Careful search for other significant injuries should be made
2 IV lines
ET intubation is a top priority
Restoration of adequate blood pressure is vital
Head CT and immediate neurosurgery consult
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
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
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
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
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
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);
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
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
Monitor any changes in the level of consciousness and associated physical signs throughout the entire exam
Glasgow Coma Scale (total=15 points)
Neuromuscular Junction: Myasthenia gravis
Weakness in all four limbs
UMN: Cervical or Brainstem
LMN: Polyradiculopathy, Peripheral Neuropathy
Unilateral limb weakness
Hemisection of cervical cord
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
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)
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
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
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
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
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)
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
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
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)
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!
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
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
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
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
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
Plain Films: Two views at least. Check entire film
Consider joint above & below injury
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.
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.
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
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
fluids: resuscitation, maintenance
Infection and swelling of the epiglottis
H. influenza, S. pyogenes, S. aureus, S. pneumonia
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
< 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?
Incarcerated inguinal hernia: Contents cannot be returned (reduced) to the abdominal cavity
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:
Acute chest syndrome
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
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
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
signs of cardiac tamponade (Beck's triad of hypotension, jugular venous distention, and muffled heart sounds)
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
D - Disability; abbreviated neuro exam
Moving all extremities
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
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
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.
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
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
Other imaging: Echocardiogram, Carotid Ultrasound, MRI/MRA
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
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
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
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
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
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
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.
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