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Traumatic Brain Injury
- Careful search for other significant injuries should be made
- 100% O2
- Cardiac monitoring
- 2 IV lines
- ET intubation is a top priority
- Restoration of adequate blood pressure is vital
- Head CT and immediate neurosurgery consult
- Seizure prophylaxis
TBI and blood pressure
- If hypotensive, resuscitate with IV crystalloid fluid to MAP of 90 mmHg;
- If hypertensive, 25-30% reduction in MAP should be achieved
TBI and Increased ICP
- Elevate the head of the bed 15-30 degrees
- volume resuscitation
- arterial oxygenation
- If signs of transtentorial herniation or progressive neurological deterioration → IV mannitol bolus
- Hyperventilation is a last resort to lower ICP
- Emergency trephination (burr holes) When all other methods to control ICP have failed and there is impending brain herniation.
TBI and Seizures
- Prophylactic anticonvulsants for posttraumatic seizures
- Benzodiazepines: lorazepam and fosphenytoin) should be administered with consult of neurosurgeon
TBI and Skull Fractures or Penetrating Injuries
For patients with basilar skull fracture or penetrating injuries should be admitted for neurosurgery consult and given prophylactic broad-spectrum antibiotics (ceftriaxone)
TBI and Traumatic Subarachnoid Hemorrhage
Administer nimodipine (reduces death/severe disability)
Glasgow Coma Scale: Motor:
- 6 – Follows commands
- 5 - Localizes pain
- 4 - Withdraws from pain
- 3 - Decorticate posturing
- 2 - Decerebrate Posturing
- 1 - No response
Glasgow Coma Scale: Eye Opening
- 4 – Opens spontaneously
- 3- Opens to voice
- 2- Opens to pain
- 1- Does not open
Glasgow Coma Scale: Verbal
- 5 – Alert and Oriented
- 4 - Disoriented
- 3 - Speaking nonsense
- 2 - Moans
- 1 - No verbal response
GCS Prediction of Outcome
- At 48 hours, a GCS = 3-4/15
- 53/54 died in coma/vegetative state
- 1/54 awakened with good recovery
- Wound Care
- Underlying Skull fracture
- Debridement v undermining
- Wound repair – sutures, staples, hair (?)
- Can be very complicated
- Focal or Diffuse
- Frequently combinations of both
- Hematoma is located outside of the dura
- Frequently seen in the temporal or temporoparietal areas
- Usually the result of arterial injury but can also occur from venous injury
- Usually result from direct mechanical force resulting in a skull fracture
- More common in younger patients, rare in the elderly and in those under 2 years because the dura is closely attached in those populations
- Classic lucid interval seen only 30% of the time
- Brain parenchyma frequently compressed to the midline
- Arterial blood
- May rapidly expand
- Ventricles shifted across midline
- More common than epidural hematomas
- Usually occur from the tearing of small cerebral cortex surface vessels
- Cover the entire surface of a hemisphere
- More severe underlying brain injury than that of an epidural
- Seen with acceleration deceleration injuries (MVA, fall)
- More common in the elderly
- Blood clot forms between the dura mater and the brain with extensive parenchymal injury at the site of the clot
- On CT - hyperdense lesion that hugs the convexity of the brain with a crescent shape
- Extends beyond the suture lines
Initial Management of Hematomas
- Primary survey and resuscitation
- Secondary survey and history
- Airway and Breathing
- Maintain C spine immobilization and secure the airway
- Treat hypotension
- Acute short term hyperventilation
- Goal is to have a pCO2 in the range of 30 to 35 mm Hg
- Reduce ICP by cerebral vasoconstriction
- Can decrease the ICP by 25% in most patients
- Consider osmotic agents (mannitol 0.25 to 1 g/kg IV) or hypertonic saline
- Results in minutes, peak effects at 60 minutes, duration over 6 to 8 hours
- Seizure prophylaxis
- Post traumatic seizures can occur in up to 12% of blunt head trauma and 50% of penetrating head trauma patients
- Goal is to prevent additional insult to the brain
- Noncontrast CT of the Head
Increased chances of an intracranial hematoma
Skull Fracture Clinical Findings
- Periorbital ecchymosis (raccoon eyes)
- Retroauricular ecchymosis (Battle’s sign)
- CSF leakage from the nose or ear
- VII or VIII nerve injury (facial paralysis or hearing loss)
Closed skull fracture
The bone is broken, but the skin is intact
Open skull fracture
The bone exits and is visible through the skin, or a deep wound exposes the bone through the skin.
Depressed skull fracture
- Usually from blunt force trauma
- 11% of severe head injuries
- Comminuted fractures in which broken bones are displaced inward.
- Depressed skull fractures carry a high risk of increased pressure on the brain, crushing the delicate tissue.
- Compound depressed skull fractures occur when there is a laceration over the fracture, resulting in the internal cranial cavity being in contact with the outside environment increasing the risk of contamination and infection. Complex depressed fractures are those in which the dura mater is torn.
- Depressed skull fractures may require surgery to lift the bones off the brain if they are placing pressure on it.
Basilar skull fracture
- Basilar skull fractures, breaks in bones at the base of the skull, require more force to cause than cranial vault fractures.
- 4% of severe head injury patients.
Basilar Skull Fx Signs
- blood in the sinuses;
- CSF leaking from the nose (rhinorrhea) or ears (otorrhea);
- periorbital ecchymosis or "raccoon eyes"
- and retroauricular ecchymosis or "Battle's sign"
Skull Fx Management
- Operative repair: Dural evaluation, Intracranial pressure management, Wire repair
- Simple Skull Fracture, Observation, Neurovascular intact
Diagnosis and Management of Intracranial Injuries
- Cervical spine radiographs should be obtained
- All patients with a GCS of 14 of less should undergo a emergent noncontrast head CT after stabilization
- Patients with GCS of 15 should undergo CT if they experienced a LOC, nausea/vomiting, posttraumatic seizure, amnesia, continued diffuse headache, history of coagulopathy, or intoxication without significant improvement after a period of observation
- Other indication for CT: neurologic deterioration, presence of distracting injuries, persistent focal neurologic or mental status deficit, and skull fractures in the vicinity of the middle meningeal artery or major venous sinuses
- Routine skull radiographs are not indicated: implicated for penetrating wounds of the skull, suspected depressed skull fracture, and presence of foreign bodies
- Lab work: type and crossmatching, CBC, electrolytes, glucose, arterial blood gas, directed toxicology screens, PTT, PT, platelets, and dissemination intravascular coagulation panel.
- Trauma-induced alteration in mental status that may or may not involve a loss of consciousness
- Mild traumatic brain injury that is caused by an impact or jolt to the head or as an immediate and transient impairment of neural function due to mechanical force
- Frequently sports related
- Usual complaints are headache, confusion, amnesia
- Neuro exam is nonfocal
- Shearing or stretching of white matter fibers
- Temporary neuronal dysfunction
- Transient alterations in neurotransmitter levels
- Temporary changes in cerebral blood flow and oxygen use
Contusions and Intracerebral Hematomas
- Represent 20 – 30 % of severe brain injuries
- Contusions can evolve over time to become a hematoma requiring intervention
- Focal hemorrhage within the brain
American Academy of Neurology Grading For Concussion And Recommendations For Return To Athletic Activity
- Grade I: No loss of consciousness, Transient confusion. Concussion symptoms or mental status changes resolving in less than 15 minutes
- Grade II: No loss of consciousness, Transient confusion. Concussion symptoms or mental status changes lasting more than 15 minutes
- Grade III: Loss of consciousness of any duration
AAN Return to play parameters
- Grade I: Remove from event. Examine on sideline and at 5 minute intervals for mental status changes or post concussive changes at rest and with exertion. May return if better in 15 minutes. A second Grade I will eliminate the player from competition with a return in 1 week if asymptomatic
- Grade II: Remove from event with no return. On site evaluation with repeat evaluation the next day. If symptom free at rest and with exertion for 1 week, neuro exam for clearance. If still with symptoms for more than a week, do CT or MRI. Need to be symptom free at rest and with exertion for 2 weeks before return to play. If the CT or MRI is abnormal, the season is over
- Grade III: If not stable transport to nearest facility. Complete neuro exam. Consider admission if abnormalities persist. After a brief Grade III, no play until asymptomatic for one week. After a prolonged Grade III, withhold from play for 2 weeks. After a second Grade III, withhold from play for at least one month. CT or MRI if symptoms persist longer than one week. Any CT abnormality will end the season
Post Concussive Syndrome
- Seen in many patients after mild traumatic brain injury
- Key elements are somatic, cognitive and affective symptoms
- SOMATIC symptoms: Headache, sleep disturbance, dizziness/vertigo, nausea, fatigue, hypersensitivity to light/sound
- COGNITIVE Symptoms: Attention/concentration difficulty, Memory problems
- AFFECTIVE Symptoms: Irritability, Anxiety, Depression, Emotional lability
Discharge Instructions for The Patient With Minor Head Trauma
- LOW RISK: No loss of consciousness. No posttraumatic amnesia. No moderate or high risk factors
- MODERATE or HIGH RISK: Loss of consciousness. Posttraumatic amnesia. Alteration of level of consciousness. Severe or increasing headache. Persistent nausea or vomiting. Intoxication. Posttraumatic seizures. Age less than 2 years. Use of warfarin. History of hemophilia or marrow suppression.
- Total intracranial volume is fixed
- The intracranial volume is equal to the sum of its components
- Fixed volume that cannot change – any change must be compensated for
- Volume (intracranial) = V (brain) + V (CSF) + V (blood)
- In the adult, the intracranial volume is around 1500 ml, with the brain representing 85-90%, cerebral blood volume 10%, CSF the remainder
Cerebral Perfusion Pressure (CPP)
- Net pressure of blood delivery to the brain
- CPP = MAP – ICP
- MAP = mean arterial pressure
- ICP = intracranial pressure
Cerebral Blood Flow constant in range of 50 – 150 mm Hg because of autoregulation
- When MAP is less than 50 mm Hg – ischemia can occur from insufficient blood flow
- When the MAP is greater than 150 mm Hg – excess CBF can increase the ICP
Hyperventilation in Head Injuries
- Hyperventilation (over breathing) will reduce Carbon dioxide – raising pH (alkalosis) – initiation vasoconstriction
- Low concentration of carbon dioxide (hypocapnia) - reduces respiratory drive, hyperventilation with lower carbon dioxide levels
- So, Hyperventilation (deep or rapid breathing) → hypocapnia → reduces PaCO2 below 40 mmHg → respiratory alkalosis → vasoconstriction
- Controversial secondary to possible tissue ischemia
- Trauma to the vertebral column must always be considered in patients with multiple injuries
- Neurologic deficits may or may not be present
- 5% of patients with a head injury will have an associated spinal injury
- 25% of patients with a spinal injury will have a head injury
- Cervical region: 55%
- Thoracic Region: 15%
- Thoracolumbar junction: 15%
- Lumbosacral: 15%
- As many as 10% of patients with a C spine fracture have a second noncontiguous vertebral column fracture
Immediate Management of Patients With Suspected Spinal Cord Injury
- Spinal immobilization with a cervical collar and a longboard
- As long as a patient’s spine is protected, evaluation of the spine and exclusion of spine injury may be safely deferred, especially in the presence of systemic instability
- IV Fluids – persistent hypotension (along with bradycardia) should raise concern for neurogenic shock
- Consider Vasopressors
- Consider high dose Methylprednisolone if a nonpenetrating injury within the first 8 hours
Immobilization of Patients with Suspected/Potential Spinal Cord Injury
- Airway compromise
- Increased intracranial pressure
- Cutaneous pressure ulcers
- Iatrogenic pain
- Increased difficulty of patient handling
- Combativeness in intoxicated patients
- Clearance Criteria: No Altered mental status, Intoxication, Neurologic deficits, Suspected extremity fracture, Spine pain
Methods to Minimize Neurologic Injury and Treat Complications After Spinal Cord Injury
- Airway assessment and management with inline cervical immobilization
- Pt should be placed on high-flow oxygen and have 2 large bore IV lines established
- Rapid assessment of other life-threatening injuries (pt should be log-rolled)
- Neurosurgical or orthopedic consult should be obtained as soon as an injury is identified
- Spinal shock should be treated with oxygen, IV fluids, and if necessary vasopressors (norepinephrine or dopamine)
- For blunt mechanism of SCI, methylprednisolone is recognized as a treatment
- Admit to hospital
- Impairment of the descending sympathetic pathways in the spinal cord
- Loss of vasomotor tone, loss of sympathetic innervation to the heart
- Vasodilatation of visceral and lower extremity blood vessels, leading to hypotension
- May become bradycardic or fail to become tachycardic in response to hypovolemia
- Need vasopressors with moderate fluid replacement
- Flaccidity and loss of reflexes after a spinal cord injury
- Variable state
Documentation Plan for Neurologic Exam Findings
- General Appearance
- Mental Status
- Gait /Coordination
- Cranial Nerve Exam
- Motor System Exam
- Sensory Testing
- Light Touch: Posterior column
- Pinprick: Spinothalamic tract
- Temperature: Spinothalamic tract
- Joint position sense: Posterior column
- Vibration: Posterior column
- Graphesthesia: Cortico-sensory function
- Two-point discrimination: Posterior column, Cortico-sensory function
- Reflex Testing
- Cerebral Vascular Exam
- Gastrointestinal exam
- Inspection: Abnormal postures, bodily asymmetries, face
- Mental Status
- Visual spatial skills: Clock drawing, figure copying
- Judgment: Includes insight, thought content. Is patient psychotic?
- Mood: Is patient depressed, manic, anxious
- Memory: Short and/or long term
- Language: Naming, repetition, comprehension
- CN II – XII
- Muscle strength: Upper and lower extremities bilaterally
- Rapid alternating movements
- Romberg / Pronator Test
- Gait: Include heel-toe walking
- Superficial pain, touch and vibration: Check the distal point in each extremity
- Deep tendon reflexes: Upper and lower extremities bilaterally
Documentation Plan for General physical exam
- Head: Trauma, dysmorphism, bruits, hair distribution, scalp disorders, external cranial lesions
- Neck: Tone, bruits, thyromegaly
- Cardiovascular: Heart rate, rhythm, and murmurs; peripheral pulses, jugular venous distention
- Pulmonary: Breathing pattern, cyanosis
- Abdomen: Hepatosplenomegaly
- Musculoskeletal: Skeletal abnormalities, peripheral edema, straight-leg raise
- Skin: Neurocutaneous and hepatic stigma
Documentation Plan for Level of consciousness
- Can your patient talk to you?
- Level of alertness
- Appropriateness of responses
- Orientation to date, time, and place
- Drowsy, confused, stuporous, comatose
- Monitor any changes in the level of consciousness and associated physical signs throughout the entire exam
- Glasgow Coma Scale (total=15 points)
- Nerve: Polyradiculopathy
- Neuromuscular Junction: Myasthenia gravis
- Muscle: Myopathy
Weakness in all four limbs
- UMN: Cervical or Brainstem
- LMN: Polyradiculopathy, Peripheral Neuropathy
Unilateral limb weakness
- Hemisection of cervical cord
- Cerebral lesion
- UMN: Lesion above highest involved level
- LMN: Single nerve = Mononeuropathy
- Single nerve root = Radiculopathy
Weakness in both legs
- UMN: Spinal cord lesion
- LMN: Cauda equina lesion
- Increased DTRs: Indicative of UMN lesion
- Decreased DTRs: Indicative of LMN lesion
- Increased DTRs or clonus: UMN lesion above the root at that level
- Absent reflexes: (Generalized) Consider peripheral neuropathy. (Isolated) Either a peripheral nerve or more commonly, a root lesion.
- Babinski: Extension of the great toe. If present indicates UMN lesion
- Glabellar: Inability to stop blinking in response to tapping on the forehead, nasal bridge, or maxilla. Consistent with Parkinson disease or frontal lobe damage
- Snout: Scratching the upper lip induces a puckering movement. If present can indicates frontal lobe dysfunction
- Palmomental: Vigorous scratching of the thenar eminence causes ipsilateral contraction of the muscles of the chin. If present usually indicates frontal lobe damage to the opposite side
Complete spinal cord lesion
- It causes complete and permanent loss of ability to send sensory and motor nerve impulses and, therefore, complete and usually permanent loss of function below the level of the injury, paraplegia or tetraplegia.
- The completeness of many injuries isn't fully known until 6-8 weeks post injury.
- The spinal cord normally goes into what is called spinal shock after it has been damaged.
- The swelling and fluid masses showing on any resultant X-ray, MRI or CT scans, may well mask the true extent of the underlying injury.
- Hemisection of the cord
- From penetrating injuries
- Ipsilateral motor loss with loss of vibration, pressure, all proprioception as well as contralateral loss of pinprick, pain, temperature sensations
Central cord syndrome
- Disproportionately greater loss of motor power in the upper extremities than in the lower extremities
- Varying degrees of sensory loss
- Ligamentum flavum buckles into the spinal cord, causing a concussion or contusion to the central regions of the cord
- Forced hyperextension injury (forward fall with facial impact)
- Most common of the incomplete spinal cord lesions
- Better prognosis than other incomplete injuries
Anterior cord syndrome
- Paraplegia and dissociated sensory loss with loss of pain and temperature sensation
- Posterior column (position, vibration, deep pressure) preserved
- Due to infarction of the cord in the region supplied by the anterior spinal artery
- Also the result of disc herniation, bony fragment protrusion, cord contusion from cervical hyperflexion
- Poorest prognosis of the incomplete injuries
Clinical Indications for Thoracic or Lumbar Imaging
- High force mechanism
- GCS < 15
- Pain or tenderness along spine
- Local signs of injury
- Neurologic deficit
- Previously identified spinal injury
- Diagnostic option, especially in high energy blunt trauma
- Better sensitivity than plain films
- Disadvantage of higher doses of radiation
- Offers the best evaluation of the biomechanical integrity of the spine’s supporting ligaments, disc interspace, and vertebral artery patency
- Provides the only evaluation of the spinal cord itself (best when considering ligamentous injury and SCIWORA)
C Spine Plain Films
- Normal 3 view
- AP: Check alignment, Intervertebral spacing, Gross fractures
- Lateral: (4 lines) anterior longitudinal ligament line, posterior longitudinal ligament line, spinolaminar line, spinous processes line.
- Additional features: Soft tissues. False (+) widening on expiratory films in children <2 years
- Odontoid: (aka “Open Mouth odontoid”) Dens (odontoid) fractures. C1 (atlas) fractures. Ex: Jefferson aka blowout. Distance from dens to ring of c1 should be symmetrical
- Lateral film adequacy: C1-T1, Otherwise cannot rule out sublux of C7 on T1
- Odontoid film adequacy: Entire dens, lateral borders of C1/C2 should align
- No posterior midline cervical spine tenderness
- No evidence of intoxication
- Normal level of alertness
- No focal neurologic deficit
- No painful distracting injuries
- Compression fx
- Hyperflexion injuries
Spinal Cord Injury
- C3 vertebrae and above: Typically lose diaphragm function and require a ventilator to breathe.
- C4 : May have some use of biceps and shoulders, but weaker
- C5: May retain the use of shoulders and biceps, but not of the wrists or hands.
- C6: Generally retain some wrist control, but no hand function.
- C7 and T1: Can usually straighten their arms but still may have dexterity problems with the hand and fingers. C7 is generally the level for functional independence.
- Complete tear of anterior longitudinal ligament and intervertebral disk with disruption of posterior ligamentous complex
- Aka traumatic spondylolisthesis of the axis
- Located in pedicles of C2, with C@ displacing anteriorly on C3
- Anterior longitudinal ligament avulses inferior portion of anterior vertebral body
- Unstable in extension
- Spinal cord injury without evidence of radiographic abnormality
- Acute traumatic myelopathy despite normal imaging studies
- More frequent in the pediatric population
- Transverse atlantal ligament injury
Acute bacterial otitis externa
- Remove debris
- Place Oto-Wick if canal is too narrow
- Topical antibiotic drops
Acute fungal otitis externa
- Fungal ear infections are usually very itchy
- They can look like bacterial infections
- Suspect fungal infections if antibiotic drops fail to resolve the problem
- Culture if fungus is suspected
- Treat with Acetic acid drops (Vosol)
Malignant otitis externa
- aka Temporal bone osteomyelitis
- Chronic otorrhea in an immunocompromised patient, especially uncontrolled DM
- Pseudomonas aeruginosa
- Needs non-contrasted CT temporal bone and/or bone scan
- ENT consult and IV abx
Acute otitis media
- Symptoms: Ear Pain, Hearing Loss, Tinnitus, Ear Fullness
- Treated with oral antibiotics
- Complication of OM and is defined as spread of infection to the mastoid air cells
- Physical exam findings include fever, otalgia, post auricular erythema, swelling, and tenderness with protrusion of the auricle.
- CT scan can help delineate the amount of bone involvement
- Treatment includes IV abx, ENT consult, admission for observation and often mastoidectomy
- Very painful, especially when coughing, sneezing
- Likely caused by Mycoplasma, H. Flu, or Strep pneumo
- Treat with antibiotics (macrolide like Biaxin) and topical antibiotics if vesicles rupture
- Pain management with opiate is acceptable for the short term.
Unilateral Hearing Loss
- Must distinguish between outer ear, middle ear and inner ear causes
- External Ear: Cerumen impaction, infection, foreign body
- Middle Ear: ETD/Otitis media with effusion (OME)
Otitis media with effusion Physical Exam findings:
- Appearance: Opaque TM, Air-fluid line, bubbles, amber discoloration.
- Pneumatic otoscopy: Immobile TM
- Tuning Forks: Weber Lateralizes to affected ear, Rinne BC>AC in affected ear
Sudden SNHL Physical exam findings:
- Appearance: Normal TM, Normal Landmarks, Translucent TM
- Pneumatic otoscopy: Mobile TM
- Tuning Forks: Weber Lateralizes to good ear, Rinne AC>BC in affected ear
- An otologic emergency, refer to ENT without delay
- When in doubt, refer! When in doubt, treat with steroids!
- Any SNHL that has occurred within 72 hours. Usually has no warning. Some patients will hear a “pop” in their ear
- 30 dB loss in 3 frequencies
- Possible causes: Viral Labyrinthitis, Autoimmune, Vascular compromise
- Treated with high dose prednisone: 60mg x 8 days, 40mg x 2 days, 20mg x 2 days
- Needs MRI of IAC with contrast
Benign Paroxysmal Positional Vertigo (BPPV)
- Vertigo which lasts less than a minute, usually seconds
- Provoked by supine head movements to the right or left
- Better when holding head still
- Caused by displaced otoliths in the semicircular canals
- Positive Dix-Hallpike maneuver
- Treated with Epley maneuvers
- A disorder of increased endolymphatic fluid pressure
- Classic Triad: Episodic SNHL, Vertigo x hours, and Roaring Tinnitus
- SNHL is low-frequency, usually unilateral.
- Treatment: Diuretics, Low sodium diet, Anti-vertigo medication, Surgery (to prevent vertigo)
- Surgical options: Endolymphatic sac decompression, Gentamicin injection, Selective vestibular nerve resection, Labyrinthectomy
- Infection or inflammation of the inner ear.
- V. Neuritis: affects semicircular canals only
- Acute Labyrinthitis: vertigo and hearing loss
- Vertigo is severe, lasts 24-48 hours, is disabling.
- Vertigo subsides and the patient will have several weeks of imbalance
- Treat with steroids and physical therapy
- BPPV: lasts seconds, head movements, no hearing loss
- Ménière’s: lasts several hours, associated hearing loss, tinnitus, ear fullness
- Neuritis/Labyrinthitis: Severe disabling vertigo lasts 1-2 days, gradual recovery
- Anterior: Kiesselbach’s plexus
- Posterior: Woodruff’s plexus
- Local risk factors: Digital manipulation, Septal deviation, Inflammation (allergies, infection), Cold dry air, Foreign body
- Systemic causes: Clotting Disorder, Hypertension, Leukemia, Liver disease, Medication (aspirin, Plavix, Coumadin), Thrombocytopenia
- Treatment: Manual compression, Afrin, Cautery, Anterior/Posterior Packing
- Surgical: Arterial Ligation, Embolization, Cauterization
Nasal Foreign body
- Seen often in pediatrics
- Consider if patient has foul nasal odor, chronic nasal discharge, nasal obstruction, sinusitis
- Chronic foreign bodies can cause pressure ulcers, infection, abscess
- Very common fracture, most often caused by blunt trauma.
- Look for obvious displacement of external nose
- Internal exam: Epistaxis, mucosal tear, septal deviation
- Reduction is indicated if cosmetic deformity or if there is loss of nasal function.
- Done within 3 hours or after 3-7 days (swelling makes the nose more stable).
- Non-displaced fractures do not require reduction.
- If viral URI does not clear in 7-10 days
- Double Sickening
- Signs and Symptoms: Localized Facial Pain, Upper Tooth Pain, Purulent nasal discharge; Fever, cough, fatigue may still be present, Facial Pain upon percussion
- Primary Treatment: Antibiotics (10-14 days)
- Pathogens: Strep. pneumo, H. flu, M. catarrhalis, Staph. aureus
- Adjunct Therapy: Nasal saline lavage, Nasal steroid, Antihistamine/Decongestant, Mucolytic (guaifenesin) , Afrin (for 4 days or less)
Dental Fractures and Avulsions
Fractured teeth can mostly be treated with sealing the fractured portion and referral to a dentist within 24 hours
Dental Luxations and Avulsions
- Commonly result from trauma to the mouth, and are common in small children
- Extrusive luxations: should be repositioned manually and splinted into place as promptly as possible
- Splinting can be performed with commercially available splinting material which is applied to the gingival surface of the tooth or by suturing the tooth into place by placing a suture through the anterior and posterior gingival mucosa and around the tooth. The pt. should have follow up within 24 hours with a dentist
- Intrusive luxations: the most serious but should not be manipulated initially but should be allowed to extrude themselves or be performed by an orthodontist and an also be referred out as an outpatient
- Lateral luxations: treated in the same way that extrusive luxations are but are commonly associated with an alveolar bone fracture
- <5 days duration
- sore throat
- nasal congestion
- Treat symptomatically.
Treat with antibiotics: PCN, Amox, EES, Quinolones.
- A collection of mucopurulent material in the peritonsillar space
- Often follows tonsillitis
- S/S: “Hot potato” voice, Severe throat pain and dysphagia, Inability to open jaw, Asymmetric swelling, Copious salivation
- Tx: Requires I&D and antibiotics
- Sx: Nuchal rigidity, Stridor, Sore Throat, Drooling
- Posterior pharyngeal space extends to base of skull and mediastinum
- Potential sequelae include: Mediastinal infection, airway obstruction, epidural abscess, necrotizing fasciitis, Sepsis, erosion into the carotid artery, Jugular venous thrombosis
- Treatment: Airway management, I&D, and antibiotics.
- Viral, aka acute laryngotracheitis
- Symptoms: Stridor, seal-like cough
- Treatment: Glucocorticoids, Nebulized epinephrine
- Most commonly seen in adults due to childhood vaccination against HIB
- Most common pathogens are haemophilus influenzae type b, staph. Species, strep. Species
- Can lead to rapid and unpredictable airway obstruction
- Symptoms: Trismus, drooling, dysphagia
- Lateral Neck X-Ray will show “Thumb Sign.”
- ENT Consult, avoid touching the epiglottis, treat with IV antibiotics
- Physical trauma to the auricle which causes shearing of the tissues and a perichondral hematoma.
- The auricle will be very swollen.
- Treat with I&D, then bolster both sides with dental rolls.
- Failure to treat early can lead to permanent remodeling of the auricle, cauliflower ear.
- Can occur in embryonic pits. Can be cystic which then becomes infected.
- May also present as a perichondral abscess.
- Treat with I&D and may empirically treat with antibiotics which cover GP organisms. Culture will help focus antibiotic course if no improvement.
- If recurrent infection occurs, will need to take to OR for excision of the cyst.
- Debride the wound
- Excise any protruding cartilage which prevents closure.
- Approximate the wound and use interrupted sutures
- Cover with antibiotics.
- If avulsed part is to be reattached, treat it like any other avulsed body part and consult plastics
Foreign Body in Ear Canal
- Attempt to remove if it appears you can get it on the first try.
- If completely obstructing EAC, if TM perf present, or if touching the TM, consult ENT
- Do not attempt to remove batteries, consult ENT and do not lavage.
Ear Canal Insect
- If alive, kill the insect using mineral oil, alcohol, or lidocaine
- Remove with microscopic forceps using binocular microscopy for best results.
- May need ENT consult
- Usually posterior
- Get audiogram
- Put on non-ototoxic ear drops (Floxin, Ciprodex)
- Keep ear dry and give TM time to heal and recheck hearing in 1-2 months
- If chronic perf results, may need surgical repair.
- Rapid pressure changes cause negative pressure in the middle ear resulting in effusion and ruptured blood vessels.
- Treat with nasal steroids and time, generally will resolve
- Audiogram will help determine if any significant hearing loss occurred.
- Etiology unknown.
- Facial paralysis thought to be caused by inflammation of the 7th CN after it leaves the brainstem, possibly viral (HSV?).
- Signs: Abrupt onset of upper and lower facial paresis or paralysis, mastoid pain, hyperacusis, dry eyes, altered taste.
- Treatment: Rule out serious pathology. Steroids and anti-viral. Protect the eye- lubricant
- Post extraction alveolar osteitis
- Occurs when the clot is dislodged from the socket of the extracted tooth and results in severe pain due to the exposure of the bone to the environment
- Plain films should be ordered to rule out retained root tip
- If there are no retained bodies present treatment consists only of analgesia and follow up with a dentist within 24hrs.
Acute Necrotizing Ulcerative Gingivitis (ANUG)
- Most commonly associated with HIV infection and/or prior ulcerative gingivitis
- Can be life threatening if left untreated
- Treatment includes chlorhexidine rinses, debridement by an oral surgeon or otolaryngologist, and PO Flagyl three times daily
- Marked swelling of the oral soft tissues
- Can be a result of hereditary C1 esterase inhibitor deficiency, allergic reaction, ACE inhibitor therapy, or may be idiopathic
- Treatment should include Benadryl, steroids, and epinephrine if airway compromise is imminent or the symptoms are rapidly progressing
- Exudative tonsillitis may be viral or bacterial.
- Can treat with antibiotics if symptoms persist or if airway is becoming compromised.
- Treat with GP coverage: Amox, EES, Quinolones, Bactrim.
- Bacterial infection of the floor of the mouth
- Treatment: Airway Management, IV antibiotics, Surgical
Airway Foreign Body
- Occur most often in children (toddler-preschool).
- Smooth Foods- grapes, hotdogs, nuts, seeds
- Non-food- coins, balloons, toys.
- Signs/Symptoms: Coughing, Wheezing, Stridor, Pneumonia, Decreased breath sounds, Bronchiectasis
- Airway Foreign bodies usually require surgical intervention: rigid bronchoscopy.
- If airway is compromised and cannot be resolved, tracheostomy is performed.
- Example: (subglottic stenosis, laryngeal cancer, laryngeal crush injury, severe obstructive sleep apnea).
- Anterior dislocation is the most common
- Can also have posterior, lateral, and superior dislocations.
- Symptoms: Jaw pain, trismus, malocclusion
- Evaluate ear canals, cranial nerves.
- Give analgesia and muscle relaxants prior to reduction
- Protect thumbs when reducing (can wrap in gauze).
- Tongue Blade Test, Imaging
- Evaluate for malocclusion
- Look for mucosal injury
- Closed Reduction- Non-displaced fractures
- ORIF- Displaced fractures, condylar fractures
- Wire Osteosynthesis for 6 week
LeFort Facial Fracture
- High energy blunt force trauma to the skull
- The mechanism of injury is important in determining the type of fracture.
- Secure airway, control bleeding
- ORIF- Align back into normal anatomic position and stabilize with fixation.
Temporal Bone Fracture
- Severe head and body trauma
- Skull base fracture
- Temporal bone houses the cochlea, semi-circular canals, carotid, jugular, facial nerve
- Complications include: hearing loss, facial paralysis, CSF leak, vertigo, TM perforation, nystagmus
- CT Temporal Bone, non-contrasted
- ENT Consult
“Rule of Nines” for Adult
- patient’s hand is approx 1% TBSA
- Chest: 9%
- Abdomen: 9%
- Anterior arm: 4.5%
- Posterior arm: 4.5%
- Face: 4.5%
- Head: 4.5%
- Anterior legs: 4.5%
- Posterior legs: 4.5%
- Genitals: 1%
- Upper and Lower Back and Buttocks: 18%
“Rule of Nines” for Children
- Head: 18%
- Front torso: 18%
- Back torso: 18%
- Arm: 9%
- Leg: 14%
- Genitals: 1%
1st degree - Superficial burns
- Epidermal only
- caused by sun or minor flash
- no blisters/edema
- skin is pink or red and is dry
- rapid healing, 3-6 days
2nd degree - Partial Thickness
- Involves dermis
- Superficial or deep
- Appearance and healing time vary on severity of burn
- Heals in 2-3 weeks
Superficial Partial Thickness
- Caused by flame, scalding, and chemicals
- Minimal damage to skin appendages
- Edema/blister formation
- Skin is pink or red and often blisters
- Healing 10-21 days
Deep Partial Thickness
- Deeper dermis involved some skin appendages
- caused by grease, flame, or chemical
- moderate edema
- skin pale and dry
- decreased sensation, decreased circulation,
- healing takes greater than 21 days
3rd degree - Full Thickness
- Destruction of both epidermal and dermal layers
- Prolonged exposure to heat
- Extensive edema
- Skin often dry, leathery or charred
- No sensation, circulation
- Will not heal spontaneously
- Requires skin grafting
Pre-Hospital Management First Aid for Burns
- Stop the burning process
- Remove clothing, irrigation of chemicals, etc.
- Cool the burn surface
- Cover/protect burn wound
- prevent heat loss, keep clean
Emergency Management of Burns
- Initial care is focused on the patient, not the burn wound
- Airway: assess airway patency, asses for smoke inhalation injury, constantly reassess: upper airway edema develops as fluid resuscitation progresses
- Breathing: Assess for spontaneous respiration, Assess for bilateral airflow
- Circulation: Assess circulatory status- peripheral pulses, Establish IV access
- Disability: Quick assessment of disability
- Exposure: remove all clothing, keep room warm, protect patient against heat loss with blanket
- Fluid Resuscitation: physiologic salt solution (LR, NS) according to formulas
- Pain Control: analgesics, IV morphine, titrate as needed, reassess often
- Secondary Survey: full examination, nasogastric decompression, urinary catheter to monitor resuscitation efforts
- Baseline labs: ABG, CBC, electrolytes, glucose, urinalysis, carbon monoxide level
- Tetanus booster or immunoglobulin and immunization
- Care of burn wound can wait for disposition, continue wound protection
Fluid Resuscitation for Burn Patients
- Edema maximum in 2nd 24 hrs post burn
- decreased intravascular fluid
- decreased CO
- increased PVR
- BURN SHOCK (distributive and hypovolemic)
- hypoperfusion of tissues leading to Acute Renal failure and possible brain damage.
- Adequate resuscitation ameliorates burn shock
- LR solution is a relatively isotonic crystalloid solution that is the key component of almost all resuscitative strategies, at least for the first 24-48 hours.
- LR is preferable to NS for large-volume resuscitations because its lower sodium concentration (130 mEq/L vs 154 mEq/L) and higher pH concentration (6.5 vs 5.0) are closer to physiologic levels.
- Another potential benefit of RL solution is the buffering effect of metabolized lactate on the associated metabolic acidosis.
- The rate of fluid administration should be titrated to a urine output of 0.5 mL/kg/h or approximately 30-50 mL/h in most adults and older children (>50 kg).
- In small children, the goal should be approximately 1 mL/kg/h.
- Burn injury can result in shock due to damage to the microcirculation and resultant capillary leak.
- In larger burn injuries, the release of chemical mediators causes a systemic increase in capillary permeability.
- The leakage of fluids, electrolytes, and protein from the intravascular space into the interstitium results in massive burn edema and, if the patient is not resuscitated adequately, circulatory collapse.
- Burn shock results from both distributive and hypovolemic processes because of the generalized microvascular damage and the third-spacing of fluids.
- 2-4 cc of LR x weight in kg x % BSA burned = total volume for 1st 24 hours
- ½ in 1st 8 hrs
- ¼ in 2nd 8 hrs
- ¼ in 3rd 8 hrs
- e.g. 100 kg patient with 30% BSA burn: 4 x 100 x 30 =12,000 cc: 6000 cc LR in first 8 hours post burn, then 6000 cc over next 16 hours
- monitor urine output (0.5ml/kg/hr in adults and 1ml/kg/hr in children <30kg)
- monitor pulmonary status
- monitor BP and pulse
Myoglobinuria & Hemoglobinuria (Red Pigmented Urine)
- High voltage electric injury or soft tissue injury due to mechanical trauma
- Administer fluids to maintain UOP 1.0-1.5 ml / kg / hr in adults
- Often clears urinary heme pigments & eliminates need for diuretic
- May add Na+ bicarbonate to IV fluid to maintain a slightly alkaline urine
Carbon monoxide poisoning
- Hemoglobin affinity 240X that of O2
- 5-10 % CO: Mild Headache and Confusion
- 11-20 % CO: Sever HA, Flushing, Vision Changes
- 21-30 % CO: Disorientation, Nausea
- 31-40 % CO: Irritability, Dizziness, Vomiting
- 41-50 % CO: Tachypnea, Tachycardia
- > 50 % CO: Coma, Seizures, Death
- >7% carboxyhemoglobin
- Cherry red skin color, agitation and ↓ LOC
- Cyanosis & tachypnea unlikely (CO2 removal unaffected)
- PaO2 and SaO2 may be normal
- Only carboxyhemoglobin level may be abnormal
- Treatment- administration of 100% O2, hyperbaric O2 rarely needed
Burn Injury above the glottis
- Heat exchange capacity efficient
- Most heat damage occurs above the vocal cords
- Laryngeal edema may occur at any time
- Usually within 24 hours of the injury
- Intubate preemptively, may need surgical airway
Burn Injury below the glottis
- Almost always a chemical injury
- Aldehydes, sulfur oxides & phosgenes adherent to surface of smoke particles cause direct damage to epithelium of large airways
- Diagnosis: Fiberoptic bronchoscopy
- Erythema; edema; mucosal ulceration, or carbonaceous material below vocal cords
- 33% of patients admitted to burn centers
- Clinical suspicion if: enclosed space, facial burns, singed nasal and facial hair, carbonaceous deposits in oropharynx
- Smoke particles and toxins cause damage to airways triggering inflammation, mucosal ulceration or necrosis of epithelium which causes pulmonary edema, bronchospasm, pneumonia and ARDS
- pneumonia is the most common cause of morbidity in smoke inhalation patients
Inhalation Injury Treatment
- Mostly supportive
- humidified O2
- pulmonary physiotherapy
- mucolytic agents and bronchodilators
- Consider intubation: copious secretions, edema
- Usually heal within 2-3 weeks
- “Tip of the iceberg” – The grand Masquerader
- Small surface injuries may be associated with devastating internal injuries
- Types: High voltage – 1,000 volts or greater; Low voltage
AC Electrical Current
- Alternating (AC) by reversal of electron flow every half cycle
- Contact sites, but no true entrance / exit sites – causes flexion contraction – sticks to source
- More dangerous (tetany, death from cardiac fibrillation, respiratory muscle paralysis)
DC Electrical Current
- Direct Current
- Travels in one direction – sudden contraction of muscles- thrown off
- Entrance & exits sites may be seen
Extent of Electrical Injury Dependent Upon:
- Type of current
- Pathway of flow
- Local tissue resistance
- Duration of contact
- Current (I) = V (voltage)/R (Resistance)
- Skin, bones and fat have high resistance
- Current flows along bone surface
- Generated heat damages adjacent muscle
- Deep muscle injury may occur when superficial muscle appears normal
- Fasciotomy - extensive muscle damage
- if red pigmented urine (muscle break down – myoglobinuria), increase fluid to obtain urine output of 100 ml/hr
- alkalinize urine with NaCO2 50 mEq/liter
- Cardiac monitoring for potential arrhythmias X 24 hrs
- Frequent neurologic examination and distal pulses
- 1/3 of patients with significant electrical injury will require amputation
- Most common: Alkalis
- Hydroxides, carbonates, caustic sodas of sodium, potassium, ammonium, lithium, barium, calcium
- Oven cleaners, drain cleaners, fertilizers, industrial cleaners
- Structural bond for cement, concrete (pH wet cement = 12)
- Tissue damage by liquefaction necrosis & protein denaturation – cause more damage than acids
- Common household items
- Hydrochloric acid in many bathroom cleansers
- Oxalic & hydrofluoric acids common in rust removers
- Concentrated hydrochloric & muriatic acid for pools
- Concentrated sulfuric acid in drain cleaners
- Tissue damage by coagulation necrosis & protein precipitation
Hydrofluoric Acid (HF)
- Industrial Use : Etch glass, Teflon, Clean semiconductors, Home use – rust removers
- Weak acid, but fluoride ion very toxic
- Severe pain for 6 – 18 hrs
- Tissue necrosis
- Hypo-calcemia as fluoride binds free serum calcium
HF Acid Burn Treatment
- Flood wound with water
- Neutralize with topical calcium gel
- 1 amp calcium gluconate in 100 gm lubricating jelly
- Apply with gloved hand
- High concentrations may be life threatening
- Cardiac monitoring
- IV line for treatment of hypocalcemia
- Wound excision may be required
- Burn center consultation
- Rare patients may require intra-arterial calcium infusion or subeschar dilute calcium gluconate
Organic compounds--petroleum products
- Phenols: chemical disinfectants
- Petroleum: creosote, gasoline, kerosene
- Cutaneous damage due to fat solvent action- (cell membrane solvent action)
- Systemically absorbed: toxic effects on kidneys and liver
Organic Compound Burn Treatment
- Remove saturated clothing
- Brush off powder agents
- Continuously irrigate with copious amounts of water
- If agent is dry powder, first brush off before rinsing
- Neutralizing chemical contraindicated; potential of heat generation
- Use litmus paper to get pH to 7, especially in eyes
- Wounds may initially look superficial but develop to full thickness in 2-3 days.
Burn Pain Management
- Pain management and topical medication application are two therapeutic interventions for burns.
- Rapid and effective pain reduction is central to the care of patients with burns.
- With few exceptions, the EP should not hesitate to insert an intravenous line, preferably in a non burned area, and provide intravenous analgesia.
- Intravenous administration is ideal for the acute treatment of patients who require immediate pain relief.
- Oral medication is more suitable for patients who will be discharged to home.
- For most patients with only minor burns, nonsteroids anti-inflammatory drugs (NSAIDS) and acetaminophen are adequate for pain relief. However, the EP should not hesitate to use opioid analgesics for pain relief, especially in those patients with severe burns.
- If the patient has a burn that requires the patient to be transferred to a burn center, treatment should be limited to removing the source of the thermal burn, debriding contaminated tissue, and covering the burned area with a nonadhesive cover (petroleum-based gauze) then a sterile, dry towel or sheet.
ABA Burn Center Referral Criteria
- 2nd degree burns > 10% TBSA
- Burns to face, hands, feet, genitalia, perineum, major joints
- 3rd degree burns (Any body part anywhere)
- Electric injury (lightning included)
- Chemical burns
- Inhalation injuries
- Burns accompanied by trauma
Burn Wound Management
- Cleanse and debride
- Debride blisters > 2cm
- daily cleaning and debridement, often use tub bath or whirlpool
- Apply topical antibiotics
- Antibiotics: All burn wounds will become colonized.
- S. Aureus and Pseudomonas are most common pathogens
- Topical antibiotics prevent invasion
- Usually apply twice per day
Topicals Abx for Burn Wounds
- Silver nitrate: applied as an occlusive dressing. No eschar penetration!
- Silver Sulfadiazine (SSD): limited eschar penetration
- Mafenide Acetate (Sulfamylon): good Gram-positive and negative coverage. Penetrates eschar. extremely painful
- Routine systemic antibiotics not indicated
- Systemic Abx Indications: Suspected wound invasion, discoloration of the wound, erythema and induration at wound margin, Fever > 101.5 F, Positive blood cultures, Positive wound biopsy/culture
Burn Surgical Management
- Burn wound excision to viable tissue
- Tangential Excision and Split thickness Skin grafting for third degree burns and deep second degree. Often done in stages. Accelerates hospital course and rehabilitation.
- Fascial excisions with Split thickness Skin grafting for some deep 3rd degree burns
Skin Graft Harvesting
- Dermatome used to harvest skin
- Graft may be meshed to increase coverage 1:1, 2:1, 3:1….
- graft glued, stapled or sewn over affected area
Biological Dressing for Temporary Burn Coverage
- Gold standard: Human allograft, last 2-3 weeks until rejection
- Porcine xenografts: cheap, available, last approximately 1-2 weeks
- Synthetic skin substitutes: Integra 2-3 weeks
Burn Management Summary
- Remove source of injury
- Patient is priority: ABCDE
- Overall Assessment
- Fluid Resuscitation
- Pain Management
- Referral to Burn Center or Wound Care
- Risk is 1 in 280,000
- Kills 80 – 100 people in US annually
- Associated with 30% mortality
- 70% of survivors suffer serious complications
- Direct current
- Not associated with deep burns
- Cardiac & neurological damage
- Lichtenberg – fern like dendritic pattern on skin
Burn Zones of Injury
- Zone of coagulation: A nonviable area of tissue at the epicenter of the burn
- Zone of ischemia or stasis: Surrounding tissues (both deep and peripheral) to the coagulated areas, which are not devitalized initially but, due to microvascular insult, can progress irreversibly to necrosis over several days if not resuscitated properly
- Zone of hyperemia: Peripheral tissues that undergo vasodilatory changes due to neighboring inflammatory mediator release but are not injured thermally and remain viable
Surgical incision into necrotic skin resulting from a severe burn; inelastic leathery dead skin causing a tourniquet like effect.
Indications for escharotomy/ fasciotomy (5 Ps)
- Pallor: Cyanosis of distal unburned skin on limb
- Pain: Unrelenting deep tissue pain
- Paraesthesia: Progressive tingling/numbness
- Paralysis: usually late finding
- Pulselessness: Progressive decrease or absence of pulse
- Surgical excision of fascia to relieve tension or pressure in muscle compartment
- indicated for compartment syndrome
- Indicated in electrical burns with muscle injury
Extremity Compartment Syndrome
- Edema within (beneath) deep investing muscle fascia
- Results from: High-voltage electric injury, Massive IV fluid infusion, Crush injury, Delayed escharotomy (ischemic-perfusion injury)
- Early irrigation is essential!! Use 1-2 L of saline or water with Morgan Lens and irrigate until pH is neutral.
- May use a topical anesthetic to aid in pain management.
- Fluorescein exam of cornea if indicated
- Alkalis bond to tissue proteins: require prolonged irrigation—use pH paper to help with diagnosis if the nature of the chemical is unknown.
- Consider early Ophthalmologic consult
- The injury should be managed as an open fracture with appropriate antibiotics and tetanus prophylaxis.
- The amputated part should be kept clean, motioned with sterile saline, wrapped in a sterile dressing, placed in a plastic bag, and put on ice.
- Cooling the amputated part will increase viability from approximately 6 to 8 hours to 12 to 24 hours.
- Post-reimplantation limb shortening may create significant disability.
- Proper use of post injury prosthetics may be the better option.
Amputation and Extremity Arterial Injury
- Torn or lacerated artery risks loss of limb
- Vascular repair of warm ischemia within 6 hours of injury
- Arteriogram for multilevel trauma
- Signs of arterial injury: Pulsatile hemorrhage, Expanding hematoma, Audible bruit, Pulseless limb
- Injuries associated with arterial damage: Knee dislocations, displaced tibial plateau fx, floating joint, GSW or knife wounds, mangled extremity
Mangled extremity & traumatic amputations
- Significant destruction of soft tissue endangering limb
- Vascular assessment, fracture management, limb salvage vs. amputation.
- MESS score > 7 needs trauma center
- Proximal stump pressure dressed with Ringer’s Lactate
- Avoid tourniquets
- Amputation wrapped in Ringer’s moistened sponge, placed in plastic bag and cooled in a container with ice. Not in direct contact with ice.
- Time from amputation to replantation: warm or cold ischemia
- Warm ischemia: 6 hrs
- Cold ischemia: 12 hrs; up to 30 hrs for digits
- Better prognosis for sharp cut injury than crush or tear.
- Absolute indications: Thumb, pediatric amputations
threatened soft tissue / open fracture
- Reduce displaced fractures and dislocations that are tenting or opening skin to relieve vascular, neurologic, & skin compromise.
- Open fractures are covered with saline moistened dressings and brought to the OR for repair.
Septic Joint and Osteomyelitis
- Hematogenous or traumatic in origin
- Bone: Gp A Strep, S. aureus
- Joint: H. influenza, Gp A Strep, E. coli, N. gonorrhea
- Sx: Fever, joint or bone pain, leukocytosis
- Dx: Bone scans localize osteomyelitis. Joint aspiration to identify organism
- Rx: Parenteral Abx, I&D
Describe the clinical findings and treatment of compartment syndrome.
- Compartment syndrome develops when the pressure in the inelastic fascial space increases to a point where it causes compression and dysfunction of venous outflow.
- Five "Ps": pallor, paresthesias, poikilothermia, paralysis, and pulselessness.
- Compartment syndrome may result from exertion, circumferential burns, frostbite, constrictive dressings, arterial bleeding, severe soft tissue injury, and fracture.
- The earliest symptom is severe pain out of proportion to the physical findings.
- The involved compartment is extremely firm.
- The pain is worsened with passive range of motion due to ischemic muscle fiber stretch.
- Paresthesia is a later sign of nerve compromise, commonly with vibratory sensation lost first.
- Motor weakness, pallor, poikilothermia, and pulselessness are very late signs and only occur after irreversible muscle, nerve, and vascular damage have occurred.
- The most common areas of the extremities affected by compartment syndrome are the anterior compartment of the leg due to proximal tibial fractures and the volar compartment of the forearm secondary to fractures of the ulna or radius, as well as supracondylar fractures.
- Sx: Pain out of proportion to injury, Pain with passive stretch, Paresthesias, Pulslessness (late finding).
- Measure compartment pressures
- > 30 mm Hg: warrants decompression with fasciotomy
Red Flags for Child Abuse Injuries
- Multiple fractures and fractures in various stages of healing: Multiple fractures in various stages of healing are seen in 70% of children <1 yr, 50% over all
- Metaphyseal corner fractures: less common
- Long bone fractures in child <2 yr: Fractures through femur, tibia or humerus suggestive of abuse in child < 2
- Vertebral compression fractures, spinous process avulsions: Fairly specific for child abuse, spinous process avulsions > vertebral fractures. Most asymptomatic, identified on skeletal survey
- Epiphyseal separation: physeal separations usually the result of violent traction or rotation
- Miscellaneous fractures
- Delayed union: Slow callus formation
- Nonunion: No clinical or radiographic signs of progression of bony union within 3 months
- Infection: Especially with open fractures- Osteomyelitis: S. aureus, Beta strep
- N/V injury: Always evaluate circulation & sensation distal to injury site.
- Closed reduction
- CRPP: Pinning
- ORIF: Screws, plates
- Plain Films: Two views at least. Check entire film
- Consider joint above & below injury
- Stress films
- CT: Defines bony anatomy
- MRI: Defines soft tissues
- Nuclear medicine studies: Help define tumors, etc
- EMG: Evaluates denervation of muscle units
- NCS: Evaluate conduction velocities
Diagnosis and Treatment of Clavicle Fractures
- Usually resulting directly from an impact on the superior aspect of the acromion.
- Patients complain of pain at the AC joint and will actively splint the injured shoulder.
- Ecchymosis may be present; however, an obvious deformity is not always seen.
- There is significant tenderness upon palpation of the AC joint.
- Standard radiographs should include AP and axillary lateral views of the shoulder.
- Type I and type II injuries are treated with rest, ice, analgesics, and a simple sling until acute pain with movement is relieved.
- Treatment of type III injuries is controversial with the literature supporting both nonoperative and operative management.
- Types IV, V, and VI are treated operatively.
- Referral to a musculoskeletal specialist is essential for all AC joint injuries since many patients who initially appear to have minor injuries will have more obvious deformity after the swelling and pain have subsided.
- Anterior shoulder dislocations are the most common dislocations seen in the emergency department.
- Most frequently caused by falling with the arm externally rotated and abducted.
- Acutely, patients present with the affected extremity held in adduction and internal rotation.
- Often, the patient complains of shoulder pain, refuses to move the affected arm, and may support the dislocated shoulder with the other arm.
- The acromion becomes prominent and there is a loss of the rounded contour of the deltoid.
- A neurovascular examination of the upper extremity should be performed to rule out associated injury, most commonly of the axillary nerve (sensation over the deltoid), and of the musculocutaneous nerve (sensation on the anterolateral forearm).
- Posterior shoulder dislocations are commonly missed because of subtle radiographic findings.
- The arm is held internally rotated and slightly abducted.
- Patients are unable to externally rotate their shoulder.
- On examination, a posterior prominence exists.
- Anterior: 95%
- Bankart lesion: Avulsion of the antero-inferior glenoid labrum
- Hill-Sachs lesion: Compression fx of posterior humeral head
- Posterior: Anterior force, Seizure, Electric shock
- Rx: Closed reduction is treatment of choice
- Rowe maneuver: touch opposite ear over head
- Stimson maneuver: prone, weights off table
- Hippocratic: traction / counter traction
- X-Ray: Standard views: AP (Grashey), Scapular Y, Axillary views
- Elevated humeral head = RCT
Olecranon and Radial Head Fractures
- Anterior fat pad: Small is often present – large is pathologic
- Posterior fat pad: Always pathologic
- MUGR: Monteggia – ulnar, Galeazzi – radial
- Direct trauma or fall on an outstretched hand may result in elbow fractures.
- Supracondylar fractures often occur in pediatric patients.
- Neurovascular insult occurs in 7% of supracondylar fractures, with the anterior interosseous nerve most commonly injured.
- This can be checked by having the patient make an "ok" sign. This neurapraxia usually resolves in 6 months.
- Arterial injury to the brachial artery occurs approximately 5% of the time and arteriography is indicated if the radial pulse is decreased either before or after reduction.
Radial head fractures
- Can be treated with a sling for comfort and patients should be told to discontinue the sling as early as possible.
- Capitellum fracture is commonly associated with fractures of the radial head.
- Fractures of the wrist and elbow usually involve a fall onto the outstretched arm, while fractures of the ulnar shaft are more commonly the result of a direct blow.
- Monteggia fracture-dislocation is an ulna fracture (usually proximal third) with associated proximal dislocation of the radial head. This fracture is occasionally associated with radial nerve injury.
- Galeazzi fracture-dislocation is a fracture of the distal one-third of the radius with dislocation of the distal radioulnar joint. It occurs three times more often than a Monteggia fracture. This fracture can be associated with an ulnar nerve injury.
- 90% are posterior
- Some are s/p total hip replacement
- PE: hip flexed, adducted & internally rotated
- X-ray, pain relief, reduction
- Possible N/V entrapment
Femoral Shaft Fx
- Significant hematoma formation is extremely common.
- Patients with comminuted femoral shaft fractures are at risk for fat emboli syndrome.
- For distal fractures, it is important to rule out intraarticular involvement.
- Initial management includes stabilization and evaluation for any life-threatening injuries.
- 1000 mL blood loss can occur.
- An open fracture is an orthopedic emergency; these patients require tetanus prophylaxis, antibiotic coverage, and emergent irrigation and debridement in the operating room.
- Orthopedic consultation should be obtained with any femur fracture since the majority require operative fixation and stabilization.
Tibial and Fibular Fx
- Isolated fibular fractures are caused by direct trauma to the lateral leg.
- Isolated fractures of the fibula are anatomically splinted by an intact tibia.
- Distal fibular fractures may include a disrupted ankle joint, as evidenced by a widened mortise on the anteroposterior (AP) radiograph.
- Tibial fractures are classified by their location, amount of displacement, and presence of comminution.
- Compartment syndrome can be seen following a tibia fracture and distal neurovascular status should always be documented.
- Suspect tibial fractures with trauma to the lower extremity, pain, and inability to bear weight.
- Maisonneuve fracture
- Combination of an oblique proximal fibular fracture, disruption of the interosseous membrane and tibiofibular ligament distally, and a medial malleolar fracture or tear of the deltoid ligament.
- Occurs when an external rotational force is applied to the foot, producing a fracture of the proximal third of the fibula.
- Physical examination findings include tenderness at the medial and anterolateral ankle joint in combination with proximal fibular tenderness.
- Treatment of tibial fractures depends on whether they are open or closed and on the degree of displacement.
- All open fractures require immediate orthopaedic evaluation.
- Closed fractures that cannot be reduced may also need open reduction.
- Patients with isolated nondisplaced tibial fractures may be splinted, started on ice therapy, and referred for outpatient treatment.
- Displaced tibial fractures should also be evaluated by an orthopaedic surgeon since these are at risk for developing compartment syndrome.
- Treatment of a Maisonneuve fracture is most commonly operative.
assessment of children with medical emergencies and trauma
- Initial assessment- ABCs
- Rapid Cardiopulmonary Assessment (RCA)
- Airway patency: able to be maintained, maintainable with positioning, requires assistance
- Breathing: rate, mechanics, air movement, color
- Circulation: HR, peripheral/central pulses, skin perfusion, BP
- CNS perfusion: responsiveness (AVPU), recognizes parents, pupil size, posturing
- Identify deficits in oxygenation and organ perfusion
- Respiratory distress/failure: Respiratory failure frequently leads to cardiac arrest in children
- Respiratory Distress: Increased RR and effort, Tachypnea, nasal flaring, use of accessory muscles, retractions
- Respiratory Failure: Inadequate oxygenation
- Respiratory Arrest: Apnea, absence of breathing
- Shock: Inadequate perfusion
- Compensated: Inadequate perfusion with normal BP
- Decompensated: Inadequate perfusion and hypotension
- Hypotension: >1mo SBP <60; 1-12 mo SBP <70; 1-10 y/o SBP <70 + 2x age in yrs; >10 y/o SBP <90
- RCA needed if HR: > 200 in infant; >180 in 1-8 y/o, > 160 in > 8 y/o, Less than 60 (indication for chest compression)
- CPR Infant and child: ABC, One rescuer - 30:2, Two rescuer – 15:2
- Potentially Reversible Causes of Arrest:
- 4H’s & 4T’s: Hypoxemia, Hypovolemia, Hypothermia, Hypo/Hyperkalemia, Tamponade, Tension pneumothorax, Toxins/poisons/drugs, Thromboembolism
- 4 C’s added in trauma cardiac deterioration: CNS or Cervical spine injury, CV injury, Chest wall disruption, Comorbid injury (head trauma, seizure…)
- initiate resuscitation
- D & E: disability & exposure. thorough neurologic and musculoskeletal exam
- Normal Heart Rate: < 3 mo 85-205; 3 mo-2y 100-190; 2-10y 60-140; >10y 60-100
- Normal Respiratory Rate: Neonatal 40-60; 1 y/o 24; 18 y/o 12; RR > 60 needs RCA
- History: may not be fully obtained until after assessment of ABCs
- Physical exam
- Labs/Diagnostic tests: pulse ox, glucose, CBC; blood cultures, electrolytes, CXR
Causes of Respiratory Failure:
- Upper airway obstruction: stridor, hoarseness, distress; epiglottitis
- Lower airway obstruction: wheezing, prolonged expiration, retractions; asthma
- Parenchymal lung disease: grunting respiration; pulmonary edema, pneumonia, atelectasis
- Abnormal ventilation: Brain injury, OD
- varies with severity
- oxygen via mask or nasal cannula
- bag/mask ventilation
- if oxygen saturation fails to improve intubation and mechanical ventilation should be initiated (via rapid sequence induction)
Rapid Sequence Intubation- PALS
- Pre-medicate: Fentanyl for analgesia in awake pt. Atropine to decrease secretions and Vagal stimulation. Lidocaine reduces rise in ICP. Defasciculating agent inhibits muscle fasciculation from succinylcholine.
- Sedation with one of these agents: Thiopental, Midazolam, Propofol, Ketamine, Etomidate
- Paralyze after sedation: Succinylcholine . Vecuronium or Rocuronium are safe in renal and hepatic failure & have less CV side effects
- Primary & Secondary confirmation of tube
- Secure tube
- vascular access
- fluids: resuscitation, maintenance
- Infection and swelling of the epiglottis
- H. influenza, S. pyogenes, S. aureus, S. pneumonia
- Abrupt onset of: High fever, sore throat, stridor, dysphagia & drooling
- Caution on PE
- Lateral neck film in extension during inspiration
- Treatment: Humidified O2, Nebulized epinephrine, Heliox; Intubate, blood culture; Cefuroxime, Cefotaxime, Ceftriaxone
- Subglottic inflammation
- Most common in 6 mo – 3 y/o
- Peaks in late fall/early winter
- Etiology: Parainfluenza viruses I, II, II
- Sx: 1-5 day prodrome of cough and coryza Followed by 3-4 days of barking cough. Peaks on day 3
- Steeple sign on AP of neck
- Rx: Humidified O2, Monitor O2 sat; Dexamethosone 0.6 mg/kg PO/IM; Nebulized epi, 0.05 mL/kg. Up to 0.5 mL of 2.25% solution
- Discharge: No stridor, 3 hrs since last epi, Well appearing, O2 sat > 90% on RA, Reliable parents
Foreign body aspiration
- Toys, balloons, hot dogs, nuts, grapes, PB
- Upper airway obstruction: Weak cough, inability to speak, stridor
- Responsive Infant: 5 back blows/5 chest thrusts
- Responsive Child: Abdominal thrusts (Heimlich)
- Unresponsive Infant & Child: Look for FB, CPR
- Lower airway obstruction: Unilateral wheeze, cough, dyspnea
- Intubate unstable pt.
- etiology : Respiratory Syncitial Virus (RSV) Fall through Spring, Virus shed 1-2 days before & 1-2 wks after Sx. Also - Parainfluenza, Adeno & Rhinovirus, Mycoplasma
- Sx: URI Sx with wheezing and + fever
- Dx: CXR - hyperinflation, interstitial pneumonitis, RUL/RML infiltrate. ELISA RSV nasal wash specific and sensitive. WBC, O2 sat
- Sx: Cough, expiratory wheeze, SOB, tachypnea
- PE: Expiratory wheeze, retractions, nasal flaring
- Dx: Clinical, O2 Sat, PEF
- CXR: Hyperinflation with flattened diaphragms
- PEF: Severe < 60%, Moderate > 60 - < 80%, Mild > 80%
- ER Rx: O2 if Sat < 94%; Fluids
- Nebulized albuterol: 0.15 mg/kg (2.5-5mg) q 20 min. 0.5ml of 0.5% sol (2.5mg) in 3 ml saline. One 3ml unit dose (.083%). Syrup 2mg/5ml – 0.1-0.2mg/kg/dose TID
- Nebulized Xopenex (levoalbuterol): 0.63 - 01.25 nebulized q 20 minutes
- Methylprednisolone: 0.5-1mg/kg IV, IM q6h
- Solu-Medrol: (40, 125, 500 mg/vial)
- Prednisolone: 1-2mg/kg/day PO
- Prelone: (15mg/5ml),
- Pediapred: (5mg/kg)
- SC epinephrine: 0.01 mL/kg SC – rarely used now
- Admit: Unable to keep O2 Sat > 93% on RA
- Most common in kids < 5 y/o
- Etiology: GABS, S aureus
- Sx: Fever, sore throat, odynophagia, dysphagia, stridor, HOT POTATO voice
- PE: Tender cervical adenopathy, pharyngeal erythema and unilateral pharyngeal edema
- Dx: Lateral neck soft tissue x-ray, Cultures
- Rx:Clindamycin 600mg q8h IV; Unasym 3 g q6h IV
- Operative I&D
- Quinsy; GABS
- Sx: Sore throat, fever, dysphagia, drooling
- PE: Unilateral tonsillar enlargement, Uvula edema & contralateral displacement
- Dx: Clinical
- Rx: Clindamycin 600mg q8h IV; Unasym 3 g q6h IV.
- Operative I&D
Evaluation and treatment of fever in infants and children
- Fever: rectal temp > 38° C (100.4 ° F) or oral temp > 37.5°C (am) or 37.8°C (pm)
- Common bacterial infections associated with fever: pharyngitis/tonsillitis, cellulitis, meningitis, sepsis, UTI, pneumonia
- toxic infant: lethargy, poor perfusion, resp. distress
- 10% of well appearing young infants with temp >38° C have infection
- < 2% of older infants with temp > 39 ° C have bacterial infection
- Give appropriate dose of antipyretic
Rochester Criteria for Identifying Febrile Infants at Low Risk for Serious Bacterial Infection
- Infant appears generally well
- Infant has been previously healthy: Born at term (≥37 weeks of gestation). No perinatal antimicrobial therapy. No treatment for unexplained hyperbilirubinemia. No previous antimicrobial therapy. No previous hospitalization. No chronic or underlying illness. Not hospitalized longer than mother.
- Infant has no evidence of skin, soft tissue, bone, joint or ear infection
- Infant has these laboratory values: White blood cell count of 5,000 to 15,000 per mm3. Absolute band cell count of ≤ 1,500 per mm3. Ten or fewer white blood cells per high-power field on microscopic examination of urine. Five or fewer white blood cells per high-power field on microscopic examination of stool in infant with diarrhea.
Empiric Abx for FUO Infants < 3 mo:
- Ampicillin 100-200 mg/kg/day q6h IV, plus
- Gentamycin 7.5 mg mg/kg/day q8h IV, Or
- Ceftriaxone 50 mg/kg/day in a single IV dose, Or
- Cefotaxime 150 mg/kg/day q8h IV
Empiric Abx for FUO Infants older than 3 months
- Ceftriaxone 50 mg/kg/day in a single IV dose
- Cefotaxime 150-200 mg/kg/day q6-8h IV
- 3 mo – 5 y
- Recurrence common
- < 5% develop epilepsy
- LP, MRI, EEG only if indicated
- Rx: Evaluate for source of fever. Temperature control. Prophylactic Phenobarbital not recommended. Lorazepam or Diazepam for Status Epilepticus
Vomiting in infants and children.
- Define: projectile, persistent, spitty
- Is there diarrhea? - Gastroenteritis
- Is there blood or bile?
- Bilious vomiting
- Nonbilious vomiting
- TE fistula
- Incarcerated inguinal hernia: Contents cannot be returned (reduced) to the abdominal cavity
- Diabetes mellitus
Bilious vomiting a sign of intestinal obstruction
- duodenal atresia: double bubble sign
- malrotation w volvulus: ischemia
- meconium ileus: retained meconium
- necrotizing ileus: blood in stool
- Hirschsprung’s: aganglionosis
- Rx: NG tube, IV fluids, imaging, surgery
- Pyloric stenosis
- Hypertrophic pyloric sphincter causes gastric outlet obstruction.
- 3 – 6 weeks old
- More common in first born males, 4:1 male predominance, positive family history.
- Persistent, Progressive, Projectile (non-bilious) vomiting. Everything including water.
- Poor weight gain
- Visible peristaltic waves
- Palpable Pyloric “olive”
- Most common cause of intestinal obstruction in infants <1y/o
- Intestinal invagination around ileocecal valve.
- 3 mo. – 36 mo.
- Sx: Intermittent “colicky” abdominal pain. Bloody “currant jelly” stools
- PE: Palpable mass, “sausage” RUQ
- Dx: Plain films show small bowel obstruction
- BE reduction successful 50 - 90% of the time
- Surgery if not reduced
Evaluation and treatment for children with sickle cell disease.
All children with SCD presenting with fever, pain, respiratory distress, or a change in neurologic function require a rapid and thorough ED evaluation.
Sickle cell emergencies include:
- Vasoocclusive crisis
- Pain crisis
- Acute chest syndrome
- Hematological crisis
SSD Vasoocclusive crisis
- due to intravascular sickling, which leads to tissue ischemia and infarction
- Pain may be the only symptom
SSD Pain crisis
- Clinical features: classic sickle cell pain crisis is usually typical in location, character, and severity of pain
- symptoms may be triggered by stress, extremes of cold, dehydration, hypoxia, or infection but most often occur without a specific cause
- initially may present with dactylitis, a swelling of hands or feet, and low-grade temperature caused by ischemia and infarction of the bone marrow
- As children age, the array of presentations may expand from the extremities to the abdomen, chest, and lumbosacral area
- Treatment: Pain management must be individualized
- Aggressive hydration: attempted with oral fluids as tolerated or age-appropriate IV maintenance fluids
- 5% dextrose (D5) in 0.25 normal saline solution (NS). D5½NS at 1.5 the maintenance rate
- Mild to moderate pain: managed with oral hydration and analgesics, such as narcotic and acetaminophen combinations and NSAIDs
- Parenteral, long-acting narcotics, morphine 0.1 to 0.15 mg/kg IV or hydromorphone 0.015 mg/kg IV, are indicated for failure of oral regimens
- Admission: is warranted for poor pain control or inadequate oral fluid intake
- child discharged from the ED for a pain crisis to be reevaluated within 24 hrs by the child's pediatrician or hematologist
SSD acute chest syndrome
attributable to a combination of pneumonia, pulmonary infarction, and pulmonary emboli from necrotic bone marrow
SSD hematological crisis
- acute sequestration crisis
- the second most common cause of death in children with SCD younger than 5 years
- Such crises are often preceded by a viral infection
- Classically, children present with sudden onset left upper quadrant pain; pallor and lethargy; a markedly enlarged, tender, and firm spleen on abdominal examination; and signs of cardiovascular collapse, including hypotension and tachycardia
- Treatment: Early recognition and prompt initiation of treatment. rapid infusion of resuscitative crystalloid or colloid fluids. Transfusion with packed RBCs or exchange transfusion
SSD Aplastic episodes
- precipitated primarily by viral infections (typically parvovirus B19) but also can be caused by bacterial infections, folic acid deficiency, or bone-marrow suppressive or toxic drugs
- gradual onset of pallor, dyspnea, fatigue, and jaundice
- Pain is not a hallmark of this crisis unless there is an associated vasoocclusive crisis
SSD Hemolytic crisis
- Bacterial and viral infections in children with SCD also can precipitate an increasing degree of active hemolysis
- Onset is usually sudden
- Increased jaundice and pallor may be noticed on physical examination
- Care should be directed toward treating the underlying infection
- Distal 1/3 clavicular fracture
- Supracondylar fractures – fat pad sign
- Radial head subluxation
- Greenstick / plastic deformation injury
- Torus fracture
- Legg-Calve-Perthes disease
- Femur fx – non-ambulatory, suspect abuse
- Toddler’s fx – oblique fx of distal tibia in child <5y/o
Child Abuse - Non-accidental Trauma
- 1.4 million children suffer abuse
- 160,000 suffer serious or life threatening injuries
- 1000-2000 children die each year
- Red Flags: Multiple lesions in different stages, Lesions w/ shape of object, Trauma inconsistent with history, History that shifts with retelling, Injury involves an un-witnessed event
- Risk factors: Social isolation, Poor role models, Unrealistic expectations, Economic difficulty, Illness, Drug or alcohol abuse
- History: History of multiple injuries, Injuries not consistent with mechanism, Inconsistent story
- Physical Exam: Patterns, Inconsistent findings, Fractures
- The Injury Prevention Program: TIPP
- Accidents are the #1 cause of death < 1y
- Bicycle helmet
- Firearms safety
- Drowning awareness
- Choking: BLS
- Poison prevention
- Burns, water temp <120
- Car seats
Car Seat Recommendations
- < 20#: rear facing seat
- 20-40#: front facing
- 40-60# booster seat
- > 60# lap belt
- 4 y/o regular shoulder/lap belt
Sedation and pain relief in children
- Sedation reduces awareness: Benzodiazepines (Versed, Valium, Ativan), Barbiturates
- Analgesia reduces pain: Morphine, Fentanyl
- Dissociative anesthetic provides sedation and anesthesia: Ketamine
- Minimal sedation for non-painful procedures: Versed, Valium, Ativan
- Moderate sedation: Conscious sedation, Procedural sedation
- General anesthesia
- Reversal agents: Naloxone for narcotics, Flumazenil for benzodiazepines
- AMPLE Hx
- O2, Bag mask, Suction
- Monitor: O2sat, BP, Cardiac
- IV access
- Meds: Short acting benzo (Versed) + opioid (Fentanyl) or Ketamine + atropine + benzo
Acetaminophen 10 - 15 mg/kg/dose every 4 - 6 hrs.
5mg/kg is used for fever < 102.5F; 10mg/kg is for fever > 102.5F
- 0.5mg/kg/q6hr IV, IM
- 10 mg/dose q6hr PO Child > 50kg.
- 0.05-0.15 mg/kg PO q4-6h
- 5, 15, 30 mg tab, 5mg/5ml
Differentiate innocent from dangerous rashes
- Differential Dx
- Dangerous: Meningococcemia, RMSF, ITP
- Benign: Viral Exanthems (Measles, Scarlet fever, German measles, Fifth disease, Roseola), Infestations, Dermatitis
- Many conditions are normal variations
- Reassurance is important for parents
- Calculate as follows
- children weighing 10 kg or less: administer 100 mL/kg/d
- 11–20 kg: administer 1,000 mL plus 50 mL/kg for each additional kg >10 kg over 24 hrs
- > 20 kg: administer 1,500 mL plus 20 mL/kg for each additional kg >20 kg over 24 hrs
- A rapid means of calculating maintenance fluid rates is as follows: 4 mL/h for every kilogram up to 10, plus 2 mL/h for every kilogram between 10 and 20, plus 1 mL/h for every kilogram over 20
- Standard solutions
- young infants: 5% dextrose in 0.2 NS (ie, one fourth NS)
- older infants and children: 5% dextrose in 0.45 NS (ie, D5½ NS)
- Standard solutions for deficit fluid replacement are the same as those for maintenance fluids
- If patient weighs 15 kg on presentation and is estimated as 10% dehydrated, then it is estimated that 15 kg x 10% = 1.5 kg of water has been lost: 1.5 kg water equals 1.5 L water
- Therefore, 1500 mL is the estimated deficit.
- Half of this total is given over the first 8 hrs and the remaining half is given over the following 16 hrs
- The hourly IV fluid rate is determined by the sum of maintenance and deficit fluid requirements for the patient
Chest Pain in Children DDx:
- Cardiac disease rare: Arrhythmias, IHSS, Mitral prolapse, Pericarditis, Myocarditis
- Musculoskeletal: Strains, Trauma, Costochondritis
- Respiratory: Asthma, Pneumonia, Pneumothorax, PE
- Psychogenic - Hyperventilation
- GI: GE reflux, FB aspiration
- Others: Sickle cell, Marfan’s, Shingles
Sudden Cardiac Death
- High profile tragedy
- Unsuspected cardiac disease most common
- 1:200,000 / year, 10 - 25 deaths / year
- HCM (IHSS): 36%
- Congenital coronary artery abnl: 19%
- Marfan’s Syndrome: 5%
- Myocarditis: 3% (50% from Coxsackie B)
- Non cardiac causes: hyperthermia, asthma, anaphylaxis, trauma
- The sudden death of an infant under 1 year of age that remains unexplained
- SIDS is the most common cause of death in infants aged 1 month to 1 year
- Incidence: 1992-1.2 / 1000; 2002-0.57/1000
- The diagnosis of SIDS is one of exclusion
- Hypotheses: Prolonged QT syndrome leading to arrhythmia. Hypoxia & apnea, either obstructive, central.
- Acute life-threatening event (ALTE): unexpected change characterized by color change, limpness & apnea
- 50% have identifiable cause
- Barium swallow
- CXR, EEG, EKG
- Home Monitoring
- Breast feed
- Avoid exposure to smoke
- Avoid soft surfaces
- Back to sleep
- Parent BLS training
- Type of toxin, time of ingestion, & amount.
- Acetaminophen (APAP): N-acetylcysteine 140mg/kg. 17 doses of 70 mg/kg q4h. Peak concentration level @ 4h. Rumack nomogram
- Disc batteries: 7 days
- Iron: Little toxicity <20mg/kg dose. Lavage. Charcoal ineffective. Deferoxamine IV
- Salicylates: Toxic dose > 150mg/kg. Lavage, charcoal
- Odor on breath
- Toxic screens
- Poison Control Center
- Skin or eye exposure – flush with water
- 24-32F orogastric tube.
- Serial infusion/withdrawal 200ml
- Activated charcoal: 1g/kg PO
A - Airway maintenance with c-spine control
- Foreign bodies (blood, vomit, teeth)
- Prevent Hypoxia/hypoventilation
- Intubation, mechanical ventilation indicated when: Unable to oxygenate/ventilate. Major head trauma or GCS < 8. Agitation/intoxication.
- Radiographic and clinical assessment
- NEXUS: No posterior midline tenderness, No evidence of intoxication, Alert mental status, No focal neurologic deficits, No painful distracting injuries.
B - Breathing
- Are they oxygenating and ventilating?
- Pneumothorax/Tension pneumothorax: treated immediately with needle decompression followed by tube thoracostomy
- Hemothorax: For large hemothoraces, consideration may be given to autotransfusion and immediate operative exploration for initial chest tube output > 1,500 mL of blood.
- Flail chest: The presence of a flail chest may mandate endotracheal intubation to ventilate patients adequately
- Sucking chest wound: Require placement of an occlusive dressing followed by chest tube placement.
C - Circulation
- evaluated by pulse palpation, vital signs and cardiac monitoring
- ID sites of obvious bleeding
- Hemorrhagic shock
- signs of cardiac tamponade (Beck's triad of hypotension, jugular venous distention, and muffled heart sounds)
- Control hemorrhage
- Large bore IV access
- Fluid replacement (Crystalloid!)
- If the patient is hypotensive, then 2 L warm crystalloid should be administered to treat shock; this may be followed by administering O-negative or type-specific blood as required
- Blood products
D - Disability; abbreviated neuro exam
- Moving all extremities
- Rectal tone
E - Exposure
Undress patient and look for other problems/causes
F - Fingers/Foleys
Family and friends
- ID Mechanism of Injury
- Rapid Head to toe exam
- Identify any injury
- Plan imaging in conjunction with trauma surgery
- Arrange disposition
- FAST Scan Ultrasound: focused assessment with sonography for trauma. To evaluate the hemodynamically unstable patient for hemoperitoneum, hemopericardium, or hemothorax
- X-Ray (portable): Chest, C-Spine, AP pelvis
- CT Scan: Who needs a CT?
- Nexus II: evidence of significant skull fracture, altered level of alertness, neurologic deficit, Persistent vomiting, presence of scalp hematoma, Abnormal behavior, Coagulopathy, age 65 years
Peds and Trauma
- Trauma is the most common cause of death in children older than 1 year
- Head trauma
- motor vehicle crash is the most common mechanism of injury
- Airway: can be challenging – they have a relatively larger tongue and more cephalad location of the larynx.
- Breathing:- early appearance of tachypnea and accessory muscle use in dyspneic patients. Nasal flaring, grunting, and retractions are other signs that should be noted.
- Circulation:- tachycardia is the most sensitive and earliest sign of volume loss; hypotension is a late and ominous finding.
- Disability: Determination of coma scoring in younger children is performed by using formal age-specific adaptations of the classic Glasgow Coma Scale.
- Exposure: greater risk for hypothermia after injury. Have external warming devices such as warming lights easily available and administration of warmed intravenous (IV) fluids
- Head injury: Early signs of intracranial injury also may be subtle or nonspecific in children. liberal use of noncontrast computed tomography (CT) is warranted
- spine injuries: The increased flexibility of the spine in children is responsible for the relatively lower incidence of spinal fracture in these patients. Children with multisystem trauma or with head trauma generally need neck immobilization and cervical spine imaging
- Chest trauma: radiographic identification of any rib fracture carries great significance as a sensitive indicator of underlying lung injury
- abdominal and GU trauma: CT is indicated in patients with a suspicious mechanism of injury, those who are symptomatic, or those with more than 20 red blood cells per high-power field on urinalysis
- Burns: recognition that the Rule of Nines may be inaccurate in estimating burn surface area in children
- Child abuse: markers for abuse include the presence of retinal hemorrhages, specific pattern injuries, and unexplained bruising or skeletal fractures in various stages of resolution or healing
Indications for transfer to Peds trauma center
- MOI: Ejected from a motor vehicle, Prolonged extrication, Death of other occupant in motor vehicle, Fall from greater distance than three times the child's height
- Anatomic injury: Multiple severe trauma, More than three long-bone fractures, Spinal fractures or spinal cord injury, Amputations, Severe head or facial trauma, Penetrating head, chest, or abdominal trauma
Peds compared to Geriatrics
- Falls are the most common cause of injury in patients older than 65 years
- Motor vehicle crashes rank as the most common mechanism for fatal incidents in elderly persons through age 80 years
- A normal tachycardic response to pain, hypovolemia, or anxiety may be absent or blunted in the elderly trauma patient.
- Medications such as -blockers may mask tachycardia and delay appropriate resuscitation
- Head injury: higher incidence of subdural hematomas. More liberal indications for computed tomography (CT) are justified
- spinal injuries: increased incidence of C1 and C2 fractures with the elderly
- chest trauma: incidence of rib fractures due to osteoporotic changes. hemopneumothorax, pulmonary contusion, flail chest, and cardiac contusion, can quickly lead to decompensation in elderly individuals whose baseline oxygenation status may already be diminished
- abdominal trauma: have a high index of suspicion for intraabdominal injuries in patients who have associated pelvic and lower rib cage fractures
- orthopedic injuries: pelvic and long bone fractures are often the sole etiology for hypovolemia in elderly patients
- Starts with confusion/delirium
- Cerebral metabolic rate for glucose
- Falls faster than rate for oxygen
- Reduced synthesis of neurotransmitters
- Neuronal cell death ensues
- Treatment with dextrose
Hypoxic Caused Coma
Increase in cell water, edema, death. Brain cells die within 5 minutes. Hyperbaric oxygen therapy
Uremic Caused Coma
- From renal failure.
- Accumulation of protein / amino acid metabolites.
- Changes in sensorium: Loss of memory, impaired concentration, depression, delusions, lethargy, irritability, fatigue, insomnia, psychosis, stupor, catatonia, and coma.
- Tx: Dialysis
Hepatic Caused Coma
- Associated with cirrhosis.
- Portal blood diverted to systemic circulation through portosystemic collateral vessels
- Neurotoxic substances: Ammonia (Not converted to urea. Level may be normal in some). GABA (Brain membrane more permeable to GABA in cirrhosis. Worse with meds that effect GABA (benzos). ? Flumazenil effective).
- Tx: Lactulose (Inhibits intestinal ammonia production. Patient needs to have 2-4 loose stools daily). Antibiotics (Metronidazole, neomycin, PO Vancomyacin. Decreases colonic concentration of ammonia producing bacteria).
Toxin Caused Coma
- Poisons: Lead, Cyanide, Carbon Monoxide
- To Drugs: Opiates, Benzodiazepines – GABA, Paralytics, Methylenedioxymethamphetamine (Ecstasy), Neuroleptics
Structural Caused Coma
- Stroke: Ischemic, Hemorrhagic
- Pork Tapeworm
Initial evaluation & management of patients with altered mental status.
- As with any emergency – ALWAYS CHECK THE ABC’S FIRST!
- Airway: Is gag reflex enough to assess the airway? Consider Intubation for GCS < 8
- Breathing: Supplemental Oxygen. Hyperventilation?? Hypocapnia actually increases cerebral vasoconstriction – BAD!
- Include a finger stick glucose
- Eight Elements of the neurological evaluation: Mental status, cerebral function, cranial nerves, motor examination, reflexes, cerebellar, gait
- Sensory Examination: Light touch, Pin Prick, vibration. Dermatome levels
- Motor Examination: Gauge strength in the various muscle groups. Measured in a graded scale - +1 to +5
- Reflexes: Biceps, Triceps, Patellar, Achilles
- Cerebellar: Rapid alternating hand movements. Finger to Nose
- Gait: Romberg Test, Heel to Toe Walking, Walking backwards
- Vital Signs
- Fevers: Meningitis, Encephalitis, Cerebral Abscess
- Hypertension: SAH, HTN headache
- Hypoxia: Altered Mental Status
- Brady / Tachycardia: Decreased Cerebral Perfusion
- Hypoglycemia: Altered Mental Status
- Medications used Emergently: Narcan (nalaxone) – opioid antagonist, Romazicon (flumazenil) – benzodiazepine antagonist, Thiamine – prevents Wernickes Encephalopathy, Dextrose (D50) – correct hypoglycemia, 1 amp of D50 is 25 grams of dextrose
- Total or near total unresponsiveness
- Inability to arouse the patient
Glasgow Coma Scale Eye Opening
- 4 – Opens spontaneously
- 3- Opens to voice
- 2- Opens to pain
- 1- Does not open
Glasgow Coma Scale Verbal
- 5 – Alert and Oriented
- 4 - Disoriented
- 3 - Speaking nonsense
- 2 - Moans
- 1 - No verbal response
Glasgow Coma Scale Motor
- 6 – Follows commands
- 5 - Localizes pain
- 4 - Withdraws from pain
- 3 - Decorticate posturing
- 2 - Decerebrate Posturing
- 1 - No response
Levels of AMS/coma
- Obtundation: Lethargic, blunted cognition. Awake but somnolent or slowed. Arousable
- Stupor: Asleep/semi comatose. Only arouses when stimulated. Reverts back to sleep when stimulus withdrawn
- Coma: eyes closed, unresponsive
- 0: No muscle contraction detected.
- 1: A trace contraction is noted in the muscle by palpating the muscle while the patient attempts to contract it.
- 2: The patient is able to actively move the muscle when gravity is eliminated.
- 3: The patient may move the muscle against gravity but not against resistance from the examiner.
- 4: The patient may move the muscle group against some resistance from the examiner.
- 5: The patient moves the muscle group and overcomes the resistance of the examiner. This is normal muscle strength.
Pseudo seizure – physical movement without EEG evidence of seizure
- Non-epileptic seizure
- Often associated with Conversion disorder, Panic disorder
- Check CK, Lactate. Should be elevated in true seizure
- May respond to saline placebo
- Grand Mal (Tonic-Clonic)
- Petit Mal
- Absence: Sudden LOC without loss of postural tone. No postictal state. May occur >100x/day. Typically found in school age children
- Focal Seizures: More localized in the brain
- Simple: No change in consciousness
- Complex: Consciousness affected. Temporal lobe seizures. Can be misdiagnosed as psychiatric problems
Evaluation of seizures
- New Onset: Should have full work up
- Existing: Check finger stick. Drug Levels (Phenytoin, Carbamazepine, Valproate, Phenobarbital)
Active Seizure Management
- Prevent Injury
- Maintain Oxygen
- Check drug levels
- Some patients have breakthrough seizures even if with therapeutic drug levels
- May need to load with drug to bring level to steady state
- Phenytoin – 10-20mg/kg load at max 25mg/min
- Fosphenytoin – can be given at 150mg/min
- 5 or more minutes of seizure activity
- The longer the seizure lasts, the more difficult it is to control
- Watch for non-convulsive status
- STOP THE SEIZURE!
- Morbidity due to hypoxemia, hyperthermia, circ collapse and neuronal death
- Intubate for airway control
- Benzodiazepines: Lorazepam, Diazepam
- Phenytoin: Load with 18-20mg/kg. Use Fosphenytoin for faster loading. Should be on a monitor for loading
- Phenobarbital: 20mg/kg. Third line agent
- If the are still seizing, General Anesthesia – knock them out! Phenobarb Coma. Propofol. Up to 30% of status epilepticus patient may go on to Refractory Status
- New Onset Seizure: Neurology consult. May start on AED. Often an out-patient workup
- Existing Seizure: If typical seizure and drug level low, OK to d/c home with close neurological follow up. For different seizure or therapeutic level, may need admission to optimize therapy
Special circumstances surrounding seizures
- ETOH Abuse: Withdrawal, Trauma, Electrolyte abnormalities, May need large doses of benzodiazepines
- Pregnancy: AED’s can cause birth defects, Eclampsia (Associated with hypertension, edema, proteinuria. Treatment is delivery of the fetus)
- Any disruption of blood flow to a local region of the brain.
- May be ischemic or hemorrhagic.
- Anterior Cerebral Artery: Contra lateral leg > arm weakness. Mild cortical sensory defects
- Middle Cerebral Artery: Contra lateral weakness/numbness. Face/arm > leg. May gaze toward affected side. If dominant hemisphere, aphasia may occur
- Posterior Cerebral Artery: May be dramatic or subtle. Dizziness, vertigo, diplopia, dysphagia, CN palsies
- Basilar Artery: Brainstem, cerebellum, visual cortex. Hallmark Findings are crossed neurological deficits and Ipsilateral cranial nerve with contra lateral motor weakness.
Locked in syndrome
- Complete and severe paralysis.
- Due to injury, tumor, or stroke to a portion of the pons
- Patients are completely paralyzed except for eye movements
- They are completely alert and aware of their surroundings
- Hx: Hypertension, CAD, DM, Previous TIA’s, Timing (very important)
- PE: Attempt to localize, LOC? Visual fields, Motor, Cerebellar, Sensation/Neglect, Language, Cranial Nerves
- Dx: Emergent CT Scan, May need 6 hours to see stroke on CT. MRI with water diffusion. Hemorrhages almost always visible, May need LP to rule out SAH if CT negative.
- Timing of when patient last seen normal is crucial for consideration of thrombolysis
- EKG for presence of arrhythmia
- Labs: CBC, Chem 7, PT/PTT, tox screen, ? Cardiac markers
- Other imaging: Echocardiogram, Carotid Ultrasound, MRI/MRA
- Airway !!
- Supplemental O2
- DO NOT lower BP unless > 180/100! Labetalol, NTG. Using Nipride will eliminate TPA use
- No dextrose solutions – usually do not need significant fluids
- Antiplatelet agents: Important for secondary stroke prevention
- Aspirin: 20 to 25% stroke reduction. Decreased platelet aggregation
- Dipyridamole: Inhibits platelet function. Aggrenox (combination of Dipyridamole and ASA)
- Clopidogrel: Expensive. Marginally better than ASA, 75mg daily
- Embolic: 20% of stroke. Fragment from remote site travels to brain. Cardiac source most common. Atrial Fib
- Thrombotic: Most common. Similar mechanism to MI
- Sub Arachnoid
- Head trauma in patients on anticoagulants
AHA stroke center guidelines
- When a patient presents with CVA symptoms
- Physician/PA to assess pt within 10 minutes
- CT done within 25 minutes
- CT read within 20 minutes
Thrombolysis Inclusion Criteria
- Age > 18 years
- Time of witnessed onset < 3 hours
Thrombolysis Exclusion Criteria
- Minor symptoms
- Rapidly improving
- Prior intracranial bleed
- Glucose <50, >400
- GI bleed w/in 21 days
- Surgery w/in 14 days
- BP > 185mmHG
- Previous CVA w/in 90 days
- INR > 1.7
- Heparin use w/in 48h
- Platelets < 100,000
- 0.9mg/kg, max dose 90mg
- 10% bolus, 90% given over 60 min
- No ASA or heparin in the first 24 hours after
Post rTPA Hypertension
- Must be treated aggressively to minimize complications
- Sodium Nitroprusside
TIA Neurologic Deficits:
- resolve within 24 hours
- Often within 30 minutes
- Extra-cranial carotid artery strokes may occur
- > 10% of pts with TIA will return with CVA within 90 days
- Many variants and presentations
- 5% male prevalence, 15% female prevalence.
- Aura: Caused by vasoconstriction. Smells, scotomas, paresthesias. Most migraines are not associated with Aura
- Headache: Slow onset -> last 4-72 hours. Unilateral, pulsating, photophobia. Rebound vasodilatation. Always ask if this is the typical migraine. Sometimes patients will state it is a migraine but never been diagnosed. Ophthalmologic Migraine (Cranial nerve involvement (CN III, IV, VI))
- Nausea and Vomiting can be severe. Difficult to take PO meds
- Tx: Ergotamine (DHE-45); Triptans 5-HT1D agonist. Cranial vasoconstriction. Peripheral neuronal inhibition (Sumitriptan, Zolmitriptan, Rizatriptan, Eletriptan); Dopamine antagonists (Metoclopramide, Prochlorperzine, Chlorpromazine); Ketorolac; Dexamthasone; Opioid use (Not recommended. Should be rescue only, not first line. May actually exacerbate headache. Beware of patients who are allergic to many of the non-opioid based treatments)
- May be a spectrum from tension to migraine
- Not really associated with muscle tension
- Bilateral, non-pulsating, without nausea or vomiting
- Treated with NSAIDS
- May use triptans or other agents if headache is severe
- Again, rule out life threatening causes
- More common in men
- Trigeminal nerve dysfunction (trigeminal neuralgia)
- Very severe unilateral, lancinating pain located orbital, periorbital, or temporal
- Conjuntival injection
- Facial swelling
- Can last from 15 min to 3 hours
- May occur daily for weeks (cluster)
- Treatment: High flow oxygen, DHE-45 and triptans given parenterally, NSAIDS for prevention
Headache Secondary Syndromes
- Critical causes: Vascular, CNS Infection, Tumor, Pseudo tumor Cerebri, Ophthalmic, Drug Related, Toxic (CO), Endocrine (Pheo), Metabolic
- Reversible causes: Non-CNS Infections, Dental, Sinusitis, Systemic, Post Lumbar Puncture
Syncope is a symptom:
- Transient self-limited loss of consciousness leading to falling
- Onset is relatively rapid
- Recovery is spontaneous, complete, and usually prompt.
- The underlying mechanism is a transient global cerebral hypoperfusion
Neurally-mediated reflex syncopal syndromes
- Vasovagal faint (common faint)
- Cardiac arrhythmias as primary cause
- Structural cardiac or cardiopulmonary disease
- when pt is standing or sitting
- Lasts 10 seconds to a few minutes
- lightheadedness, nausea, pallor, sweating, and blurred vision
- No postictal period
- Decrease in arterial pressure and HR produce CNS hypoperfusion
- Precipitated by: emotional upset, sight of blood, prolonged motionless standing (your surgical rotation), medical or surgical procedures
- Carotid sinus syncope
- Situational faint
- Acute hemorrhaging
- Coughing, sneezing
- Gastrointestinal stimulation (swallowing, defecation, visceral pain)
- Micturition (post-micturition)
- Others (instrument playing, weightlifting, postprandial)
- Autonomic failure
- Primary autonomic failure syndromes: multiple system atrophy, Parkinson’s disease with autonomic failure
- Secondary autonomic failure syndromes: diabetic neuropathy, amyloid neuropathy
- Drugs and alcohol
- Volume depletion
- Hemorrhaging, diarrhea, Addison’s disease
Cardiac arrhythmias as primary cause of Syncope
- Sinus node dysfunction (including bradycardia/tachycardia syndrome)
- Atrioventricular conduction system disease
- Paroxysmal supraventricular and ventricular tachycardias
- Inherited syndromes (e.g. long QT syndrome, Brugada syndrome)
- Implanted device (pacemaker, ICD) malfunction or drug-induced proarrhythmias
Structural cardiac or cardiopulmonary disease Cause of Syncope
- Cardiac valvular disease
- Acute myocardial infarction/ischaemia
- Obstructive cardiomyopathy
- Atrial myxoma
- Acute aortic dissection
- Pericardial disease/tamponade
- Pulmonary embolus/pulmonary hypertension
- Vascular steal syndromes
Evaluation of syncope
- H&P, ECG, orthostatics
- Imaging: CT chest or abdomen/pelvis, pelvic ultrasound
- Eval for blood loss
- GI, pelvic (ruptured ectopic pregnancy), or trauma
- Determine for related symptoms
- Cardiac arrhythmias (SVT, VT, Brady, prolonged QT, Sick sinus, Brugada’s)
- Abdominal or pelvic pain (GI, AAA, ectopic)
- Chest pain (MI, PE, tension PTX, dissection)
- Neuro symptoms (basilar artery insufficiency, migraine)
- Labs: CBC, chem 7, glucose
- Perception of movement
- Imbalance of sensory input: vestibular, visual, and proprioceptive systems
- Etiologies: Vestibular (Benign Paroxysmal Vertigo most common), Ménière’s, Paget’s, Neurologic
- Onset: sudden
- Severity: intense
- Pattern: paroxysmal, intermittent
- Worse with change in position: yes
- Nausea/Sweats: frequent
- Nystagmus: rotary-vertical, horizontal
- Fatigue of sx: yes
- CNS sx: absent
- Onset: sudden/slow
- Severity: less intense
- Pattern: constant
- Worse with change in position: variable
- Nausea/Sweats: variable
- Nystagmus: vertical
- Fatigue of sx: no
- CNS sx: usually present
Dix- Hallpike maneuver
- The test will likely provoke vertigo
- Patients need to keep their eyes open
- Rotary nystagmus is a positive test
- Vomit on your shoes is a positive test
Diff to distinguish from infarction
- Sudden onset of dizziness, vomiting, truncal ataxia, can’t walk
- May rapidly progress to coma and herniation
Subarachnoid hemorrhage (SAH)
- Focal findings typical
- Occurs more commonly in women
- Severe constant headache
- Famous words: “Worst headache of my life” (and you believe them!)
- usually occipital or nuchal in location
- Sentinel hemorrhage
- Vomiting, LOC
- Precipitating hypertensive event: Cough, Intercourse, Straining, defecation
- CT Brain: CT now 93% sensitive for SAH within first 24 hours. Negative CT does not exclude SAH. Much less sensitive after 24 hrs
- LP: Xanthocromia. Seen by spectrophotometry. Will be present 12 hours after bleed. Nearly 100% sensitive for up to 2 weeks after bleed
- Tx: Nimodipine Calcium Channel Blocker Reduces Cerebral Vasospasm; Phenytoin Prophylactic against seizures
- Emergent Neurosurgery consult
- HHH Therapy: Hypertensive, Hypervolemic, Hemodilutional
- Caused by tearing of the bridging veins
- Acceleration/deceleration injury
- Atrophied brains more susceptible
- Slow bleeding
- Can be acute, sub acute, or chronic
- Tearing of middle meningeal artery
- Does not cross suture lines
- Lucid interval following initial LOC
- Hypovolemic: Hemorrhagic, dehydration
- Distributive: Sepsis, Anaphylaxis, Neurogenic
DECREASED INTRAVASCULAR VOLUME
- Trauma: external or internal bleeding (hematoma, hemothorax, hemoperitoneum, placental abruption, etc)
- Atraumatic: GIB, Ruptured AAA, Ruptured aortic dissection, ruptured ectopic
Severe dehydration Shock
- Adrenal crisis
- Vomiting, diarrhea,
- hyperosmolar state
- Pancreatitis, ascites
- AKA “warm shock”
- Abnormal distribution of vascular volume
- Decreased vascular resistance, Increased permeability
- Same amount of fluid, but increased vascular compartment
- Classic examples: Sepsis, Anaphylaxis, Neurogenic
- Others: any other class of shock that is prolonged enough that vasoconstriction cannot be maintained
- Carbon Monoxide and cyanide
- Tachy or brady
- Pump failure (Decreased HR or Decreased contractility): AMI, CHF, Arrhythmias, Cardiomyopathy, Myocarditis, Ruptured Septum or papillary muscle, Acute aortic insufficiency, Myocardial Contusion, Prosthetic valve dysfunction
- Obstructive, Blocked blood flow into or out of the heart: Decreased ventricle filling (decreased preload) or Systemic obstruction. Tension pneumothorax, Pericardial Disease (tamponade), Pulmonary obstruction (massive PE), Cardiac disease (subacute bacterial endocarditis, valve disease
Stimulation of vascular baroreceptors results in:
- arteriole vasoconstriction: blood is shunted from skin, skin membranes, and vascular beds
- Venous constriction resulting in increased preload
- Increased HR and contractility
- Release of Epi, NE, Cortisol as well as ADH and stimulation of RAAS
- Body is able to continue to perfuse vital organs
- Blood shunted away from skin/muscle, then liver, kidneys
- Clinically: the diastolic pressure is increased, tachycardic, pale, diaphoretic, decreased urinary output
- Continued cellular impairment overwhelms the body’s ability to shunt
- Severe AMS, hypotension, death
Mild Blood Volume Loss < 20%
- Decreased perfusion to skin, fat, muscle, bone. Normal arterial pH.
- Patient feels cold. Postural hypotension, tachycardia. Cool, pale moist skin, collapsed neck veins, concentrated urine.
Moderate Blood Volume Loss 20-40%
- Decreased central perfusion (liver, gut, kidneys). Metabolic acidosis.
- Thirst. Supine hypotension and tachycardia. Oliguria, anuria.
Severe Blood Volume Loss > 40%
- Decreased perfusion to heart and brain, severe metabolic acidosis. Respiratory acidosis.
- Altered mental status. Hypotensive. Rapid deep respirations.
Develop an approach to assessing the cause of shock in a trauma patient.
- Shock in trauma is classified as hemorrhagic or nonhemorrhagic
- Almost all shock states respond completely or partially to volume resuscitation
- All shock in trauma is initially treated as if the patient was hypovolemic, but it is important to identify those who have other causes of shock
- Special care should be given to evaluate pts with injuries above the diaphragm (more likely to have myocardial injury, cardiac tamponade, or tension PTX causing obstruction)
- Follow ATLS guidelines (trauma is as easy as ABCDEFG)
Shock Primary survey:
- Airway: if the pt is obtunded (GCS<8) or too agitated to allow a physical exam then intubate the patient. C-spine immobilization
- Breathing: Equal breath sounds bilaterally, trachea midline, equal chest rise? consider PTX/hemothorax, tension PTX - needle decompress and chest tube as needed. Pain control for flail chest. Pulse ox, is the pt tachypneic? ABG/shock panel
- Circulation: Does the pt have pulses? (Radial pulse disappears with sbp<80, absent pulses give clues as to where vascular injuries have occurred). Tachycardia or Hypotensive? Is the pt loosing blood (onto the floor, into a body cavity)?
- Exposure: Pt must be completely undressed for careful examination, use warm fluids to prevent hypothermia, cover with blankets.
- Fingers and Foley
- Gastric decompression
- Along the way: Consider central line for access. Bolus 1-2L in an adult (20cc/kg peds). FAST scan if unstable, CT scan if stable. Stop external (compression) or internal hemorrhage, traction on long bone fractures may help. Shock panel, CBC, Chem 7, Type and Cross
- The initial step in managing shock is recognizing shock
- Clinical appreciation of decreased tissue perfusion and oxygenation
- Tachycardia: early sign (also a sign of pain)
- Narrowed pulse pressure
- Adrenergic responses: cool, diaphoretic, delayed capillary refill, agitated
- Altered mental status: anxiety, confusion, lethargy
- Hypotension: late sign due to compensation
- Any patient that is cool and tachycardic is in shock until proven otherwise
- The second step in the management of shock in trauma is determining the etiology.
- This is usually evident from the mechanism of injury
- Most injured patients in shock are suffering from hypovolemic shock (pts die bleeding out into their thorax, abd or pelvis).
- Trauma patients may also suffer cardiogenic shock (cardiac tamponade, myocardial contusions and MI)
- Think obstructive shock /Tension PTX with penetrating thoracic injury
- Neurogenic shock may occur from injury to spinal cord
- Septic shock may even be present with delayed presentation
Assessing shock without history of trauma.
- Appear ill, pale, diaphoretic, tachycardic, tachypneic.
- ill appearing or AMS
- RR>22 or PaCO2<32
- Hypotension for >20min
- Has the pt had evidence of GI bleed, vomiting, diarrhea?
- GI tract = hematemesis, melena, (NG tube, hemoccult)
- Ectopic Pregnancy = Young women, pelvic pain, vaginal bleeding, verified by ultrasound
- BhCG >1600 with no IUP = assume ectopic
- Treat with volume resuscitation
- Does the pt have abdominal or lower back pain?
- Sudden onset back/abdominal pain in a patient with hypertension – think Aortic Dissection
- Abdominal pain, distention, palpable abdominal mass – think ruptured AAA
- Rigid abdomen – think peritonitis
- If there is concern for ruptured AAA or peritonitis call surgery
- Pt may go to the OR on clinical basis alone.
- Support ABC’s
- If pt is stable, CT may be performed
- Does the pt have a fever or hypothermia?
- Sepsis is the #1 cause of ICU death
- Treatment is EGDT (early goal directed therapy) if sepsis. Search for source of infection to guide antibiotic therapy
- Is the pt wheezing with urticaria?
Cardiogenic & Obstructive Shock
- Does the pt have CP or SOB?
- Treat as cardiogenic shock from myocardial ischemia
- Treat ABC’s, has O2, IV, and cardiac monitoring right away, get an EKG and CXR
- Ensure adequate oxygenation and ventilation.
- Treat any emergent dysrhythmias per ACLS guidelines.
- If pharmacologic support fails, the pt needs to be in an ICU for intra-aortic balloon pump counter-pulsation (IABPC). This increases diastolic coronary perfusion which disrupts hypotension induced myocardial perfusion.
- ASA if no allergy
- Heparin and arrange for angioplasty
- Cardiogenic shock may also be caused by cardiac tamponade
- In trauma the etiology is most likely penetrating
- Large effusions may occur in patients with recent viral URI’s, TB, neoplasms, recent cardiac surgery, or chest radiation (among others).
- Symptoms are usually pleuritic chest pain and SOB
- Becks Triad: tamponade (muffled HS, JVD, hypotn)
- CXR shows enlarged cardiac silhouette
- Treatment = pericardiocentesis
- Is there persistent hypoxia?
- r/o PE with CT
- If too unstable, look for signs of right sided heart strain
- Bedside ultrasound shows dilated RV
- EKG may show S1,Q3,T3 if there is considerable R heart strain
- PE requires anticoagulation with heparin
- If pt is in shock they require thrombolytics
- Is the pt bradycardic?
- Look for ingestion of negative inotropic drug
- Consider addisonian crisis or steroid withdrawal
- Treatment for BB and CCB’s includes:
- IVF, glucagon, atropine and pacing as needed
- Treatment for adrenal insufficiency includes:
- Stress dose steroids
- Treatment for hypothyroidism includes:
- Treat hypothermia, thyroxine 500mg load, hydrocortisone
Treatment of hypovolemic shock.
- First bolus 1-2L LR or NS
- Then use Shock Classes to guide need for IVF and blood
- If level of consciousness or peripheral perfusion (HR, BP) does not respond appropriately, look for another cause of shock such as cardiac tamponade or tension PTX
- If aggressive resuscitation is not enough, the pt must go to the OR for operative control of hemorrhage
- If there is any fluid in the abdomen the pt requires laparotomy
- During resuscitation look at all the compartments where the pt may be loosing blood
Blood Loss: Chest
- can hold 2L in each hemithorax
- Has there been deceleration injury?
- Associated with Aortic Tears
- CXR – widened mediastinum
- Chest CT if stable
- Aortic angiography if stable
- Rib fractures and clavicle fractures may cause lung lacerations or vascular lacerations resulting in hemothorax
- Large bore chest tube. If >1500cc initially or >200cc/hr then OR
Blood Loss: Abdomen
- The abdomen can hide severe pathology
- Shock, normal chest x-ray, and no external bleeding = assume intra-abdominal/retroperitoneal hemorrhage
- Unstable = FAST (ultrasound); Cardiac, LUQ, RUQ, bladder
- Stable = Abdominal CT
Blood Loss: Pelvis/Retroperitoneum and thighs
- each thigh can hold 3-4L of blood
- Unstable pelvis – AP/LP iliac wings
- Significant hemorrhage
- MAST trousers
- Pelvic binder
- Tightly wrapped bedsheets
- Systemic infectious response (Early): 2+ of the following; Temp >38 or <36, Pulse >90 bpm, Respiratory rate >20 or PaCO2 < 32 mmHg, WBC >12,000 or <4,000 or >10% bands
- Sepis: SIRS + evidence of infection
- Severe Sepsis: evidence of organ dysfunction (AMS, oliguria, liver failure, ARDS) Usually has hypotension that is responsive to fluids.
- Severe Septic Shock: Sepsis that does not respond to fluid resuscitation
- MODS (multiple organ dysfunction)
- Cause: Massive histamine release from previously sensitized mast cells and basophils minutes after exposure to allergen
- Food (peanuts, shellfish, eggs)
- Envenomation (Hymenoptera stings)
- Medications (parenteral Penicillin, Bactrim)
- Actions of Histamine: Mucous membrane secretion, Increased bronchial smooth muscle tone, Decreased vascular muscle tone, Capillary, Urticarial skin lesions
- Clinical signs (variable): Early – apprehension, urticaria, cough, bronchospasm/hoarse/stridor. Severe – hypotension, AMS, incontinence, death
- Treat early – don’t let them sit in the waiting room
Anaphylactic Shock ABC’s
- Continuous oxygen monitoring: Supplemental oxygen 5-10 L/min prn
- ETT if needed & prepare for emergent cricothyrotomy just incase
- Epinephrine and antihistamines early
- albuterol if wheezing (bronchospasm).
- Steroids are used for persistent or delayed reactions
- Cardiac monitoring
- Bolus fluid if hypotensive
- If still hypotensive after 2L IVF, use IV epinephrine
Anaphylactic Shock Treatment
- Discontinue exposure: take out stinger, stop offending drug, etc.
- Pulse ox and O2 as needed
- Diphenhydramine: H1 blockers (25-50mg IV) [peds 1mg/kg]
- Ranitidine/Cimetidine (Zantac/Tagamet): H2 blockers (50mg/300mg any route) [peds zantac 0.5mg/kg]
- Methylprednisolone: corticosteroids for delayed or biphasic reaction, does not help with acute presentation (125mg)
- Epinephrine: (0.3-0.5mg 1:1000 IM) [peds 0.01mg/kg], 100mcg (0.1mL of 1:1000 or 1mL of 1 10:000) IV over 5-10min if persistently hypotensive, may require continuous infusion
- Albuterol neb: for wheezing
- Always inquire about drug allergies
- Use alternative agents whenever possible
- Pt’s may be admitted to the ICU for desensitization if no other drug choices are available
- Give parenteral medications slowly and observe for at least thirty minutes after injection
- Home kits: Epi-pen, anyone who goes home after a true allergic reaction should have an epi pen