transfusion protocol, give TXA in the first hour, keep patients warm. 

TABLE 112-1   -- Categorization and Initial Treatment of Hemorrhagic Shock*






Blood loss (mL)





Blood loss (% of blood volume)





Pulse rate





Blood pressure





Capillary refill test





Respiratory rate





Urine output (mL/hr)





Mental status

Slightly anxious

Mildly anxious

Anxious and confused

Confused and lethargic

Fluid replacement (3:1 rule)



Crystalloid + blood

Crystalloid + blood


Chandra   Massive Transfusion Protocol (MTP)

Massive transfusion:  10 units of prbc’s in 24 hours,  or replacement of 50% of total blood volume in 4 hours.    Kids is >40ml/kg prbc’s  in 4 hours.

Who gets MTP?: ABC rule includes heart rate >120/bp<90/positive fast/penetrating mechanism.  More than 2 criteria activate MTP.    TASH score bp<100/hr>120/hgb<7/FAST/ Long bone fx/male gender.

1 unit of prbc’s increases hgb by 1.   Patients that receive FFP in a 1:1 ratio with prbc’s have a lower mortality.   Consensus for MTP is 1:1:1 ratio for prbc’s: platelets: ffp.   Battle field data from Iraq shows improved mortality with this ratio.

ACMC protocol: 10 units prbc’s, 6 units ffp, 1 unit aphoresis platelets, and 2 units of cryoprecipitate.  ER or  Trauma attending has to order this protocol.   The SYMS know how to order this. 

Goal of MTP: Map of 65 with adequate perfusion; basically bp of 80/60 with palpable pulses and warm extremities.    

Sam Lam comment: He questioned the component make up of the ACMC MTP because it is a little atypical based on trauma data in the literature.

OMI  Traumatic Brain Injury

Brain injury classification: Mild GCS=14-15    Mod GCS=9-13     severe GCS=3-8

Canadian head injury rule is a validated tool to identify patients at risk for positive ct or brain injury.

40% of moderate head injury patients(GCS9-13) have abnormal ct findings and 10% require surgery.

Severe head injury patients have the highest likelihood for brain injury and highest potential for benefit from surgery.   Get these patients to CT in 30minutes.   Tube all these patients.   Don’t routinely hyperventilate these patients.   PCO2 less than 25 increases mortality.

SAH from trauma are relatively benign.   Subdural hematomas tend to have significant underlying brain injury.   Epidurals often have little underlying brain injury.  Epidurals have great outcomes if manage properly.  Epidural hemorrhages may have a lucid period between initial loss of consciousness and later deterioration.    CT will be abnormal in these epidural cases from the time of initial injury.

Diffuse brain injury: concussion usually resolves in 6 hours.   Diffuse axonal injury due to shearing forces from high speed mvc’s.  Initial Ct will be normal despite severe coma.   Later CT’s or MRI will show punctuate hemorrhages.   Outcome for DAI is poor and any improvement takes months to years.

Monro-Kellie Doctrine: increasing volume inside fixed volume boney skull causes rapid increase in intracranial pressure.     


Cerebral perfusion pressure=MAP- ICP.   There is little data that medical care impacts outcome of brain injury.   Prevention of injury and prevention of secondary injury are keys to limiting morbidity/mortality.  Preventing hypoxia is probably the most important thing we can do to prevent secondary injury and  lower  patient mortality.   Hypotension is the second most powerful factor increasing mortality in brain injured patients.   After preventing hypoxia and hypotension, there is not much evidence that anything else helps outcome.

 ICP monitor:  keep ICP less than 20 and CPP>60. Improved outcome in patients who respond to hyperosmolar therapy.   This means mannitol at 1gm/kg.   Mechanism is osmotic mobilization of water across blood brain  barrier.  You can get hypotension from mannitol.   Hypertonic is an option for osmotic therapy that does not cause hypotension.

Some centers are studying hypothermia and suspended animation for severe brain injury.  The current thinking is that patients need low temp cooling for prolonged time (>48 hours).

Brain oxygenation are also being studied.

Hyperventillation:  works by dropping pco2 causing vasoconstriction.  This causes decreased brain blood flow and reduction in intracranial volume/pressure.  It can however cause brain ischemia.  So it has gone out of fmavor.

Kascia Nosek comment:  If patient is breathing over the vent settings, do you sedate them to avoid hyperventilation?   Dr. Omi,  yes.

Steroids: no benefit in brain injury.

Anticonvulsants:  Phenytoin reduces the incidence of seizures in the first week but not after.

Brett Negro comment: What are criteria for using steroids?   Dr. Omi,  patients with parenchymal brain injury including subdural hematomas should get phenytoin or phosphenytoin.  Keppra may be another option.   Anticonvulsants are all stopped at about a week.

Elise comment: Ketamine is probably a good choice for an induction agent in the hypotensive brain injured patient.   The risk of increasing intracranial pressure is low and it is less likely to cause more hypotension than etomidate.