Case-Based Presentation: Trauma

CCM Academic Half-Day

11 December 2008

Case #1: Don’t mind your own business, whatever you do…

• You are moonlighting in the emergency department in a very, very rural hospital and field a base contact call from a paramedic crew.

• A young man minding his own business in a bar was shot several times with a handgun, according to witnesses. His GCS is E2 V3 M 4, with rapid, weak pulses. His vital signs: HR 130, RR 28, BP 110/65. Primary survey reveals two penetrating wounds to his chest and one hole in his abdomen. There are no other reported injuries.

• The paramedics called for a helicopter for direct transport to Vancouver, but it will take about an hour to reach them, as the sole functioning machine is being refueled. Your hospital is approximately 50 km from the scene, with a parking lot that would serve nicely as a helipad. – The paramedics are seeking some wisdom…

• What is the current evidence regarding out-of-hospital trauma life support?

• What should the destination be for this patient?

In the ED

• He remains resistant to attempts to immobilize him, and makes a mockery of spinal precautions. The ambulance crew delivers him to your resuscitation bay with a GCS 9, with a heart rate of 150 and BP 100/60. RR is 30. He has a patent airway, quiet breath sounds bilaterally, penetrating injuries as described, a tender, firm abdomen and is moving all extremities. His skin is pale and diaphoretic.

Immediate Management Goals?

A little assistance, please…

• The trauma service at VGH is an hour away including helicopter response time. A general surgeon is on call at your hospital, and he may still be rounding. He’s not Naisan. Would you refer him to the immediately available service, or call for a helicopter? Why?

Case # 2: Deere Me

• The following week, at VGH…• A truck carrying a riding lawnmower on the

freeway dropped its payload and the wayward John Deere struck a midsize car following at 100 kph. The car then careened into the center divide and rolled several times before coming to rest in a ditch. The driver (Unknown A), a 30 year old man, was trapped in the car for 30 minutes. He was intubated in the car, then extricated after the roof was sawn off. Initial GCS was 6 (E1 V1 M4).

AC 1

• Now he is in full spinal immobilization, intubated and mechanically ventilated. GCS is E1, V(T), M 1. Vital signs are HR 140, BP 100/50, RR 12 on ACV. SPO2 is 92% on FiO2 0.35. Pupils are unequal ( R 3 mm and reactive, L 6 mm and fixed). An abraded area on his forehead and an obviously fractured left clavicle are his only immediately apparent external injuries. – Neurosurgery has arrived, and the resident has managed

to coax the radiology resident into approving a stat CT brain, but “you have to send the patient right now!”

AC 1

• What are the immediate concerns regarding his hemodynamic mangement in light of his neurologic injury?

• What will you do about it?

Main Goal• Current exam suggests severe TBI with possibility

of uncal herniation (blown pupil)• His BP is 100/50, sats 92%• Hypotension (SBP<90mmHg) and hypoxia (sats

<90%) must be avoided as they are independent risk for mortality and morbidity.– Traumatic Coma DataBase: Single episode of

hypotension from injury through resus is associated with doubling of mortality and similar increase in morbidity!.

Specific Management

• Need to decrease pressure in the head acutely.

• Try to maintain oxygenation and CPP.– Place on 100% O2– Hyperventilation to decrease CO2 (25-35 mmHg)

to acutely vasoconstrict intracranial vasculature.• This is OK for short term but unknown long term

consequences, as it will decrease cerebral blood flow…

Hyperosmolar Therapy

• Mannitol: widely accepted use to acutely treat severe increased ICP– Immediate plasma expanding effects cause

decreased hematocrit, decreased viscosity, which increased CBF and O2 delivery

– Osmotic effect delayed 15-30 min, be careful in hypotension!

– May also increase risk of renal failure

The RT appears, as if from nowhere…

• Any particular ventilation strategy for this patient?– 100% O2

– Stat ABG and hyperventilate as above.– Careful with PEEP (may exacerbate

hypotension, with possible increase in ICP)– Follow patient to CT scanner

• Hypertonic saline: mechanism of action likely:– Osmotic action to decrease cerebral water content

– Dehydrates endothelial cells and RBCs leads to increased diameter of vessels and deformability of RBC-better blood flow

– Also reduces leukocyte adhesion in traumatized brain

– Watch out in chronic hyponatremics!

CT Brain• The CT shows subarachnoid blood, a right

temporal subdural hematoma (8 mm) and surrounding edema with midline shift and uncal herniation. – Clinical correlation is required.

QuickTime™ and aTIFF (Uncompressed) decompressor

are needed to see this picture.

QuickTime™ and aTIFF (Uncompressed) decompressor

are needed to see this picture.

• An EVD is placed, with initial intracranial pressure measuring 40 cm H2O.

• The patient appears in the ICU, and the bedside nurse insists upon orders right this very second, as the neurosurgery post-op orders are illegible without the Rosetta Stone.

Orders, please.

• MAP goals?

• What about the EVD?

• Nimodipine for traumatic SAH with hypotension?

• Should we start phenytoin?

• Where did you leave your coffee?!

Next time, just let the coffee mug go…

• Unknown B is a 50 year-old woman with an unknown medical history. She was encountered 15 feet from the stopped car, and was initially unresponsive with strong pulses and spontaneous, snoring respirations. She now has an oral airway in place, is in full spinal precautions and has the following vital signs: HR 100, BP 100/40, RR 8, SpO2 92% on oxygen by face mask. You perform the primary survey, as you happen to be standing closest to the ER stretcher.

“What are my MAP goals?”

• Autoregulation:– CBF remains stable despite

rise and fall in CPP

• With severe TBI, autoregulatory function is compromised– CPP can lead to CBF

– Might need a higher CPP to avoid ischemia

Avoid secondary insult

• Single episode of hypotension during resuscitation double mortality

• Recommend SBP > 90 during initial resuscitation

• Recommendation from European guidelines MAP>90.

Br J Anaesth 2007; 99: 18-31

Avoid Secondary insult

• Brain Trauma Foundation:– Aggressive attempts to maintain CPP above 70

mm Hg with fluids and pressors should be avoided due to increase incidence of ARDS (Level II)

– CPP of 50 mm Hg should be avoided. (Level III)

Management of ICP

• Goal of balancing risk of herniation with risk of over treatment

• No large RCT comparing different levels of ICP targets

• Brain Trauma Foundation recommend:– Maintain ICP < 20mmHg (level II evidence)

aSAH

• HHH therapy: hypervolemia, HTN, hemodilution• First reported in 1976• Incidence of delayed ischemia by 50%

Nimodipine and SAH

• Goal is to avoid secondary ischemia• Delayed cerebral ischemia due to

vasospasm is the most common cause of death and disability in aSAH

• Nimodipine treatment didn't influence presence of angiographic vasospasm– benefit linked to cytoprotective rather than its

vasodilatory properties?

Nimodipine and SAH

• Cochrane review 2007 for aneurysmal SAH:– Nimodipine reduced risk of poor outcome

and (RR was 0.67 (95% CI 0.55 to 0.81))

– IV nimodipine not recommended– Recommend nimodipine 60mg PO Q4H for 3

wks– Can give 30mg PO Q2H if BP low.

Nimodipine and TBI

• Cochrane Review of CCB in TBI 2003:– No benefit of CCB in TBI patients– Subgroup analysis for traumatic SAH for risk

of death from 2 RCTs• pooled OR 0.59 (95% CI 0.37 to 0.94).

– Higher risk of hypotension in CCB group.

Unknown B

• GCS is E2 V2 M1. She coughs against the oral airway, and there are no secretions nor blood noted in her mouth. There is some blood on the backboard beneath her occiput. No chest nor abdominal abnormalities are noted. She does not move her extremities, and her skin is warm with normal capillary refill.

Radiological adjuncts

• How would you manage her airway?

• What imaging is necessary before a treatment plan can be made?– How good are CT and MRI at determining the

nature of vertebral and spinal cord injuries?

• CT brain shows suggestion of cerebral edema, but no midline shift nor evidence of uncal/tonsilar herniation. There is a C4 body and facet fracture with fragments projecting into the canal. CT angiography reveals a right cervical carotid dissection, just outside the skull. There is flow on either side. Spinous process fractures are noted at T 10 and 11. The lumbar spine is unremarkable.

• The patient is now in the ICU, with GCS E2 V(T) M1. HR is now 115 and BP is 90/40, giving her the highest unsupported MAP in the unit. The spine service is occupied in the OR, but plan to operate on her as soon as the room is turned over.

• What is the strategy for managing her hemodynamics?

Approach to hemodynamics in TBI

• Although the imaging is not as spectacularly abnormal as in Unknown A, the guidelines defined by the Brain Trauma Foundation still apply– SBP <90 mmHg should be avoided.

• In hospital, a single episode in pts w/ a GCS < 13 showed a trend toward incr mortality, while two or more episodes carried a relative risk of 8.1.

• Increased duration of hypotension is also assoc w/ incr morbidity and mortality.

Approach to hemodynamics in TBI

• The optimal choice of resuscitation fluid has yet to be defined, although there is some evidence that hypertonic saline is superior to Ringer’s lactate (improved survival). I would not use albumin in this patient, given the increased mortality for trauma pts seen in the SAFE trial (especially brain injured pts; (relative risk, 1.62; 95% CI, 1.12–2.34).

• The optimal BP has yet to be defined, although significant guidelines suggest a goal MAP > 80 or 90, which more closely correlates with CPP.

• There is insufficient evidence at present to suggest which if any vasoactive agents should be used to support arterial pressure if fluids alone are inadequate.

Dr. Mountain’s consult note

• So, to answer the question, I would volume resuscitate with blood if necessary based on her Hgb, and any active bleeding. Once bleeding and Hgb were stable, I would continue to support her pressure to a MAP > 80 with NS, and then probably levophed if necessary.

• I would aggressively avoid episodes of hypotension, and if any happened inadvertently, I would correct them as quickly as possible, and yell expletives I learned from Naisan at the responsible resident.

Is there a role for steroids in her management?

• No.

Details?

• In the 60s and early 70s, steroids were commonly given to TBI pts on the basis of their beneficial effect on brain tumor pts, and some early studies suggesting positive effects in TBI.

• Since the mid-70s, multiple studies and a meta-analysis have shown no benefit of steroids in TBI.

• In addition, one study has shown an increased risk of first late seizures in pts treated with steroids, and a large study (10,008 pts) in 2004 was stopped early due to incr mortality in TBI pts treated with methylpred (RR 1.18, 95% CI 1.09-1.27, p = 0.0001).

• TF, the Brain Trauma Foundation guidelines state that the majority of evidence indicates that steroids do not improve outcome or lower ICP in severe TBI. There is strong evidence that steroids are deleterious; thus their use is not recommended in TBI.

“Should an EVD be placed?”

• …asks the pathology resident. “They put one in the other guy…”

Endoventricular Drain

• The BTF states that Level II evidence supports the placement of an ICP monitoring device in all salvageable patients with a severe TBI (GCS 3-8 after resuscitation) and an abnormal CT scan (hematomas, contusions, swelling, herniation, or compressed basal cisterns).

• ICP monitoring should be done with a normal CT scan if two or more of the following at admission: age > 40, any motor posturing (unilateral or bilateral), or SBP < 90.

• These factors define pts at high risk for ICH (53-63%).• With a normal admission scan, the risk is about 10-15%

(followup scanning necessary).

• TF, the BTF recommends the use of ICP monitoring in pts at risk for ICH, to more accurately allow measurement of CPP, and therefore appropriate treatment, earlier detection of ICH, and treatment via CSF drainage.

• They note that ICP cannot be reliably predicted from CT scan alone, that ICP data are useful in predicting outcome and guiding therapy, and that not monitoring ICP while treating for ICH can result in deleterious outcomes.

• In this patient, there is a suggestion of cerebral edema on her CT scan, which would qualify as abnormal according to the BTF.

• Even if it was not abnormal, the fact that she is over 40, and she has absent motor responses on her GCS suggest that she is at high risk for ICH, and her ICP should be monitored, and treatment tailored to the readings.

• Nice job pathology resident!

“And the carotid is dissecting. Uhh, is there something we’re supposed to be

doing about that?”

• Incidence in blunt trauma is 1%

• Thromboemboli

• Stenosis

• Occlusion

Treatment options

• Antiplatelets

• Anticoagulants

• Stents/angioplasty

• Considerations in Trauma

Cochrane review

• No RCT’s

• No difference between anticoags and antiplatelets for death and disability

Do they heal?

• 90% heal in 3-6 months

• 50% recanalize from complete occlusion

Back to Unknown A

• As the patient is rolled to the OR, you are paged about Unknown A, whose name has since become available but nobody can remember it. In the course of performing his physical exam, the resident noted that the patient’s left pupil is the same size it was in the ER, although it was documented to be 4 mm and reactive following EVD placement. He is breathing dyssynchronously with the ventilator. “What do we do? There’s already a drain in place!”

Yikes

• What do we do? There’s already a drain in place?

• Is there a role for hypothermia here?

• Would any other monitoring modalities be useful here?

What do you do? There’s already a drain in place!

• Treatment to decrease ICP– Mannitol– 3% saline– Hyperventilation– Surgical decompression

• Treatment to decrease CMO2– Sedation– Mechanical ventilation– Normothermia

Please comment on the role of hypothermia in managing elevated

intracranial pressure.

It should work

• reduction in brain metabolic rate• effects on cerebral blood flow• reduction of the critical threshold for oxygen delivery,

blockade of excitotoxic mechanisms• calcium antagonism• preservation of protein synthesis• reduction of brain thermopoolin• a decrease in edema formation• modulation of the inflammatory response• neuroprotection of the white matter• modulation of apoptotic cell death.

It does work…..

• Animal studies are encouraging

• Appears to help in post cardiac arrest cerebral anoxia

• Some human studies in TBI appear to show a benefit

• BUT …………….

The breadth of the evidence is equivocal

Part of it is encouraging

TBI guidelines

Some people are not giving up on Hypothermia

• Surface cooling

• Intranasal selective hypothermia

• Transarterial or transvenous endovascular cooling

• Extraluminal vascular cooling

• Epidural cerebral cooling.

Time to meet the family

• Does he have brain damage?

• Is he going to get any better than this?!

• Should we start planning for discharge?

Primary vs Secondary Brain Injury

• Primary injury: experienced at the moment of traumatic incident. – There is NOTHING to be done about the primary

injury!

• Secondary injury: caused by ischemia (hence the need to avoid hypotension and hypoxia) and the sequelae of deranged intracranial pressure.– This is the opportunity to salvage neurologic function!

Prognostication

• Extremely difficult in patients who are initially comatose or who require sedation to allow for ongoing care.

• Data are suboptimal in terms of study design, definitions and timelines.

• As a result, exact percentages are nearly impossible to provide.

Glasgow Coma Scale

• GCS at first assessment (i.e. immediately post-injury): GCS 3 is associated with 80% mortality and approx. 10% functional neurologic survival across all studies.

• Note wide variation in time of “initial” GCS, from < 6 hrs to 7 days.

• Age > 60 yrs, not accounted for solely by medical comorbidity (i.e. inherent loss of ability of older brain to heal).

Prognostication

• Bilaterally absent pupillary light reflex after hemodynamic resuscitation.– Reflex pathway is adjacent to areas responsible

for cognitive function.– Correlates to approx. 88% dead or vegetative

state.– Numbers affected by orbital trauma,

hypotension, and hematomas/ subsequent surgery.

The money…Hypotension

• SBP < 90 mm Hg at any time from injury through ICU stay!– Single recording of hypotension during critical

care stay correlates to approxiately double the mortality!

– This is the most addressable of all the prognostic signs.

CT Scan Findings

• Basal Cisterns: compression or absence associated with elevated ICP

• Traumatic subarachnoid hemorrhage

• Midline Shift

• Intracranial mass lesion