Barash Chapter 53- trauma Flashcards
The general approach to evaluation Acute trauma victim has three components:
Rapid overview: seconds, is pt stable, unstable, dying or dead ?
Primary survey: ABC, Neuro assessment, external injury ? TEE= Myo contractiliy, Volume, pericardial effusion, essential labs
Secondary survey: Detailed evaluation of each anatomic region, FAST( focused assessment with sonography ) , CT ( MDCT) , MRI, pulmonary
Why do a tertiary survey within 24 hours after trauma?
To potentially diagnose missed injuries during the initial survey
What are the difficult trauma related reasons for tracheal intubation?
Maxillofacial,
Neck
chest injury
cervicofacial burns.
Signs of upper and lower airway obstruction
Dyspnea cyanosis hoarseness strider dysphonia Subcutaneous emphysema hemoptysis
What physical findings may be present before symptom indicating airway obstruction and requiring specialized technique to secure airway?
Cervical venous distention ,
crepitation
Tracheal tug and/or deviation
Jugular venous distention maybe present before symptoms appear
What are the initial steps in airway management
Chin lift
jaw thrust
Clearance of the oral pharynx placement of an oral pharyngeal and nasal pharyngeal airway
in inadequately breathing patients Ventilation with his self inflating bag
In what type of brain injury is blind passage of a nasal pharyngeal airway or NG or nasotracheal tube avoided
Basilar skull fracture because the air we may enter the anterior cranial fossa
True or false airway assessment must include a rapid examination of the interior neck for feasibility of access to the cricothyroid Membrane
True
Why is tracheostomy not desirable in the initial phase compared to cricothyrotomy
Because it takes longer to perform
It requires Neck extension which may cause or exacerbate cord trauma in patients with cervical spine injuries
If a cricothyroitomy is in place for more than 2 to 3 days what should you do?
Conversion to a tracheostomy to prevent Laryngeal damage
What are the contraindications to cricothyrotomy
Younger than 12 years ( permanent laryngeal damage)
and suspected Laryngeal and Trauma( uncorrected airway obstruction)
Why does rapid sequence induction with cricoid Pressure in Trauma patients necessary?
I assume they’re full stomach
No time to reduce gastric content pharmacologically
Awake intubation with sedation and topical anesthesia as well can be done
What is the anesthesia approach for head, open eye, and contained major vessel injuries ?(3)
- Ensure adequate oxygenation in ventilation
- Deep Anesthesia
- Profound muscle relaxation before airway manipulation= they don’t buck cough or go hypertensive»_space; less Intracranial, intraocular, intravascular pressure elevation.
In head,open eye, or contained major vessel injuries, what can happen if you allow the patient to cough , buck or go hypertensive
- Herniation of the brain
- extrusion of eye contents
- dislodgment of a hemostatic clot from an injured vessel
If the patient is not hemodynamically compromised and has a head , open eye , or contained major vessel injuries how do you perform your anesthetic sequence
1.Preoxygenation and opioid loading
2.Large doses of IV anesthetic and muscle relaxant
Watch for :
Low BP»_space; ICP, Low CPP,
Is ketamine still contraindicated in patients with head or open eye injury?
Yes! Because of its potential to increase Intracranial and intra occular Pressure they used to avoid ketamine but because it maintains the systemic blood pressure it does not cause any big increase in ICP or IOP so nowadays it is used in those type of patients
Do use ketamine in patients with contained major vessel injury ?
No ! because by increasing systemic blood pressure it can cause dislodgment of a hemostatic plug initiating bleeding in vascular injuries
Can sux be used in head , open eye or contained major vessel injury ?
Yes ! As long as fasciculation is inhibited by prior with administration of adequate dose of nondepolarizing muscle relaxant
Or
just use ROC at 1.2 to 1.5 mg/kg = same onset as Sux of 60 seconds but will lasts 2 hrs
When comparing video laryngoscopy to direct laryngoscopy what is a disadvantage
Video shows longer intubation time resulting in decline of oxygen saturation to 80% or less in a lot of patients!
Most common cause of cervical spine injuries
- High speed MVA
- Falls
- Diving
- Gunshot
- Head injuries especially if low GSC = c spine injury
What are the complications associated with the C collar:
- Pressure ulcer
- Elevated ICP
- Compromise central venous access
- Airway management challenges if reintubation is needed
* once you establish airway r/o c- spine injury to clear the neck as soon as possible
What happens to blunt trauma induced C spine injury after admission
Worsening neurological deficits either because of delay in diagnosis or improper C-spine protection and/or manipulation
What indicates a low probability of C - spine injury
- No posterior midline neck tenderness and no focal neurologic deficit
- Normal level of alertness
- No evidence of intoxication
- No painful distracting injury
What is the Canadian C-spine rule for radiography after Trauma (which identifies Low risk patients)
- Is there any high risk factor mandating radiography :
≥ 65, dangerous mechanism , extremity paresthesia
2.Are there low risk factors that permit safe evaluation of the range of motion of the neck :
Sitting and Walking in ED, rear-end accident only , no immediate neck pain, no C spine midline tenderness .
- Can the patient rotate the neck laterally left and right for 45° in each direction without pain
How do you rule out C - spine injury in pre-elementary school children ( age 4 and under )
Absence of clinical findings .
you don’t need diagnostic studies or radiation exposure
Children with persistent midline neck pain with no other clinical findings AND negative intitial findings will you get imaging to rule out C-spine injury?
No ! because that indicates a little possibility of unstable C spine injury
Gold standard for ruling C spine injury in or out?
MRI is gold standard : but it is too sensitive and show too much .
Instead MDCT with less than 3mm cuts is used . Only thing is , possibility of missing 1 unstable C spine in about 5000 patients
How to do Airway management in C- spine injury
To DL : best do Manual inline stabilization ( MILS) w/ 2 operators + the physician doing the airway.
Is a hard cervical collar sufficient to provide absolute protection . True or False
A hard collar alone does not provide absolute protection especially not against rotational movements of the neck .
How is MILS performed?
1) First operator : Stabilize and align the head in a neutral position without applying cephalad traction
2) Second operator: Stabilize both shoulders by holding them against the table or stretcher
3) The anterior portion of the hard collar which limits mouth opening may be removed after immobilization
How does MILS affect your intubation ?
Suboptimal glottic view
If patient has a hematoma from a vertebral fracture which leads to enlargement of the prevertebral space, how can anesthesia make that patient worse during DL ?
That causes greater interior pressure that needs to be applied to the tongue by the laryngoscope blade in order to visualize the larynx. The increase in ant. pressure goes to the spine = increase the movement of the unstable vertebral segment
During direct laryngoscopy Is there a higher pressure with MILS or without MILS?
With Manual Inline Stabilzation
Besides DL what other measures can be used to secure the airway in acute phase of cervical spine immobilization
VL, gum elastic bougie, Translaryngeal retrograde intubation, cricothyroidotomy
Flexible fiber optic laryngoscopy and translaryngeal guided intubation cause almost no Neck movement but why don’t we use them in the initial airway management phase
Blood
Secretion
Long preparation time
Difficulty of their use in comatose, uncooperative or anesthetized pt
Disadvantage of nasotracheal intubation
- Risk of epistaxis
- Failure of intubation
- Possibility of entry into cranial vault or the orbit if there is damage to the cranial base or the maxillofacial complex
What are the usual signs of basilar skull facture
- Battle sign : (takes 1 day to appear , bruise over the mastoid process from blood along the periauricular artery )
- Raccoon eyes
- Bleeding from the ear or the nose
- just bc those signs are not there ‘yet” does not mean the don’t have cranial base fracture
Can supraglottic device with or without the aid of FOB be used?
Yes, but has same neck movement as DL
In regards to C spine injury : when is the use of FOB preferred
In the SUBACUTE phase of the spine injury when time constraints , full stomach and patient cooperation issues do not exist!!!!!
Why is high impact maxillofacial injury challenging for airway management
Not only soft tissue Edema of the pharynx and parapharyngeal hematoma, blood or debris in the oropharynx maybe responsible for partial or complete airway obstruction in the acute stage of these injuries
How can liberal administration of fluids in maxillofacial Trauma worsen the patient
Serious airway compromise may develop within a few hours in up to 50% of patients with major penetrating facial injuries, multiple trauma, caused by progressive inflammation or Edema resulting from liberal administration of fluids
Maxillofacial Hemorrhage most frequently from what artery?
Internal maxillary artery or its branches
Less frequently : facial external carotid, sphenopalatine arteries and other small branches
Life treathening= do packing, intermaxillary fixation if that doesn’t work do angioembolization
If there is fracture induced encroachment of the airway or the mandibular movement is limited patient : pain , trismus ( lockjaw ) = pt cannot open the mouth what do you do
Fentanyl titrated 2 to 4 µg /kg over a period of 10 to 20 minutes will improve the patient’s ability to open the mouth if mechanical limitation is not present
In direct airway injury if there is bleeding into the oropharynx , will flexible fiber-optic be useful ?if not what do you do ?
Waste of time !
Retrograde technique using a wire or epidural catheter passed through a 14 gauge catheter introduced on the trachea through the crycothyroid membrane : IF THE PT CAN OPEN MOUTH
When is the surgical airway indicated in direct airway injuries
- Airway compromise
- Direct laryngoscopy has failed or is considered impossible
- When the jaw will be wired
- When a tracheostomy will be performed anyway after repair of the fracture.
Direct airway injury , WHen is Tracheostomy indicated ?
- ER
- As a delayed procedure in OR for airway control within 12 hours of arrival
- An elective sx during definitive surgery within or more than 12 hours following admission of the hospital
- Comminuted mandibular, mid-facial, bilateral LeFort III and panfacial fractures are likely to be managed by tracheostomy for definite of surgery
Can be done to avoid the complication of tracheostomy
Submental or submandibular intubation
What does submental or submandibular intubation involve
Pass the proximal end of the FLEXIBLE ARMORED OROTRACHEAL tube through a small submental incision
Mid face fx with frontal sinus or orbitozygomatic and orbitoethmoid complexes what other type of fracture is most likely involved ?
Cranial fracture
When do cervical airway injury happen usually
Blunt or penetrating Trauma
Air escape, hemoptysis, and coughing are present in almost all …
Penetrating injuries
Hoarseness, muffled voice , dyspnea , strider , dysphasia, odynophagia , cervical pain and tenderness , ecchymosis, subcutaneous emphysema , flattening of the thyroid cartilage protuberance , what diagnosis ? *
Major blunt laryngotracheal damage .
Which may actually be missed either because the patient is asymptomatic or unresponsive, or the S/S are missed *
No Resp distress or hemodynamic compromise, do you CT first or airway first ?
CT first .
Don’t go blind in the compromise airway , it will make it worse.
But if you have to , use FOB if possible or a surgical airway
There 5 grades of laryngeal injuries
1 . no Fx, minor laceration , minimal edema = minimal airway s/s
- Undisplaced fx , mucosal damage but no exposure of cartilage = mild airway compromise
- Displaced fx, vocal fold immobility = significant compromise
- Multiple fx with instability = significant compromise
- Laryngeal separation = catastrophic airway obstruction.
If there is a stab in airway already , can you use that stab to pass your tube and intubate ?
Yes
***If it’s grade 5 laryngotracheal damage ( cartilaginous fx) or mucosa abnormalities. What is your choice of intubation technique?
Awake intubation With FOB
or
Awake tracheostomy
Can’t do a cricothyroidotomy ** laryngeal damage precludes cricothyroidotomy **
Up to ____% of blunt laryngeal injury may have ______injury ; perform a _______with caution
70% blunt laryngeal
Have Cervical spine injury
Tracheostomy = be careful
If pt with cervical airway trauma is confused or cant cooperate , do you do an awake intubation ?
No, go to OR , use ketamine or inhalation gas, intubate without muscle relaxant .
If pt has episodes of apnea while under gas anesthesia, put patient upright and do the usual maneuvers
Complete transection of trachea is
Life threatening
Distal trachea will retract in to the chest - OBSTRUCTION!!!
Penetrating thoracic airway injury can occur anywhere , but where does blunt trauma usually affect?
Posterior membranous portion of the trachea and the main stem bronchi , usually 3cm of the carina .
Believe it or not , tracheal intubation can cause this injury
What are the S/S of blunt thoracic airway injury ?
Pneumo Pneumomediastinum Pneumopericardium SubQ emphysema Continuous air leak from chest tube * but these are not specific to thoracic airway damage .
What will happen to your ETT cuff if there is perforated airway ?
Can’t get a seal around the ETT ,
Or
on CXray shows large radiolucent area in the trachea corresponding to the cuff = perforated airway
What are the CXray signs of perforated airway?
Seeing the cuff on X-ray
A radiolucent line along the prevertebral fascia bc of the air tracking up from mediastinum
Peribronchial air
Dropped lung sign : complete intrapleural bronchial transection causes the apex of lung to descend all the way to the hilum
For airway techniques in thoracic airway injury , danm if you anesthetize and relax , danm if you do it awake. Why? What happens with each technique ?
Anesthesia and muscle relaxant = irreversible obstruction bc you relax the peritracheal and peribronchial structures that airway patency
Awake intubation = airway loss bc of further distortion of the airway by the ETT , pt agitation or rebleeding
Is condensation a way to verify tube placement in these patients ?
No
Auscultation and ETCO2
But you may not hear
Or ETCO2 may be low or not present if shock or circulatory collapse
What can prevent you to hear when you auscultate for tube placement in these thoracic airway trauma patients ?
Pulmonary contusion
Atelectasis
Diaphragmatic rupture w/ abdominal content migration
Pneumothorax
Tracheal injury what is preferred method of intubation then ?
ETT using a bronchoscopic guidance DISTAL to the tracheal injury . That’s the new trend vs surgical management
What type patients will not be part of the new trend and will have to have surgical management?
If the lesion is > 4 cm Is cartilaginous vs membranous Esophageal trauma also present Progressive subQ emphysema Severe dyspnea needing intubation Pneumothorax w/ air leak through chest Difficult to mechanical ventilate Mediastinitis
What are the IMMEDIATE threats to patient life after trauma that may alter respirations
Tension Pneumothorax
Flail Chest
Open pneumothorax
Other that may not be immediate : Hemothorax Closed pneumothorax Pulmonary contusion Diaphragmatic rupture with abdo content herniation Actelectasis with mucus plug Aspiration Chest wall splinting
What are the classic signs of tension pneumothorax?
- Cyanosis
- Tachypnea
- Hypotension
- Neck vein distention ( if Hypovolemic may be see this)
- Tracheal deviation ( may be difficult to see)
- Diminished breath sound
What sign is usually diagnostic of tension pneumothorax in the supine position ? Describe
Deep sulcus sign : pleural air track in the lateral and caudal region of the lung instead of the apex
What is definitive dx of Tension pneumo ?
CT
How to relieve the Tension pneumo?
Insert a 14 gauge catheter 4th or 5th intercostal space midaxillary line
Or
2nd ICS midclavicular line
Flail chest , there is costochondral separation or sternal fracture . What makes them into Resp failure ?
Underlying pulmonary contusion
Increased elastic recoil»_space; increased WOB»_space; Resp insufficiency/failure»_space; hypoxemia!
Over how long does Resp insufficient/ failure develop with flail chest ?
Develops over 3 to 6 hr period»_space; worse CXray and worse ABG ( hemopneumo, paradoxical chest wall movement , pain induced splinting make gas exchange worse )
Fraction of lung contused is indicative of
ARDS
Especially if contuse volume is > 20%
Rib score system . 1 point is assigned to each of these type of fractures
6 or more rib fx=1
Bilateral fx= 1
Flail chest =1
3 or more severely (bicortically) displaced fx =1
1st rib fx = 1
At least 1 rib fx each ant, lateral, Posterior regions of ribs= 1
Rib score and Vital capacity have linear correlation with
Development of
Pneumonia
Resp Failure
Tracheostomy
Vital capacity 50 % means what in flail chest patient ?
Little risk of pulm complications
But less than 30% = probability increase 2.5 times
Flail chest , Vital capacity below ____% means _____times likely to develop pulmonary complications
Below 30%
2.5 times increased probability
True or false . Once there is chest wall instability , must have respiratory support ?
False, only if there is gas exchange abnormalities
Liberal tracheal intubation make things worse patient mortality and complication increase
Just do effective pain relief = improve Resp function and no need for a vent . Use thoracic epidural with LA and opioids or thoracic paravertebral block
Besides pain continuous pain control what else to do for flail chest patient who do not have gas exchange issues ?
O2 , CPAP 10 -15 cmH2O using face mask , airway humidifier, IS, Bronchodilators , airway suction with FOB , nutrition. Overzealous fluid and blood make oxygenation worse bc it worsens pulmonary injury
If head injury patient does not have a known threat to cerebral herniation , avoid hyperventilation …why ?
Increased cerebral vasoconstriction = decreased perfusion + cerebral lactic acid build up
If hypovolemic , how is hyperventilation bad ?
It interferes with venous return and cardiac output , leading to hypotension , further decrease in organ perfusion and even cardiac arrest
What ventilation technique is Best to prevent hemodynamic deterioration and decrease likelihood of ARDS ?
Low TV: 6- 8 mL/kg
Moderate PEEP
Producing low inspiratory or plateau pressures
What ventilation goal to use in intubated but spontaneously breathing patient s?
Airway pressure release ventilation where breathing is superimposed on the vent by intermittent brief decreased of CPAP = improved V/Q , BP , less sedation needed , better O2 delivery, less VAP( happens in 30% of pulmonary contusion )
Bil severe pulmonary contusion use what ventilation mode ?
High frequency Jet ventilation
Severe unilateral pulmonary contusion unresponsive to other vent measures , use a…
Double lumen tube
How do you diagnose systemic air embolism which can happen after penetrating lung trauma, blast injury or blunt thoracic trauma where both distal passages and pulmonary veins are affected ?**
You will see:*** Hemoptysis Circulatory instability CNS dysfunction IMMEDIATELY AFTER ARTIFICIAL VENTILATION \+ Air in blood from the radial Artery .
If there is air bubble in the coronary arteries during thoracotomy , what is the diagnosis ?
Systemic air embolism
You know there is systemic air embolism bc of lung contusion , what Resp maneuvers do you do to prevent air entry in the systemic circulation ?
Isolating and collapsing the lacerated lung with a double lumen tube
Or
Lowest possible TV using a single lumen tube
TEE of the left side of heart to see if there is any air bubble
Most common cause of dramatic Hypotension and shock is***
Hemorrhage***
The second most common cause of mortality after trauma ***
Hemorrhage ***
First most common cause of mortality after trauma is
Head injury
What is the primary goal in bleeding
urgent surgical control of the source
Why is it important to remove the tourniquet as soon as urgent surgical control is achieved
To avoid Pressure-Induced nerve damage, skin necrosis, limb ischemia.
What is the optimal systolic blood pressure in the trauma patient?
100 to 110 mmHg mercury for elderly
And 90 for younger patient
Elderly vs young , who is more at risk for significant tissue hypoperfusion in the presence of normal blood pressure
Elderly (> 65 )
Carbon monoxide takes how long to remove it on room air, 100% O2 , and at 3 atm in hyperbaric chamber
4 hours on room air
60 to 90 minutes with 100% O2
20 to 30 minutes at 3 atm in the hyperbaric chamber
Normal IOP is
10 to 21 mmHg
What is considered a predictor of increased mortality in shock patients independent of injury , SBP, or presence of head injury?
Inability for the patient to elevate heart rate in the face of hypo perfusion!!!
What are the Early clinical indicators of the severity of hemorrhagic shock
Heart rate BP Pulse pressure Respiratory rate Urinary output Mental status
Why does hematocrit drop in hemorrhage
Because of immediate activation of transcapillary refill. Low Hct = suspect extensive bleeding
Shock index formula:
Hr / SBP
In elderly (HR/SBP )x age or
SI x age
Normal SI
.6
Closer to 1 = Increased mortality
Assessment of Bloof consumption score ask 4 questions ( used to determine the amount of transfusion)
Heart rate 120
systolic blood pressure 90
penetrating injury
Positive FAST
White blood like that level indicates major bleeding
> 2 mmol/L
Damage control resuscitation
Brief permissive hypotension
rapid control of any bleeding source minimal crystalloid infusion
early administration of plasma in other blood products in a balanced ratio 1:1:1 of packed red blood cells plasma and platelets by activation of the MTP
and TXA
What is the purpose of damage control resuscitation?
To prevent : 1.pulmonary edema 2.ARDS 3.and Multiple Organ - MOF And abdominal compartment syndrome.
If you give > 1.5 L to 1 unit blood ratio in the first 24 hrs , what will happen to the patient ?(2)
ARDS
Abdo compartment syndrome
Permissive hypotension is contraindicated in: (3)
- Brain injury
- spinal cord injury
- elderly with chronic systemic Hypertension because adequate perfusion is crucial
Most useful and practical tools of organ perfusion during all phases of shock ?(2)
1) Base deficit
and
2) Blood Lactate level
Base deficit reflects: (3)
1) Severity of shock
2) Oxygen debt
3) Changes in O2 delivery
Base deficit is better than Arterial pH
Base deficit -2 to -5 means
Mild shock
Base deficit -6 to -9 mmol/L indicates
Moderate
Base > 10 mmol/L
Severe shock
Why is blood lactate less specific than base deficit as a marker of tissue hypoxia
Because of increased epinephrine Induced skeletal muscle glycolysis accelerated pyruvate oxidation decreased hip had a clearance of lactate in early mitochondrial dysfunction
What is the half-life of lactate
15 to 30 minutes in a healthy individual failure to clear lactate within 24 hours after reversal of circulator shock is a predictor of increased mortality
What is normal plasma lactic concentration
0.5 to 1.5 mm/L
Lactate levels over 5 mm/L indicates
Lactic acidosis :significant
Recommended hemoglobin concentration in all phases of management is
729 grand per deciliter
To increase brain oxygenation in 75% of head injured patient how old should PRBC be
Less than 19 days storage to increase HgB 9 to 10g/dL
MTP means
10 unit in 24 hr
> or = 4 PRBC in first hour with need to to continue assumed
It does not take plasma into account
Can use Liquid plasma up to how many days after collection
28 days
How long does it take to Saul FFP or PF 24
30 to 45 minutes
PF 24 vs FFP
PF frozen within 24 hour collected ( only contains 60% of factors in FFP except fibrinogen bc it has a t1/2 of 12 hours )
FFP is frozen within 8 hours
A kid has massive hemorrhage if had to be given how much blood ?
> 40ml/kg
Or
Given 50% of blood volume over 24 hrs
Circulating blood volume in an infant is :
80 ml kg
90 for Barrash
Children over 3 months , circulating blood volume is
70 ml/ kg
What is the most constant vital sign indicating early volume loss?
Narrowing pulse pressure
Children have a greater hemodynamic reserve and VS only deteriorate after they have lost ____to ____% blood volume
35 to 40 %
Neonates don’t have Vitamin K and functional fibrinogen until
6 months
In pediatric actual trigger for activating the MTP
High injury severity score
Kid with base deficit > 6 or INR 1.8 predicts what ?
High chance to die .
What are the two components of coagulopathy of the trauma patient
A cute traumatic coagulopathy and resuscitation associated coagulopathy
Signs of life
Pupillary response Spontaneous ventilation Carotid pulse Palpation blood pressure Extremity movement Cardiac electrical activity
Of all the possible secondary insults in the injured brain, what has the most or greatest detrimental impact
Decreased oxygen delivery due to Hypotension and Hypoxia
40% of death from trauma are cause by …
Head injury
Most common early complication of head trauma are :
ICH Herniation Seizures Neurogenic pulmonary edema Cardiac dysrhythmias Bradycardia Systemic HTN Coagulopathy
Does phenylephrine constrict cerebral vessels ?
No
What is the most important cause of death in the head injury patient ?
Low BP
Especially < 90
AVPU alert , verbal stimuli , Response to pain , unresponsive to assess consciousness
True true
Uncal Herniation under the Flax cerebri how does the pupil look?
Dilated and unresponsive “ blown “
Pupil that is dilated and sluggish
Uncus ( temporal lobe ) is compressing. Oculomotor nerve
CT , concave border in brain , Dx?
Subdural hematoma
CT scan has convex outline aka lenticular configuration?
Epidural hematoma
In patients with brain trauma how to prevent or alleviate the secondary injury ?
Prevent Hypotension and Hypoxemia anemia raised ICP acidosis and hypoglycemia greater than 200
Are the most important therapeutic maneuvers in the patients with brain trauma
Maintaining ICP,CPP, and oxygen delivery
Head injury , where do you want MAP , PaO2, ICP and CPP
MAP > 80
PaO2 over 95
ICP below 20 to 25 mmHg
CPP at 50 to 70 mmHg
Why CPP > 70 no longer practiced ?
Bc it causes ARDS
LR solution Na 130 , Osmolality 255 mOsm/L not given in brain injury bc ?
Slightly hypotonic , may promote swelling in uninjured of brain if given in large quantities
How is Mannitol IV administered ? What you rate .
0.25 to 0.5g/kg
Repeat every 4 to 6 hrs to control ICP
Some say up to 2mg/kg
How does mannitol Improve cerebral blood flow
By decreasing the Hct
Signs and symptoms of Manitou toxicity are
Hyponatremia
high serum osmolality
Gap between calculated in measured serum osmolality over 10 mOsm/L
When given to patients with renal failure or at doses of 2 to 3 g/ kg
Can mannitol make edema of the injured brain tissue worse ?
Yes !
What other fluid is as efficacious as mannitol to manage ICP and at what rate is it infused?
Hypertonic Saline 15% at 0.42mL/kg
What does long period of hypertonic saline cause ?
Hypernatremia
Hyperosmolality
Hyperchloremic acidosis BC of renal HCO3 loss secondary to increased level Cl-
When do you D/C hypertonic saline ? When plasma sodium reaches
160 mEq/L
When CPP is maintained above the recommended 50 mmHg to 70 mmHg, hyperventilation is good practice ?
No , bc hyperventilation will cause brain ischemia . And even if CPP. 50 to 70 , the first 6 hrs will always have brain ischemia in the brain injured patient
When and how should hyperventilation be used ?
Short term ,
For patients with severe head injury and elevated ICP not responding to normal ventilation and diuretics
BUT
Not in the first 24 hours after injury
Hyperventilation can cause ALI ?
Yes
Everything you do can’t fix the ICP , what med can you give ?
Pentobarbital
Hypoglycemia can cause ( in the brain injured ) <40
Metabolic crisis
Hyperglycemia > 200
Detrimental effects through excitotoxicity ,
oxidative stress
and inflammation cytokines release
Patient from ICU getting surgery keep VS, PaO2 , and PaCO2 should be maintained at
The same level
Flacid areflexia , loss of patient rectal sphincter tone , paradoxic respiration, bradycardia in a hypovolemic patient suggest what diagnosis ?
Spinal cord injury
In cervical spine trauma , what S/S indicate cord injury ?
Ability to flex but not extend the elbow
Response to painful stimuli above but NOT below the clavicle
How do you rule out cervical spine injury without radiology according to the guidelines ?
Absence of neck pain
Absence of paresthesia
A negative physical examination :lack of tenderness with palpation
No tenderness during voluntary flexion and extension of the neck
In a neurologically intact , conscious patient
Complete spinal cord injury vs incomplete
Incomplete: intact sensory perception over the sacral distribution and voluntary contraction of the anus are present
Complete : those above not present and no possibility of recovery
Spinal Shock
Absolute flaccidity
Loss of reflexes
So spinal shock does not allow you to figure out if it;s complete vs incomplete spinal cord injury Initially , so don’t stop therapy . Spinal shock subsides in 3 to 5 days .
Do not leave a patient on a hard board for more than
1 hr
If patient has cervical spine fx how do you move pt ?
If it’s thoracic or lumbar , how do you move ?
C Spine : immobilization or MILS ( Manual Inline Stabilization)
Thoracic lumbar : Log rolling
Canadian C-Spine rule . High risk factors :
Age >/= 65
Dangerous mechanism
Parathesia in extremities
Canadian C-SPine low risk factors allowing beck range of Motion
Simple rear-end MVW Ability to sit or ambulate in ED No immediate- onset neck pain No midline C spine tenderness if no , do CT
Canadian C-spine , third question is
Able to rotate neck 45 degrees left and right ? If unable do Radiography.
Spinal shock is also called Neurogenic Shock which is
Hypotension ,
bradycardia (bc of loss of vasomotor tone and sympathetic innervation of the heart)
Spinal shock is usually present in what injury
Cervical or thoracic spine
But gets better in 3 to 5 days
Intubation of Neck injuries , Tracheal intubation may cause bradycardia bc of unopposed vagal stimulation , so what do you do prior to intubation
Pre oxygenate and give .4 to .6 mg of atropine
If Brady happens during intubation : give atropine , glyccopyrrolate , isoproterenol or cardiac pacing
Injuries at C5 or lower vs Injuries at C4 or above .
C5 and below = Normal Tidal Volume
C4 or above = permanent ventilatory assistance
Huge catecholamine release after acute trauma May be short but has lasting effects …
Pulmonary edema from pulmonary capillary damage and shifting of a large portion of blood volume into the pulmonary circulation + LV dysfunction .
3 to 5 days after injury , what will be developing in the patient if pt was given overzealous fluid ?
Acute pulmonary edema
Paradoxic respiration
Partial chest wall collapse during inspiration . = TV , increased risk Hypoventilation.
Worse in upright position. Bc the diaphragm cant keep its dome-shaped since the weight of the thoracic contents is not opposed by normal tone
Supine or upright is best for quadriplegic patient ?
Supine
But the comorbities like sleep apnea may not allow much of that
What to do to manage the hemodynamic of a Quadriplegic patient ?
Central Line
PAC ( swan )
LV dysfunction in 25% = hypotension , keep MAP >85
Increase the preload to a PCWP of 18 mmHg= avoid pulmonary edema
Hypotension desire adequate fluid, acidosis , or low mixed venous Po2 , give …
Inotropes such as dopamine
How soon after injury to we initiate DVT prophylaxis ?
Within 72 hours : LMWH or low dose UFH Rotating bed SCD Electrical stimulation
Neck Injury
.
If you don’t treat neck injury promptly what can ensue ?
Hemorrhage Asphyxia Mediastinitis Paralysis Stroke Death
FAST
Focused assessment sonography in Trauma
Signs of cervical artery injury ?
Absent or decreased upper extremity/distal carotid pulses
+ carotid bruit or thrill
Penetrating neck injury zones :
Zone 1 = narrow area above clavicles from cricoid to the sternal notch
Zone 2 = between the cricoid and the angle of the mandible ** most common
Zone 3 =between the angle of the mandible and the cranial base.
Hard vs Soft signs of neck injury . Compare and contrast .
Hard signs : urgent/emergent sx
Soft signs : just a CT will do
Hard signs : hypotensive/shock , active bleeding, expending hematoma , neurologic deficit , airway compromise , air bubbling through the wound, massive Sub Q emphysema and hemetemesis
What indicated esophageal injury ?
Dysphasia Odynophagia Hematemesis SubQ crepitus Prevertebral air on lateral cervical radiograph
Partial Spinal Cord injury produces what syndrome . Describe the syndrome
Brown Sequard : ipsilateral motor and contralateral sensory deficits
Amaurosis fugax
Can’t see out of 1 or both eyes due to low blood flow
Cervical blunt trauma , usually cause hematoma that may compress the cervical veins , displace the airway , laryngeal congestion . If artery is involved___,___,___ or ___can occur . And if carotid or vertebral artery : ____may occur.
Intimal tear, pseudo aneurysm, fistula, or thrombosis.
Cerebral Ischemia
Patients with cervical vascular injury may have :
Cervical bruit AMS Lateral icing neurologic deficits Hemiparesis TIA Amaurosis Fugax Horner syndrome
Chest Injury
.
Single rib fracture do not usually need ———can be treated instead with ———
No need for mechanical ventilation
Can treat with analgesics
What kind of chest wall fractures have severe underlying thoracic abdo cranial ,skeletal injury and interfere with breathing ?
Rib, Scapula, sternal fractures,
What must come to mind when a chest injury patient has SubQ emphysema, pulmonary contusion , and rib fractures .
Suspect pneumothorax
What are the s/s of tension pneumothorax?
It’s present in >50% pneumothorax Dyspnea Tachycardia Cyanosis Agitation Diaphoresis Neck vein distention Tracheal deviation Displacement of maximal cardiac impulse to the opposite side
Upright X-ray is best to detect pneumothorax, you can’t do upright or pt will die ( being dramatic ) what do you look for in the X-ray done supine to detect pneumothorax? Why ?
Deep sulcus sign .
Bc air accumulates in the anteromedial sulcus first , then lateral and caudal regions
Can you use an Ultrasound to diagnose a pneumothorax?
Yes , put probe longitudinally over the intercostal space . Use that in case of an emergency
Definitive diagnosis of pneumothorax is
CT chest
Once a pneumothorax is diagnosed in a trauma patient , small pneumo vs large pneumo , how do you treat ?
Doesn’t matter the size , they need a chest tube and that should be before intubation and before positive pressure ventilation.
Pneumothorax chest tube catheter size
26 to 32 French
Hemothorax catheter size
30 to 40 French catheter
If pt drains 1000ml or 200ml/hr for several hours , what intervention is indicated ?
Thoracotomy
Also : white lung on X-ray and continuous air leak from chest tube mean thoracotomy is needed
Classic findings of pericardial tamponade
Tachycardia, hypotension, distant heart sounds, distended neck veins , pulses paradoxus, pulsus alternans
But pt with hypovolemia may not show that …😒
TEE showing pericardial sac and presence of ventricular diastolic collapse has —-% reduction of cardiac output
20
How do you perform anesthesia for the patients with pericardial tamponade ?
Ketamine or etomidate since they produced relatively little myocardial depression.
Commotio Cordis is …
Agitated heart ,
Sudden V tach, cardiac arrest and oftentimes death in young people who receive a big to the chest during the 10 to 20 milliseconds of T wave upstroke .
It’s different from myocardial contusion because there is no structural heart damage
VSD can be detected on chest X-ray by seeing …
Increased pulmonary vascularity with a normal Heart size
In thoracic aorta injury , where along the thoracic aorta does blunt trauma usually occur ?
The isthmus : where where the free and fixed portions of the descending aorta ( just distal to the left subclavian .
2nd place is the roots of the thoracic aorta
Because the TEE can cause aortic rupture in the already injury thoracic aorta , what is the preferred imaging to diagnose the injuries there ?
CT :
Multi detectector CT ( accurate )
Use a TEE only when you had to go to surgery immediately without prior CT
3 grades of traumatic aortic injury :
Grade 1 : intramural clot , intimal flap and or mural clot
Grade 2 : subadventitia ( under the adventia) rupture , media is injured , the geometry of the aorta is changed and/or hemomediastinum
Grade 3 : TRANSECTION w/ huge blood extravasation , obstruction inside the lumen causing pseudo coarctation and ischemia
Vancouver classic action has a 4th grade : contrast extravasation
Clamp and sew technique during left thoracotomy to fix blunt aortic injury , what are the potential complications ?
Mortality, Morbidity especially paraplegia or renal dysfunction are also frequent with this technique
Why is lung isolation with a double-lumen Endobrinchial tube is necessary ?
To prevent contamination of the contralateral lung from blood entering the airway during dissection of the aorta in proximity to the lung .
What labs or parameters should be monitored during aortic clamp release ? What are the treatments ?
Systemic BP and Potassium
If potassium is high a rise in K+ should be treated with insulin and glucose
Endobascular aortic repair vs thoracotomy ?
Minimally invasive and less complication than thoracotomy. But an endoleak between graft and vascular wall is an early complication .
Why place radial artery on the right ?
Because subclavian artery is covered by stent
During aortography and stent placement what may have to be done
Stop ventilation and lower the mean BP at 60mmHg
Diaphragmatic injury
.
What happens when the diaphragm is injured ?
The contents of the abdomen migrate in the chest = lung compression , abnormal gas exchange, or heat compression»_space; dysrhythmias and/or hypotension.
What organ protects the right side of diaphragm ?
The liver , so more often damaged are on the left . That also means …right side damage are missed all the time
Looking at CXray , how do you know that the stomach is deplaced into the chest ?
NG tube is found ABOVE the diaphragm
Anesthesia induction for diaphragmatic injury , what precautions?
Avoid aspiration of gastric contents
Abdominal and pelvis injury
.
If there is no abdominal distention, does it mean you can rule out intra-abdominal bleeding ? Why ?
No because 1 L of blood and accumulate before a very small change in abdominal circumference is seen
+
The diaphragm can moved upward (cephalad) to make more room to allow more blood without having abdo distention
Can CT abdomen some mesenteric or bowel injury
No . Unless its a 64 slice CT
Fast is most needed for _______patient who may not be safely transported to _____
Hemodynamically unstable
CT
advantage and disadvantages of FAST ( focused assessment with sonography )
Inferior to CT , operator dependent, only moderate sensitivity , can’t diagnose injuries that do not have intraperitoneal fluid
Cannot determine severity of injuries
What it can do well…
Has good specificity Dx injury also with intraperitoneal fluids Less expensive Requires 1/3 of the time And no hazard radiation
What 4 distinct regions do we screes during FAST
Subxiphpid = detect pericardial bleed RUQ = detect hepatorenal punch LUQ = detect perisplenic blood Just above the pubic symphysis = detect blood In rectovesical pouch
Which patient groups cannot be managed non-operatively?
Patients with blunt trauma who have advanced age low admissions systolic pressure high injury severity score metabolic acidosis lower GCS requirement for multiple Transfusion
Why does Hypotension happen on opening the peritoneal cavity filled with blood
One. Because of hemorrhage
two. Because of sudden release of compression on the splanchnic vessels causing capacitance vasodilation
Patients with pelvic fracture should get what exam before installation of a urinary catheter? Why?
Urethrogram should be performed because pelvic fractures may also enjoy your bladder in the urethra
What are the key diagnostic measure for pelvic fracture on a CT scan
Pelvic ring disruption Arterial extravasation elevated blood pressure secondary to compression by hematoma volume is greater than 500 ML
also
hemodynamic instability after adequate fracture Stabilization is suggestive of pelvic Hemorrhage
Extremity injuries
.
What complications can occur, if fracture repair is delayed
Increased risk of DVT
pneumonia
sepsis
Pulmonary and cerebral complications of fat embolism
Open factors have additional risk of——-
One left and repaired for more than —— hours are likely to become——
Infection
> 6 hours»_space; septic
What are the signs and symptoms of the classic syndrome for vascular injuries( 5 Ps)
Pain pulselessness pallor paresthesias paresis
The definition of diagnosis for vascular trauma is
Arteriography
Some patients may receive duplex ultrasound study as a screening test
If patient is unconscious what are the signs of compartment syndrome
Swelling and tenseness of the extremity
What is a definite of diagnosis for compartment syndrome and when is surgery indicated
Measure compartment pressures using a transducer attached to a fluid field extension tube and a needle inserted into the various compartments of the extremity.
A pressure greater than 30 cm of H2O means immediate surgery
Burns
.
What are the three wrist factors determining the death rate in burn injury patients
Inhalation injury
Burn size greater than 40% of TBSA
Age greater than 60
How many TBSA % is involved in full thickness burns
> 10% TBSA
How many %nof TBSA is involved in partial thickness burns
> 25% in adults but > 20% in extremes of age
What are major burns
Burns in face and feet or perineum Inhalation, chemical and electrical burns
burns in patients with severe pre-existing medical disorders
What are the two phases of burn injury
Burn shock phase
and
hyper metabolic and hyperdynamic phase
Describe the burn shock phase
Continued plasma lost from intravascular space into burned and often intact tissues for about the 1st or 2nd day after injury
How long does the subsequent hyper metabolic and hyperdynamic phase of burn last
Months
What happens to patients with burns over 40% of TBSA
They consistently develop catabolism ,weight loss which may last up to 1 year
Hey severe burn is a systemic disease what gets stimulated and released ?
Release of inflammatory mediators such as interleukins and tissue necrosis factor locally (wound edema ) and into the circulation resulting in immune suppression hypermetabolism, protein catabolism,insulin resistance ,sepsis and MOF
What interventions may decrease the extent of catabolism
Prevention of sepsis
maintain normal body temperature and management of pain
What is the color of a partial thickness burn
Red,
blanches to touch
sensitive to painful stimuli and heat
Describe a superficial partial thickness burn
A.k.a. first-degree burn
Involves the epidermis and upper dermis and heal spontaneously
Describe a deep partial thickness burn
A.k.a. second-degree burn
Involves the deep dermis and require excision and grafting to ensure rapid return of function
Describe a full thickness burns
A.k.a. thirddegree burn
it does not Blanch even with deep pressure and
has no sensation
There is complete destruction of the dermis it requires would excision and grafting to prevent wound infection that may lead to local sepsis and systemic inflammation
What Structure does a fourth-degree burn involve
Muscle fascia and bone
It necessitates complete excision and leaves the patient with limited function
What tool imaging is used to judge the death of the burn
Laser Doppler imaging
The child Palmar surface excluding the digits represent what percent of TBSA?
0.5%
What is the more accurate is specific estimation of the TBSA
The lund-Browder table
Singed hair , facial burns, soot in the mouth or nose , swallowing difficulties , dysphonia or hoarseness with or without respiratory distress may indicate
Upper or lower airway injury
What physiological complications occur if there is lower airway burns
Decreased surfactant and mucociliary function ,
mucosal necrosis and ulceration , edema , tissue sloughing ,
and
secretions produce bronchial obstruction , air trapping and bronchopneumonia.
How long after does parenchymal lung injury take place ?
1 to 5 days and looks like ARDS
When does pneumonia or PE occur ?
They are late complications and occurs 5 days or more after burns
By how much does presence of lung injury in burns increase fluid requirements ?
By 30 to 50 %
Also increases mortality and rate from thermal injuries
If patient is moderately burned and has a patient airway , what is the top priority ?
Highest possible O2 concentration via face mask
In what occasions is immediate tracheal intubation indicated ?
Massive burns Stridor Respiratory distress Hypoxemia ‘hypercarbia Loss of consciousness AMS
Can kids sustain an awake fiber optic ?
No .
Use inhaled O2 and Sevo then use FOB or regular DL which ever is more appropriate
Since we consider those traumatic burn patients a full stomach what medication can be given to facilitate emptying of the stomach without causing agitation ? Don’t say reglan please …
Methylnaltrexone
Bc it antagonizes the peripheral but not the central effects of morphine = antagonizes gastric effect of morphine without causing agitation
What Significant risk does surgical airway carry
Pulmonary sepsis in late upper airway sequelae
Only ones who should get those are those at risk to develop complications such as dysphasia dysphonia after prolonged tracheal intubation
Why do we use low levels of peep immediately after securing the airway
To prevent pulmonary eDema that may happen secondary to loss of laryngeal auto peep in patients with significant area obstruction before intubation
Tracheal intubation should be based on clear criteria. What are those criteria
Large full thickness burns
inability to protect the airway
or
signs of airway obstruction
What does the treatment for smoke inhalation in Burns involve
Ventilatory management intensive care treatment of carbon monoxide and cyanide Toxicity
Why is there hypoxemia in the first 36 hours after airway injury despite Tracheal intubation ,Ventilation ,peep , bronchodilators, etc..
Because of acute pulmonary edema
Why does hypoxemia Occur from these 2 to 5 in airway injury patient displayed trickle into Bashan Ventilation peep Bronchodilators
Atelectasis bronchopneumonia airway edema resulting from Mucosal necrosis and sloughing viscous secretions distal airway obstruction
How does CO produce tissue hypoxia
By imparing O2 unloading
CO impairs unloading of O2 , what else it causes ?
1 mitochondrial function interference
Interferes with Uncoupling oxidative phosphorylation
Reduces ATP
Causes metabolic acidosis
Co is a myocardial toxin bc of its effects on the mitochondrial function . True or false
True . So true that even after hyperbaric O2 and resuscitation, patient won’t come back
Normal oxygen saturation reading on pulse ox does not exclude the possibility of CO Toxicity but a _——measured by coax immature should raise a suspicion
A low arterial O2 saturation
Crab on oxide toxicity alone without line injury but with a decreased PaO2 , Will you see tachypnea or will it be absent
Tachypnea will be absent
Classic cherry red color of the blood is absent in most patient but it occurs only at carboxyhemoglobin concentration above
40%
What are the carotid bodies are sensitive to?
Sensitive to arterial P02 and not to the O2 content
What are the advantages of 100% FiO2 in carbon monoxide poisoning
Improves oxygenation by promoting elimination of carbon monoxide by decreasing the blood half-life of carboxyhemoglobin from 4 hours at room air to about 60 to 90 minutes when on 100% O2
and
the half-life is reduced to 20 to 30 minutes at 3 atm in a hyperbaric chamber
If you have unexplained metabolic acidosis in the absence of cyanosis what diagnosis do you suspect
Cyanide toxicity
The reason why plasma Lactate levels can be elevated in severe burns
Hypovolemia
carbon monoxide Toxicity
or cyanide Toxicity
Patient has no major burn half after smoke inhalation but has lactic acidosis what are you suspecting
No toxicity
The definition of diagnoses that can be made for cyanide Toxicity
That cyanide level which is toxic above 0.2 mg/L and lethal at levels be on 1 mg/L
Is the half-life of cyanide
One hour
> 155 TBSA burn, what intervention is essential?
Fluid resuscitation in the early care
For small burns how do you manage Fluid replacement
Oral or IV at 150% of calculated maintenance rate
1 1/2 times the maintenance rate pretty much
What can occur if resuscitation volume exceeds 300 ML per kilogram for 24 hours
Abdominal compartment syndrome with impedance of Venous return
What is fluid creep
Administration of fluid in excess of the amount recommended by the park and formula in modern burn management
Is the addition of glucose necessary when using resuscitation formula as it is
Only in children especially weighing less than 20 kg
Silver sulfadiazine without free water , what can happen
Hypernatremia along with CNS effects including intracranial bleed
What does aqueous 5% nitrate solution cause
Hyponatremia , cerebral edema
What is the rule of 10
The total body surface area is multiplied by 10 to determine the estimated hourly fluid rate then for every 10 kg above Eddie kilo of body weight 100 ML per hour is added to the calculated rate
What stroke pressure variation and what delta down suggest Hypovolemia in responsiveness to fluid
SPV over 5 mmHg
And Delta down over 2 mmHg
Suggest hypovolemia and responsiveness to fluid
What 2 levels are considered acceptable markers of organ hypoperfusion ?
Base deficit and Blood lactate level
Another one is the
Arterial to end tidal CO2 difference
What arterial to ETCO2 difference to measure organ hypoperfusion predict mortality
> 10 mmHg after resuscitation
What variables are included in the O2 delivery index ?( DO2I )
Hgb concentration
Arterial oxygen saturation
Cardiac output
Normal is 500ml/ min/m2
What O2 consumption index value indicated a flow dependent phase of O2 utilization ?
Less than 170/mL/min/m2
What O2 extraction ration value suggest absence of dysoxia ?
When lO2 extraction ratio is less than 0.25 to 0.3 ( 25 to 30% )
CVP > 10, MAP > 65 and Hgb > 10 g/dL mean…
Adequate organ perfusion
What 5 major clinical conditions should anesthetic be tailored to ?
1Airway compromise 2Hypovolemia 3Head and eye injuries 4Cardiac Injury 5 Burns
If patient have hypoxia and hypercarbia and you give them succs, you might as well Hand your license over because the patient is going to ….
Brady , dysrhythmias then die !!! To the morgue
For a patient in shock , how do you dose Propofol?
Reduce the dose by 10 to 20%
How do you adjust the etomidate dose in shock ?
No evidence of required adjustment of dose of Etomidate is shock . But … the author reduces the dose by 25 to 50 % when hypovolemia is present
How do you calculate dose for fentanyl or remifentanil when given on hypovolemia
Give 1/2 dose that of healthy ppl
What happens when you give opioids to hypovolemic trauma patients ?
Hypotension by inhibition of central sympathetic activity , not bu cardiovascular nor bardo receptor depressant effects .
And these trauma depends on that sympathetic activity to compensate and maintain there low BP .
How can you prevent recall in traumatic patient in whom you cannot use anesthetics ?
0.6 mg scopolamine and midazolam ( if patient can tolerate that ) before airway management may decrease likelihood of recall
What BIS level may prevent recall in Trauma patients ?
BIS lower than 60
By how much does hemorrhagic shock decrease MAC
By 25%
Bc the trauma/shock make them release natural endorphins
ISO can impair CO, organ blood flow and eventually cardiovascular depression despite causing little impairment of tachycardia . So can DES , so can SEVO. But at least they have _____solubility in blood and can come off quickly . What MAC should be used in these gases then ?
Low solubility
< 1 MAC
If patient has severe head injury where Autoregulation and CO2 responsiveness are impaired can ISO with hyperventilating at MAC less than 1 help decreased ICO and CBF ?
Not even if less than 1 MAC or with hyperventilation it will not , Instead it will cause increase ICP and CBF . So wait until the skull is opened before using the ISO . Start with opioid, midazolam or etomidate
The anesthetic agents selected for management of brain injury should produce 3 important effects :
1) least increased in ICP
2) Least decrease in MAP
3) greatest reduction in CMRO2
What is most important factor causing cerebral ischemia in head injury patients ?
Increased ICP from intracranial hematoma
Since anesthetics cause hypotension which goal should you maintain to prevent cerebral ischemia that results from hypotension ?
Avoid hypotension : MAP<60 to 70 mmHg or SBP <90 to 100 mmHg .
CRMO2 is reduced by all IV anesthetics. TRue or false
Yes , even ketamine
All IV anesthetics cause cardiologist depression which in turn reduces CPP . True or false ?
False , Ketamine is the only one that does not depress the heart and therefore does not reduce CPP
You can always give opioids : fentanyl 2 to 3 mcg/kg for example which decreased the amount of these IV anesthetics needed
Why would etomidate or propofol cause increase in ICP ? ( not a trick question )
Etomidate > propofol cause myoclonus which can raise ICP or IOP which can be prevented by carefully timin muscle relaxant.
All inhalation agents can decrease CBF and CBV and thus ICP . True or False
FALSE !
They all increase CBF»_space;CBV» ICP
All inhalation agents decrease CRMO2 while increasing CBF . True or False ?
While …
IV anesthetics decrease both CBF and CMRO2 .true or false ?
- True IA = decreased CRMO2 but increase CBF
2. True IV Anesthetics = decreased CMRO2+ CBF
Which gas has the least uncoupling ( low CRMO2 and high CBF ) , or least vasodilatory effect and thus most widely used ?
Isoflurane , but DES and SEVO have comparable effect on cerebral circulation .
But ISO < 1 Mac + hyperventilation in patient with cerebral tumors or mild edema = no raise in ICP.
When does ISO have the potential to increase CBF and ICO even when given at less than 1 MAC with hyperventilation?
When there is severe head injury which means cerebral auto-regulation and CO2 responsiveness are impaired .
It’s prudent not to use ISO in these patients , at least not until the skull is open . Best to use : Propofol, Midazolam or etomidate instead .
N2O = increase CBF , CBV , ICP . You can fix that issue by by giving
Adequate Doses of barbiturates or hyperventilation .
How can you give N2O so that it is not deleterious in patient with MINIMAL ICP elevation ?
When you give it AFTER a bolus or DURING infusion of IV anesthetics.
Cardiac Injury
.
If pt has cardiac tamponade, what 2 things MUSt be maintained .
Preload
And
Myocardial contractility
If you don’t the RV inflow obstruction will be worse !
When do you administer anesthetics when caring for patient with cardiac tamponade and why ?
After evacuation of the pericardial blood under local. Because all anesthetics can depress myocardial contractility and cause vasodilation .
If general anesthesia is required , you only induce after patient is prepped and draped
What vent mode goal do you have for general anesthesia with patient with cardiac tamponade ?
Bc both anesthesia and controlled ventilation with PEEP = decreased CO , avoid deep anesthesia and high airway pressures before evacuation of the hemopercardium .
If its chronic or chronic : use ketamine since it increases CI better than other anesthetics .
Ketamine is the agent of choice : give small doses after IV fluid blouses/infusions
Smallest possible doses of anesthetics ***
What is your anesthetic goal if patient suffered blunt myocardial injury ?
Maintain contractility
Lower pulmonary vascular
resistance that result from concomitant
pulmonary contusion , etc..
only give anesthesia after restoring intravascular volume
Use inotropes preferably amrinone or milrinone
Since the have advantage of pulmonary vasodilation
Best technique to consider for maintenance
Is IV anesthetics +opioids to avoid myocardial depression produced by inhalation agents
Anesthesia for Burns .
.
what are the characteristics of hyper metabolic state :
Tachycardia , Tachypnea , catecholamine surge , Increased O2 consumption, augmented catabolism
Why is early extensive and repeated escharotomy important in burn patients ?
It attenuates :
Hyper metabolic response
Insulin resistance
Decreases fluid loss and improve survival
What regional block would you do for analgesia of donor site .
Tumescent infiltration in the form of continuous infusion of LA
Harvesting of skin is usually taken from the lateral thigh , what block would you do ?
Lateral cutaneous nerve , or a TAP block
If its anterior thigh harvest . What block ?
Fascia iliaca
Burnet Torso , what block
Paravertebral block
For How long after burn injury succinylcholine should be avoided
At least 1 year because of risk of lethal increase in potassium level when the burn size is greater than 10% TBSA
Non depolarization and depolarising muscle relaxant response doe not change in the the 1st _____hours after burn injury
24 hours
How does succ in burn cause hyperkalemia ?
Upregulation of of acetylcholine receptor which covers the entire muscle membrane
Extra expression of 2 new type of acetylcholine receptors + new nicotinic neural alpha-7 acetylcholine receptors
And the new nicotinic a-7 receptor can be depolarized by both succinylcholine and choline = hyperkalemia galore !
All nondepolarizing muscle relaxants including cisatricurium in patient with burn > ___% of TBSA . That starts at _____week and peaks at ____ weeks after injury
> 30 % TBSA
Starts at week 1
Peaks at week 5 to 6 weeks after injury
What is the onset delay of rocuronium used as rapid sequence induction or as treatment of laryngospasm when succ is contraindicated ?
Delay onset time by 50 seconds when 0.9mg/kg dose is used .
The 50 seconds is a 30% delay compare to patients without burn …
So increasing the dose to 1.2mg/kg decrease the delay by 30 seconds , but onset is still 25 to 30 seconds longer than in patient without burn .
What are the deleterious effects of crystalloid in Trauma/Massive hemorrhage patients ?That is the physiological mechanism of it ?
Crystalloids have effect on the glycocalyx and the syndicate-1 ( A network of soluble plasma components on the endothelium stabilizing membrane integrity)
Massive hemorrhage alters the integrity of the endothelial glycocalyx; damage to the cell plasma is thought to be the primary mechanism of shock in these patients .
Although plasma is able to reconstitute syndican-1 , the main component of glycocalyx , crystalloids cause further destruction , worsening of the endothelial dysfunction .
How can overinfusing fluids before the control of the hemorrhage may lead to further bleeding ?
By increasing arterial and venous pressures , Displacing a hemostatic plug Diluting clotting factors and platelets Reducing body temperature Decreasing blood viscosity
What is the dose of TXA ?
Given in first 3 hrs of injury
Then 1 g in 10 minute bolus followed by 1 g over 8 hours .
Or
Usual of TXA : is 10 to 15 mg/kg followed but 1 to 5 mg/kg/hr .
If given over 3 hrs , TXA can cause what ?
Increase risk bleeding related of mortality
Other benefits of TXA :
It helps protect the mucosa lining of the instestine and helps protect against over inflammation
What is TXA ?
Competitive inhibitor of Plasmin and Plasminogen
What is the dose for Aminoproceic acid ?
100 to 150 mg/kg followed by 15mg/kg/hr
Is the leading cause of mortality after blood transfusion
TRALI
Pulmonary eDema with subsequent hypoxia happening six hours after blood transfusion
TRALI
Coagulopathy after trauma . 2 main categories :
ATc and RAc
Each 1C drop in temp causes
Platelet dysfunction decrease by 10% plus enhancing fibrinolytic
Burn hyper metabolic phase
Tachycardia Tachypnea Catecholamine Increase o2 consumption Augmented catabolism
Why early extensive eschorotomy 2nd day to 2nd week help stop hyper metabolic
Decrease insulin resistance
Decrease fluid requirement
Improval survival
N2O effects on CBF CBV
Up the CBF CBV ICP when used with inhaled anesthetics if PaCO2 is normal or increased
