MVA EVENT

Victim status
Location inside the vehicle
Type of vehicle
Vehicle speed
Type of collision
Static object
Type of collision
Moving object
Type of Impaction
Front
Type of Impaction
Rear
Type of Impaction
T – Bone
Seat Belt
Ejected Victims
Deaths
Way of evacuating Victims
 Air bags
Inflated??
CASE STUDY
MVA TRAUMA
 Code 3 Trauma Team Activation
• December 12, 2006, around 11 a.m.
• MVA rollover with three teenage females involved.
• The teens were reported to be driving around on
their lunch break from high school. Later
investigation discovered that the three girls were
“Huffing” or “Dusting” which is when someone
inhales gas from a compressed can of air that is
usually used to clean computer keyboards.
• The car left the road at a high rat or speed, traveled
greater than 300 feet, with multiple rollovers, finally
impacting a telephone pole.
 Patient Medical History/ Physical
Examination:
• No known drug allergies.
• On arrival into the ER the patient had a:
• pulse rate of 121
• blood pressure of 125/61
• respiratory rate 20-22
• O2 saturation of 96% on a nonrebreather.
ON THE SCENE PICTURE OF THE PATIENTS
VEHICLE
 Chest x-ray:
film critique
• Two flat plate AP Chests were obtained pre and post-
intubation by placing a 14x17 film lengthwise underneath the
backboard of the patient.
• The findings from this were:
a normal heart, the mediastinum is not wide
lungs are normally aerated without disease
no fractures are demonstrated
chest x-rays have adequate density and contrast
• The lungs include the required anatomy, which includes the
apices of the lungs to both costophrenic angles.
• Since the patient is on a backboard and the spine has not
been cleared the patient is not in the upright positioned for
both chests.
 C-Spine Film Critique
• Two cross-table lateral cervical spine x-rays were
performed. (the first view was not low enough to
demonstrate all seven cervical vertebra.)
• In the second radiograph you can see that the patient
was intubated. There is reversal of the cervical
lordosis without evidence of subluxation or fracture.
• The pre-intubation view reveals no evidence of soft
tissue swelling.
 Femur Critique
• The articulation with the hips are normal.
• There is a comminuted, butterfly type,
fracture of the middle one-third
• The backboard strap obscures the proximal
knee joint.
• The distal joint is cut off.
• Film is acceptable for trauma
 Pelvis Critique
• demonstrated normal articulation of the hips.
• The backboard obscured some areas in detail.
• There is a left pubic fracture with slight
comminuted (small particles of bone). The
break involves the body of the pubis and likely
the rami.
 Glasgow Coma Scale
• is a neurological scale which seems to give a reliable,
objective way of recording the conscious state of a person, for
initial as well as continuing assessment.
• A patient is assessed against the criteria of the scale, and the
resulting points give the Glasgow Coma Score (or GCS). It has
value in predicting ultimate outcome of the patient.
• The scale comprises three tests: eye, verbal and motor
responses. The three values separately as well as their sum
are considered. The lowest possible GCS (the sum) is 3 (deep
coma or death), and the highest is 15 (fully awake person).
(http://.en.wikipedia.org/wiki/Glasgow_Coma_Scale)
 The Patients rating on the GCS
• Initially the patient could open her eyes in response
to voice, giving her a 3. The patient had
inappropriate but comprehensible words, giving her
a 3. The patient had localization of painful stimulus,
giving her a 5, for a total initial score of 11.
• Aproximately 90 seconds later the patient didn’t
open up her eyes giving her a 1. No verbalizations,
giving her a 1, and she did not obey commands,
giving her a 1.
 CT SCAN FINDINGS

• Right Femur Fracture

• fracture of the left pubic bone at the
symphysis pubis
• Significant closed head injury
• Right lung pulmonary contusions
• transverse fracture of the posterior aspect of
the right 10th rib
 CT technical factors
• A 21 cm FOV (field of View) and a window width of
3077 was used for the head scans.
• The cervical spine was scanned helically without
contrast. Axial, sagittal, and coronal 3-D
constructions were created for review. A 12 cm FOV
was used for this scan with a window width of 3077.
• The chest, abdomen and pelvis scans used a FOV of
36 cm with a window width of 545.
 Ultrasound Findings

• A limited abdominal ultrasound and lower extremity

Doppler venous ultrasound was ordered.
• The limited abdominal ultrasound study was ordered
to evaluate free fluid in the abdomen.
• A very minimal amount of free fluid was
demonstrated in the pelvis, which is not an abnormal
finding in a young female.
• The radiologist reported no evidence of a DVT in the
right lower extremity or the left thigh.
 Emergency Room Decision:

• The patients were transport the patient to

Emmanuel Hospital for further care. The
latest update on the patient was that she was
moved to fair condition at Emmanuel on
December 11, 2006.
CASE PRESENTATION

R MAHARAJ
 CASE STUDY
• 11 year old LM...involved in a pedestrian –vehicle accident on Koeberg
Road.
• Taken to nearby fire station by motorist – attended to by paramedic.
• Initial assessment – BP 80/55, P 121, sats 82%, B/S 5
GCS –E 1, V 2, M 5
• Injuries – haematoma L temporal area, swollen L elbow, deformed L lower
leg (clinically fractured) no vascular deficit, Abrasion L Hip
• On scene management:
• A- intubated – after sedation with midazolam, morphine, C collar
• B-ventilated
• C- IV access before intubation, given 200ml R/L bolus
• Packaged and airlifted to Red Cross Hospital
 AT RED CROSS TRAUMA:

• PRIMARY ASSESSMENT:
• A – size 6 ETT in situ, C-collar in situ
• B- ventilated – sats 87% on FiO2 100%
• C – no obvious bleeding, BP 109/57 P110
• D- GCS – E 1, M 4, V T …PEARL
No focal signs
blood sugar 5.7
• SECONDARY SURVEY:
• Injuries as noted
• Lodox – C spine –no fractures
• Chest – R midzone infiltrate, no visible hemo or pneumothoraces
• Pelvis no fractures
• Fracture L proximal ulna, L tib-fib
• Urine dipstix – 1+ blood
• CT Brain – small subdural L parietal area, brain swelling, no midline shift
• CT abdomen – no evidence of solid organ injury, no free fluid
• HB, U/E – normal
• ABG – Ph 7.35, PCO2 6.49, PO2 6.46, HCO3 25.2, BE 1.6, Sats 85%

• Patient taken to theatre for insertion of intracranial pressure monitor(Licox

device)
• Fractures put in casts
• Transferred to ICU for neuro-intensive care & monitoring
 DISCUSSION POINTS

• Aims in mxn of paediatric head injury.

• Secondary insult to brain – what are they, how can they be

prevented/addressed early in the Pre-hospital/ ED phase.

• What is Neuro-intensive care and current evidence.

 AIMS IN THE MANAGEMENT OF HEAD INJURY

• Prevention of secondary insult

• Maintain adequate Cerebral perfusion pressure
• Prevent rise in intracranial pressure
• Early neuro-surgical intervention
 WHAT ARE SECONDARY INSULTS TO BRAIN

• HYPOXIA – give supplemental oxygen, intubate/ventilation

early
• HYPOVOLAEMIA – look for other injuries that may cause
hypovolaemia, early control of bleeding and fluid
resuscitation
• HYPO/HYPERGLYCAEMIA
• HYPERCARBIA
• HYPERTHERMIA
 ANATOMICAL CONSIDERATIONS
ADULT vs CHILD

• OPEN SUTURES –more prone to injury, allow for greater

amount of intracranial expansion, delayed onset of herniation
• Brain tissue LESS MYELINATED cf to adult – predisposed to
greater shearing forces
• SECONDARY INSULTS – result in more profound secondary
brain injury – worse outcomes cf adults
PATHOPHYSIOLOGY OF SECONDARY BRAIN
INJURY
 PRE-ICU CONSIDERATIONS

• AIRWAY MXN
• Intubation if GCS </= 8, or hypoxia
• RSI
• WHAT DRUGS TO USE: “ IDEAL AGENT – KEEPS PATIENT HAEMODYNAMICALLY
STABLE”
• Thiopentone, Propofol, Midazolam – use with caution -> can cause hypotension,
and decreased CPP
• Ketamine – not usually used – Increases ICP and cerebral oxygen consumption.
• Recent studies downplay these adverse effects -> Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of
sedation with ketamine in severe head injury patients: comparison with sufentanil. Crit Care Med 2003;31:711–7.
• Bourgoin A, Albanese J, Leone M, Sampol-Manos E, Viiand X, Martin C. Effects of sufentanil or ketamine administered in targetcontrolled infusion on
the cerebral hemodynamics of severely brain-inured patients. Crit Care Med 2005;33:1109–13.
• Himmelesher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005;101:524–34.

• Etomidate – safe agent – minimal changes in BP, also thought to have

neuroprotective effects
• Premedication with Lignocaine – no conclusive evidence
• PARALYTIC AGENT:
• Scoline – agent of choice
• May transiently increase ICP – no clinical evidence that that this increases
mortality/morbidity. Brown MM, Parr MJ, Manara AR. The effect of suxamethonium on intracranial pressure
and cerebral perfusion in patients with severe head injuries following blunt trauma. Eur J Anaesth 1996;13:474–77.
• Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity,
or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994;78:469–73.

• Other agents: Rocuronium, Atracurium(RXH ICU)

• Cochrane review – scoline superior d/t shorter duration of action. Perry JJ, Lee
JS, Sillberg VAH, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database
Syst Rev 2007;(3):CD002788.
• VENTILATION:
• Current recommendation: EUCAPNIA
• HYPERVENTILATION – reserved solely for patients with impending cerebral
herniation

• CIRCULATION:
• hypotension increases short term mortality the most.
• Mortality increased when SBP < 75th centile Vavilala MS, Bowen A, Lam AM, et al. Blood
pressure and outcome after severe pediatric traumatic brain injury. J Trauma 2003;55:1039–44.

• Look for sources of blood loss

• Fluid resus with normal saline
 NEURO-INTENSIVE CARE

• INTRACRANIAL PRESSURE DIRECTED vs CEREBRAL PERFUSION

PRESSURE DIRECTED

• Indications for ICP monitoring:

• Severe TBI with GCS<8, and abnormal CT Brain changes …
( Haemotoma, cerebral contusion, cerebral oedema, compressed basal
cisterns) Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic
brain injury in infants, children and adolescents. Chapter 5 Indications for intracranial pressure monitoring in pediatric
patients with severe traumatic brain injury. Pediatr Crit Care Med 2003;4(3Suppl):S19–24.

• Aim to keep ICP<20cm H20

• CONTROL OF ICP:
• MEDICAL:
• FLUID THERAPY – Head Injury Fluid (5% dextrose saline, K suppl) for maintainence
• Hyperosmolar fluid therapy: Hypertonic saline vs Mannitol
• Mannitol: IV bolus 1g/kg – lowers ICP in 1-5 min, peak effect 20-60 min
Action – osmotic effects
- rheologic effects
- free radical scavenger
• Disadvantage – osmotic diuresis  hypovolaemia
• Hypertonic saline – some studies – hypertonic saline more effective in reducing
ICP, dose 3 -5ml/kg
• Advantages over mannitol – no osmotic diuresis, augments I/V volume
• Disadvantages- bleeding diathesis, hypernatraemia ( RXH – keep Na 145-150)
• STEROIDS – not recommended – CRASH TRIAL

• HYPOTHERMIA – decreases inflm response, excitotoxicity and metabolic

demands
suggested temp 32 – 34 degrees C.
RXH – aim for normothermia. Treat hyperthermia aggressively.

• EARLY SEIZURE PROPHYLAXIS – some studies recommend anticonvulsants.

No superior agent identified. Adelson PD, Bratton SL, Carney NA, et al.
Guidelines for the acute medical management of severe traumatic brain injury in infants, children and
adolescents. Chapter 19. The role of antiseizure prophylaxis following severe pediatric traumatic brain

injury. Pediatr Crit Care Med 2003;4(3 Suppl):S72–5 .

• ADEQUATE SEDATION/ANALGESIA
• NO one sedative regimen is superior.
• Benzodiazapines – decr CMRO2 and CBF, no change in ICP
• Narcotics nil effect on above
• Watch for hypotension

• SURGICAL:
• Cerebral spinal fluid drainage
• Decompressive craniectomy

• OTHER MEASURES:
• avoid cerebral venous blood flow restriction –
• Keep head in midline, avoid compressive dressings around neck, head elevation to
30 degrees
 PATIENT PROGRESS

• ICP stabilised with neuro-intensive measures

• Hypoxia corrected with ventilation – weaned by day 3 and extubated day 4
• GCS 14/15
• Transferred to trauma ward:
• 2 days post d/c from ICU – GCS deteriorated 8/15, developed seizures
• Needed reintubation, given phenobarbitone 20mg/kg for seizures

• CAUSES FOR DETERIORATION…

• REBOUND INCREASE IN ICP- reflex brain oedema, rebleed
• INFECTION – meningitis vs systemic infection
• ELECTROLYTE ABN.
• HYPOGLYCAEMIA
• THROMBO-EMBOLIC
• HYPOXIA
• DIRECT COMPLICATION OF HEAD INJURY-
 SIADH vs CEREBRAL SALT WASTING vs DIABETES INSIPIDUS
 INVESTIGATION

• ELECS – Na 117, K 4.7, Ur 2.3, Cr 60

• FBC – normal
• CRP – NO increase
• Rpt CT brain – no new bleeds, resolving brain oedema. No midline shift

• Readmitted to ICU –
• Ventilated
• Hyponatraemia corrected slowly with hypertonic sline
• Phenytoin
• Investigated for SIADH, cerebral salt wasting
• Extubated 24 hrs later
• SIADH – Hyponatraemia -dilutional
-intravascular volume normal/mildly incrd
- urine osmolality > serum osmolality
- urine sodium normal
• CEREBRAL SALT WASTING- Hyponatraemia (imprd renal tubular function –
unable to conserve salt)
- intravascular volume depletion – incr urea, serum protein.
- incr urine sodium
• DIABETES INSIPIDUS – post. pituitary lesion(ADH def)
- polyuria
- low urine sodium
 REFERENCES

• Neurointensive Care for Traumatic Brain Injury in Children, Felice Su, MD, FAAP, Instructor of
Pediatrics, Division of Critical Care Medicine, Stanford University; Attending Physician,
Department of Pediatrics, Division of Critical Care Medicine, Lucile Packard Children's Hospital

• Evaluation and Management of Moderate to Severe Pediatric Head Trauma

Anand Swaminathan, MD, MPH; Phil Levy, MD; Eric Legome, MD
EMERGENCY MEDICINE ONLINE
Published: 08/31/2009
Case Based Presentation

TRAUMA # 2
 Case
• You’re on call on a Saturday in the ICU at
VGH when the head nurse tells you that 2
traumas from an MVA had just come into the
ER. Both the driver and the passenger were
belted when their car lost control and hit a tree.
The trauma team is currently assessing them
and will let you know if they need any ICU
services.
 Case
• After speaking to the trauma senior, you find
out that the driver is unstable. A FAST showed
free fluid in the abdomen, and the patient is
now being rushed to the OR for an exploratory
laparotomy. She thinks that the patient will
likely need to come to the ICU post-
operatively.
 Question 1

• What are the most common organ injuries

associated with a) blunt and b) penetrating
abdominal trauma? What organ injuries are
associated with deceleration injury? (Yoan)
 What are the most common organ injuries
associated with blunt abdominal trauma?
• Liver and spleen : most frequently.
• Small and large intestines : next most injured.
– Crush, Deceleration, trapped air
• Pancreas (10-12%): in crush injury, direct blow,
seat belt...
• Kidney, bladder

Source: emedicine 2007, Salomone et al

 What are the most common organ injuries
associated with penetrating abdominal trauma ?
• Stab
– liver (40%) • Gunshot wound
– small bowel (30%) – small bowel (50%)
–
– colon (40%)
diaphragm (20%)
– liver (30%)
– colon (15%)
– vascular (25%)
• pancreas, duodenum, vascular, gastric, rectum,
porta hepatis, kidneys, ureters

Source: emedicine 2008, Testa et al

 What organ injuries are associated with
deceleration injury?
• Classic deceleration injuries include hepatic
tear along the ligamentum teres and intimal
injuries to the renal arteries. As bowel loops
travel from their mesenteric attachments,
thrombosis and mesenteric tears, with
resultant splanchnic vessel injuries, can result.

Source: emedicine 2007, Salomone et al

 Case Study 9:
Blunt Abdominal Trauma

Questions & Answers

What are the initial assessment
priorities for a patient with
blunt abdominal trauma?

Question 1
Answer:

Always remember your A, B, C priorities. For trauma, here is a good way to remember
your primary survey priorities:

Airway- Is the patient’s airway open?

Breathing- Are respirations effective? Does the patient require

assistance or ventilation?

Circulation- Monitor for signs of hypovolemic shock as these

patients are high risk.

Disability- Perform a quick neuro assessment as well as LOC

and motor function evaluations.

Exposure and Evacuation- Undress patient to see injuries, consider transport

if necessary.

(Wagner, 2010)
*Question 1
 Explain the initial alterations in
hemodynamic values presented.

Describe the stages of

hypovolemic shock.
What stage is he in?
What treatment should be provided?

Question 2
Answer:

Stages of Hypovolemic Shock:

Stage I- Up to 15% of the circulating volume, or approximately 750 mL of blood,

is lost. These patients often exhibit few symptoms because compensatory
mechanisms support bodily functions.
Stage II- When 15% to 30%, or up to 1,500 mL of blood, of the circulating
volume is lost. These patients have subtle signs of shock, but vital signs usually
remain normal.
Stage III- when 30% to 40% of the circulating volume, or from 1,500 to 2,000 mL of
blood, is lost. This patient looks acutely ill.
Stage IV- Loss of more than 40% of circulating volume, or least 2,000 mL of blood.
Patient is at risk for exsanguination.

Treatment priority is fluid replacement and RBC if necessary.

*Question 2
(Unbound Medicine, 2011)
Malik, T. (2013) Adapted from various sources
*Question 2
What diagnostic tests are done
to evaluate and treat patients
who have sustained a blunt
abdominal trauma?

Question 3
Answer:

Arterial Blood Gases

Complete Blood Count
Hemodynamic Parameters: cardiac output and cardiac index, oxygen delivery,
oxygen consumption, central venous pressure,
pulmonary capillary wedge pressure, and systemic
vascular resistance
Blood Lactate Level
Hemoglobin & Hematocrit
Urinary Bladder Pressure Measurement

Radiographic and imaging studies are important depending on the location of interest
and might include chest and abdominal x-rays, transesophageal echocardiography,
aortography, computed tomography, magnetic resonance imaging, or focused
abdominal sonography for trauma.

*Question 3
What are the management
guidelines for a patient with
blunt abdominal trauma?

Question 4
Answer:

*Question 4
(Kirkpatrick,
2013)
 What is meant by abdominal
compartment syndrome/ intra-
abdominal hypertension?

Question 5
Answer:

The pressure within the abdominal cavity, or intra-

abdominal pressure in a normal person is 0-5 mmHg.
Various factors, including blunt trauma can lead to
increased abdominal pressure or intra-abdominal
hypertension which is defined as sustained pressures
over 12 mmHg (Lee, 2012).
If untreated, high pressures are sustained and the illness
progresses to Abdominal Compartment Syndrome (ACS).

ACS is defined by the World Society of Abdominal

Compartment Syndrome as a sustained intra-abdominal
pressure (IAP) of > 20 mmHg (with or without an
abdominal perfusion pressure (APP) < 60 mmHg) that is
associated with new organ dysfunction/failure
(Cheatham, M.L., 2009).

*Question 5
 What is a pulmonary contusion?

What other factors may be contributing

to Mr. Reynold’s poor oxygenation status?

Question 6
Answer:

A pulmonary contusion is an injury to the lung without

laceration that may not be visible on X-ray for up to 48
hours (trauma.org, 2004).

Contributing factors for poor oxygenation:

• Shallow, short breaths (due to contusions)

• Increased abdominal pressure (reduced lung compliance)
• Poor cardiac output
• Increasing systemic vascular resistance

*Question 6
What are the nutritional needs of a patient with a
blunt abdominal trauma?

What type and when

should feeding be started?

What complications should the nurse be

concerned with at each stage of recovery?

Question 7
Answer:
Feeding should be started as soon as possible
following trauma. The patient will move from the
Ebb phase (hypometabolism) to the Flow phase
(hypermetabolism) and will require additional
nutrients as they heal.
Patients are at risk for amino acid and electrolyte
deficiencies (Wagner, 2010).
www.jspen.jp

Institutional
guidelines should be
followed.

Feeding protocol
from Vanderbilt
University Medical
Center (Diaz, 2004)

*Question 7
The formula used in this case study is Perative. Here is more
information about that formula specifically:
http://abbottnutrition.com/brands/products/perative
Cheatham, M. L. (2009). Abdominal compartment syndrome: pathophysiology and
definitions. [Review]. Scand J Trauma Resusc Emerg Med, 17, 10. doi: 10.1186/1757-
7241-17-10.
Diaz, J. (2004). Critical Care Nutrition Practice Guidelines- Vanderbilt University
Medical Center. Retreived from www.mc.vanderbilt.edu
/surgery/trauma/Protocols/nutrition-protocol.pdf
Kirkpatrick, AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML … Olvera C. (2013). Intra-
abdominal hypertension and the abdominal compartment syndrome: updated
consensus definitions and clinical practice guidelines from the World Society of the
Abdominal Compartment Syndrome. Intensive Care Medicine. 39(7):1190-206. doi:
10.1007/s00134-013-2906-z
Lee, R. (2012). Intra-abdominal Hypertension and Abdominal Compartment
Syndrome: A Comprehensive Overview. Critical Care Nurse 32 (1):19-31.
Retrieved from www.aacn.org/wd/Cetests/media/C1212.pdf
Trauma.org. (2004, February). Chest trauma: Pulmonary contusion. Retrieved from
http://www.trauma.org/archive/thoracic/CHESTcontusion.html
Unbound Medicine. (2011). Hypovolemic/Hemorrhagic Shock. Retrieved from
http://nursing.unboundmedicine.com/nursingcentral/ub/view/Diseas es- and-
Disorders/73631/0/hypovolemic_hemorrhagic_shock
Wagner, K. D., Johnson, K.L., Hardin-Pierce, M. G. (2010). High-acuity nursing (5th ed.).
Saddle River, NJ: Pearson Education Inc.

*References