Emergency Medicine Flashcards
What is the approach to posioning?
ABCD3EFG
- A Airway (consider stabilizing C-spine) - perform endotracheal intubation if unable to protect airway (aspiration imminent)
- B Breathing
- C Circulation
- D1 Drugs - ACLS as necessary to resuscitate the patient, universal antidotes
- D2 Draw bloods
- D3 Decontamination (decrease absorption)
- E Expose (look for specific toxidromes)/Examine the patient
- F Full vitals, ECG monitor, Foley, X-rays
- G Give specific antidotes and treatment
Essential tests for poisoning?
Essential tests:
- CBC, electrolytes, BUN/Cr, glucose, INR/PTT, osmolality
- ABGs, O2 sat +/- co-oximetry (if suspect CO poisoning)
- ASA, acetaminophen, EtOH levels
Other potential tests for poisoning?
- Drug levels – this is NOT a serum drug screen
- Ca2+, Mg2+, PO43–
- Protein, albumin, lactate, ketones, liver enzymes, CK – depending on drug and clinical feature
Ddx for increased AG metabolic acidosis?
“GOLDMARK”
- Glycols* (ethylene glycol, propylene glycol)
- Oxoproline (metabolite of acetaminophen)*
- L-lactate
- D-lactate (acetaminophen, short bowel syndrome, propylene glycol infusions for lorazepam & phenobarbital)
- Methanol*
- ASA*
- Renal failure
- Ketoacidosis (DKA, EtOH*, starvation)
What are the universal antidotes?
DON’T – Dextrose, Oxygen, Naloxone, Thiamine give before dextrose
Signs and symptoms of minor withdrawal from opioids?
Minor withdrawal may present as lacrimation, rhinorrhea, diaphoresis, yawning, piloerection, HTN, and tachycardia
Signs and symptoms of severe withdrawal from opioids?
Severe withdrawal may present as hot and cold flashes, arthralgias, myalgias, N/V, and abdominal cramp
A necessary cofactor for glucose metabolism; may worsen Wernicke’s encephalopathy if glucose given before
Thiamine
Ddx for increased osmolar gap?
“MAE DIE” (if it ends in “-ol”, it will likely increase the osmolar gap)
- Methanol
- Acetone
- Ethanol
- Diuretics (glycerol, mannitol, sorbitol)
- Isopropanol
- Ethylene glycol
Ddx for decreased AG?
- Electrolyte imbalance (increased Na+/K+/Mg2+)
- Hypoalbuminemia (50% fall in albumin ~5.5 mmol/L decrease in the AG)
- Lithium, bromine elevation
- Paraproteins (multiple myeloma)
Drugs/meds to consider if hypoventilating (high pCO2)?
CNS depressants (opioids, sedative-hypnotic agents, phenothiazines, EtOH)
Ddx for decreased AG?
- Carboxyhemoglobin
- Methemoglobin
- Sulfmethemoglobin
Ddx for normal AG?
- Renal HCO3- loss: renal tubular acidosis, hyperparathyroidism
- GI HCO3- loss: diarrhea, fistula
- Other: NS infusion, acetazolamide, hyperkalemia, hypoaldosteronism
Drugs/meds to consider if hyperventilating (low pCO2)?
Salicylates, CO, other asphyxiants
Drugs/meds to consider if hyperkalemic?
Hyperkalemia: Digitalis glycosides, fluoride, potassium
Drugs/meds to consider if hypokalemca?
Hypokalemia: Theophylline, caffeine, β-adrenergic agents, soluble barium salts, diuretics, insulin
Drugs/meds to consider if hypoglycemic?
Hypoglycemia: Oral hypoglycemic agents, insulin, EtOH, ASA
Drugs/meds to consider if wide QRS complex?
Wide QRS complex: TCAs, quinidine, other class Ia and Ic antidysrhythmic agents
Drugs/meds to consider if prolonged QT interval?
Prolonged QT interval: Terfenadine, astemizole, antipsychotics
Drugs/meds to consider if atrioventricular block?
Atrioventricular block: Ca2+ antagonists, digitalis glycosides, phenylpropanolamine
What to look for on abdominal Xray for poisoning?
“CHIPES”: Calcium, Chloral hydrate, CCl4, Heavy metals, Iron, Potassium, Enteric coated Salicylates, and some foreign bodies
Contraindications for single dose activated charcoal?
Unprotected airway, late presentation aer ingestion, small bowel obstruction, poor toxin adsorption
Indications for whole bowel irrigation?
- Awake, alert, can be nursed upright OR intubated and airway protected
- Delayed release product
- Drug/toxin not bound to charcoal
- Drug packages (if any evidence of breakage emergency surgery)
- Recent toxin ingestion
Contraindications for whole bowel irrigation?
Evidence of ileus, perforation, or obstruction
Indications/criteria for hemodialysis
Toxins that have high water solubility, low protein binding, low molecular weight, adequate concentration gradient, small volume of distribution, or rapid plasma equilibration
Toxidrome for anticholinergic?
- Hyperthermia “Hot as a hare”
- Dilated pupils “Blind as a bat”
- Dry skin “Dry as a bone”
- Vasodilation “Red as a beet”
- Agitation/hallucinations “Mad as a hatter”
- Ileus “The bowel and bladder “
- Urinary retention, Tachycardia
Toxidrome for cholinergic?
“DUMBELS”
- Diaphoresis, Diarrhea, Decreased BP
- Urination
- Miosis
- Bronchospasm, Bronchorrhea, Bradycardia
- Emesis, Excitation of skeletal muscle
- Lacrimation
- Salivation, Seizures
Toxidrome for extrapyramidal?
- Dysphonia, dysphagia
- Rigidity and tremor
- Motor restlessness, crawling sensation (akathisia)
- Constant movements (dyskinesia)
- Dystonia (muscle spasms, laryngospasm, trismus, oculogyric crisis, torticollis)
Toxidrome for symphathomimetic?
- Increased temperature
- CNS excitation (including seizures)
- Tachycardia, HTN
- N/V
- Diaphoresis
- Dilated pupils
Toxidrome for serotonin syndrome?
Mental status changes, autonomic hyperactivity, neuromuscular abnormalities, hyperthermia, diarrhea, HTN
Toxidrome for opioid, sedative/hypnotic/EtOH?
- Hypothermia
- Hypotension
- Respiratory depression
- Dilated or constricted pupils (pinpoint in opioid)
- CNS depression
What should be done for exposing and examining the poisoned patient?
- Vital signs (including temperature), skin (needle tracks, colour), mucous membranes, pupils, odours, and CNS
- Head-to-toe survey including
▪ C-spine
▪ Signs of trauma, seizures (incontinence, “tongue biting”, etc.), infection (meningismus), or chronic alcohol/drug misuse (track marks, nasal septum erosion)
▪ Feel the patient’s axillae; in the average patient, should be somewhat moist (if dry, may indicate anticholinergic toxicity) - Mental status
Treatment for acetaminophen overdose?
- Decontaminate (activated charcoal)
- N-acetylcysteine - NAC protocol
Antidote for bentos?
Flumazenil
Treatment for B blockers overdose?
- Consider decontamination (activated charcoal, consider whole bowel irrigation for extended-release ingestion)
- IV glucagon, IV calcium chloride, IV high-dose insulin (with dextrose), IV intralipid
Treatment for insulin IM/SC/Oral hypoglycemic overdose?
- Glucose IV/PO/NG tube
- Glucagon: 1-2 mg IM (if no access to glucose)
Etiology of chest injuries
- Aortic disruption
- Blunt cardiac injury
- Cardiac tamponade
- Flail chest
- Hemothorax
- Pneumothorax (traumatic pneumothorax, open pneumothorax, and tension pneumothorax)
- Pulmonary contusion
Definition of tension pneumothorax
Clinical diagnosis; One-way valve causing accumulation of air in pleural space
Physical exam of tension pneumothorax
Respiratory distress, tachycardia, distended neck veins, cyanosis, asymmetry of chest wall motion, Tracheal deviation away from pneumothorax, Percussion hyperresonance Unilateral absence of breath sounds
Management of tension pneumothorax
Needle thoracostomy – large bore needle, 2nd ICS mid clavicular line, followed by chest tube in 5th ICS, anterior axillary line
Definition of open pneumothorax
Open connection from pleural space to the atmosphere; air preferentially enters through the chest would rather than through the airway
Physical exam of open pneumothorax
Gunshot or other wound (hole >2/3 tracheal diameter) ± exit wound, Unequal breath sounds, subcutaneous emphysema
Management of open pneumothorax
Air-tight dressing sealed on 3 sides, Chest tube, Surgery
Definition of massive hemothorax?
> 1500 cc blood loss in chest cavity
Physical exam of massive hemothorax?
Pallor, flat neck veins, shock Unilateral dullness, Absent breath sounds, Hypotension
Investigations of massive hemothorax?
Usually only able to do supine CXR – entire lung appears radioopaque as blood spreads out over posterior thoracic cavity
Management of massive hemothorax?
- Restore blood volume, Chest tube
- Thoracotomy if: >1500 cc total blood loss ≥200 cc/h continued drainage
Definition of flail chest?
Free-floating segment of chest wall due to >2 rib fractures, each at 2 sites Underlying lung contusion (cause of morbidity and mortality)
Physical exam of flail chest?
Paradoxical movement of flail segment, Palpable crepitus of ribs Decreased air entry on affected side
Investigations of flail chest?
- ABG: decreased pO2, increased pCO2
- CXR: rib fractures, lung contusion
Management of flail chest?
- O2 + fluid therapy + pain control
- Judicious fluid therapy in absence of systemic hypotension
- Positive pressure ventilation ± intubation and ventilation
Definition of cardiac tamponade?
Clinical diagnosis; Pericardial fluid accumulation impairing ventricular function
Physical exam of cardiac tamponade?
- Penetrating wound (usually), Tachycardia, tachypnea, Pulsus paradoxus, Kussmaul’s sign (increased JVP with inspiration)
- Beck’s triad
Investigations of cardiac tamponade?
Echocardiogram, FAST
Management of cardiac tamponade?
IV fluids, Pericardiocentesis, Open thoracotomy
Physical exam of pulmonary contusion?
Blunt trauma to chest Interstitial edema impairs compliance and gas exchange
What is Beck’s triad?
Hypotension, distended neck veins, muffled heart sounds
Investigations of pulmonary contusion?
CXR: areas of opacification of lung within 6 h of trauma
Management of pulmonary contusion?
Maintain adequate ventilation Monitor with ABG, pulse oximeter, and ECG, Chest physiotherapy, Positive pressure ventilation if severe
Physical exam of ruptured diaphragm
Blunt trauma to chest or abdomen (e.g. high lap belt in MVC)
Investigations of ruptured diaphragm
CXR: abnormality of diaphragm/lower lung fields/ NG tube placement. CT scan and endoscopy: sometimes helpful for diagnosis
Management of ruptured diaphragm
Laparotomy for diaphragm repair and associated intra- abdominal injuries
Physical exam of esophageal injury
Usually penetrating trauma (pain out of proportion to degree of injury)
Investigations of esophageal injury
CXR: mediastinal air (not always), Esophagram (Gastrograffin®), Flexible esophagoscopy
Management of esophageal injury
Early repair (within 24 h) improves outcome but all require repair
Definition of aortic tear
90% tear at subclavian (near ligamentum arteriosum), most die at scene. Salvageable if diagnosis made rapidly
Physical exam of aortic tear
Sudden high speed deceleration (e.g. MVC, fall, airplane crash), complaints of chest pain, dyspnea, hoarseness (frequently absent). Decreased femoral pulses, differential arm BP (arch tear)
Investigations of aortic tear
CXR, CT scan, transesophageal echo, aortography (gold standard)
CXR findings of aortic tear
ABC WHITE
- Depressed left mainstem Bronchus
- pleural Cap
- Wide mediastinum (most consistent) Hemothorax
- Indistinct aortic knuckle
- Tracheal deviation to right side
- Esophagus (NG tube) deviated to right
Management of aortic tear
Thoracotomy (may treat other severe injuries first)
Indications for trauma thoracotomy
- Resuscitative thoracotomy is a temporizing measure that allows direct control of hemorrhage from exsanguinating thoracic injures or decompression of cardiac tamponade and allows control of the aorta to limit bleeding from infradiaphragmatic injuries to facilitate resuscitation.
- Hemodynamically unstable from chest injury
- Hemothorax with >1500cc output from chest tube
- Hemothorax with ongoing blood loss from chest tube (200cc/hr for 2-4 hours)
- Resuscitative thoracotomy (aka ED thoracotomy) – rarely indicated – almost always on penetrating traumas
Indications for tube thoracostomy
- Pneumothorax
- Hemothorax
- Open sucking chest wound
- Trauma Code
What should be asked on history for spinal trauma?
- Mechanism of injury, previous deficits, SAMPLE
- Neck pain, paralysis/weakness, paresthesia
Physical exam of spinal trauma?
- ABCs
- Abdominal: ecchymosis, tenderness
- Neurological: complete exam, including mental status , reflexes
- Spine: maintain neutral position, palpate C-spine; log roll, then palpate T-spine and L-spine, assess rectal tone (voluntary anal sphincter contraction)
- When palpating, assess for tenderness, muscle spasm, bony deformities, step-off, and spinous process malalignment
- Extremities: check capillary refill, suspect thoracolumbar injury with calcaneal fractures
Investigations for spinal trauma
- Bloodwork: CBC, electrolytes, Cr, glucose, coagulation profile, cross and type, toxicology screen
- Imaging:
- Full C-spine x-ray series for trauma (AP, lateral, odontoid)
- Thoracolumbar x-rays: AP and lateral views
Indications for thoracolumbar x-rays
- C-spine injury
- Unconscious patients (with appropriate mechanism of injury)
- Neurological symptoms or findings
- Deformities that are palpable when patient is log rolled
- Back pain
- Bilateral calcaneal fractures (due to fall from height) – concurrent burst fractures of the lumbar or thoracic spine in 10% (T11-L2)
- Consider CT (for subtle bony injuries), MRI (for soft tissue injuries) if appropriate
According to Canadian C Spine rules what are the high-risk factor that mandates radiography
- Age ≥ 65 yr
- Dangerous mechanism
- Paresthesias in extremities
What is considered a dangerous mechanism according to Canadian C Spine rules
- Fall from ≥1 meter / 5 stairs
- Axial load to head (e.g. diving)
- MVC high speed (>100 km/h), rollover, ejection
- Motorized recreational vehicles
- Bicycle collision
Can clear C-spine if
- Oriented to person, place, time, and event
- No evidence of intoxication
- No posterior midline cervical tenderness
- No focal neurological deficits
- No painful distracting injuries (e.g. long bone fracture)
Low-risk factor that allows safe assessment of ROM according to Canadian C Spine rules?
- Simple rear-end MVC excluding: • Pushed into on coming traffic • Hit by bus/large truck • Rollover • Hit by high-speed vehicle - Sitting position in ED - Ambulatory at any time - Delayed onset of neck pain - Absence of midline C-spine tenderness
Stabilization and initial evaluation of cord injury?
- Immobilize, ABCs
- Inserting NG and Foley catheter
- Hypotension: maintain sBP >90 mmHg with pressors (dopamine), hydration, and atropine
- Monitor CBC/electrolytes
- Signs of autonomic dysfunction
- Radiographic evaluation
- Continually reassess high cord injuries as edema can travel up cord
- If cervical cord lesion, watch for respiratory insufficiency
Signs of autonomic dysfunction
Altered level of perspiration, bowel or bladder incontinence, priapism
Low cervical transection (C5-T1) produces
Abdominal breathing (phrenic innervation of diaphragm still intact but loss of innervation of intercostals and other accessory muscles of breathing)
High cervical cord injury (above C4) may require
Intubation and ventilation
3-view C-spine series?
- Lateral C1-T1 +/- swimmer’s view
- Odontoid view: space between lateral mass of C1 and odontoid should be equal, the lateral aspects of the lateral masses should be less than 1mm
- AP view: alignment of spinous processes in the midline
Approach to cervical spine radiograph?
- Adequacy: Must see C1 to C7-T1 junction
- Alignment – anterior spinal line, posterior spinal line, spinolaminar line
- Line extending inferiorly from clivus should transect odontoid
- Atlanto-axial articulation, widening of predental space (normal: <3 mm in adults, <5 mm in children) indicates injury of C1 or C2
- Bodies
- Cortical outline - fractures
- Disk spacing – should be the same heights - wedging anteriorly or posteriorly suggests vertebral compression
- Edges and soft tissues – prevertebral soft tissue thickness C2/3 <7mm (1/3 of the vertebrae body width), C6 <22mm (1 vertebral body width). Increase in this space may be due to hematoma or infection
Fanning of spinous processes suggests
Posterior ligamentous disruption
Signs and symptoms of cauda equina syndrome?
Cauda Equina Syndrome can occur with any spinal cord injury below T10 vertebrae. Look for incontinence, anterior thigh pain, quadriceps weakness, abnormal sacral sensation, decreased rectal tone, and variable reflexes
Treatment of spinal cord injury?
- Warm blanket, Trendelenburg position (occasionally), provide airway support, fluids
- Monitoring and controlling BP - atropine (for bradycardia), vasopressors for BP support
What is spinal shock?
Transient loss of all neurologic function below the level of the SCI, causing flaccid paralysis and areflexia for variable periods
What should you watch out for in acute phase of SCI?
- Spinal shock
- Neurogenic shock
What is neurogenic shock?
Hypotension that follows SCI (sBP usually <80 mmHg)
What causes neurogenic shock?
- Interruption of sympathetics (unopposed parasympathetics) below the level of injury
- Loss of muscle tone due to skeletal muscle paralysis below level of injury - venous pooling (relative hypovolemia)
- Blood loss from associated wounds (true hypovolemia)
What should be watched for in neurogenic shock?
Hypotension (lacking SNS), bradycardia (unopposed PNS), poikilothermia (lacking SNS so no shunting of blood from extremities to core)
Signs and symptoms of autonomic dysreflexia?
Pounding headache, nasal congestion, feeling of apprehension or anxiety, visual changes, dangerously increased sBP and dBP
Common triggers of autonomic dysreflexia?
- GU causes: bladder distention, urinary tract infection, and kidney stones
- GI causes: fecal impaction or bowel distension
What should you watch out for in chronic phase of SCI?
Autonomic dysreflexia: in patients with an SCI at level T6 or above
What are the two categories of TBI?
- Open head injuries involve penetration of the scalp and skull (and usually the meninges and underlying brain tissue)
- Closed head injuries typically occur when the head is struck, strikes an object, or is shaken violently, causing rapid brain acceleration and deceleration. Acceleration or deceleration can injure tissue at the point of impact (coup), at its opposite pole (contrecoup), or diffusely; the frontal and temporal lobes are particularly vulnerable to this type of injury.
Types of TBI?
- Concussion
- Hematoma: Acute subdural hematoma, Chronic subdural hematoma, epidural hematoma
- Diffuse axonal injury
- Skull Fractures: Vault fracture, Basal skull fractures
Definition of concussion?
Transient mental status alteration (eg, loss of consciousness or memory) lasting < 6 hours
CT findings of acute subdural hematoma?
Hyperdensity in subdural space, classically crescent-shaped. Degree of midline shift important
Symptoms of chronic subdural hematoma?
Gradual headache, somnolence, confusion, sometimes with focal deficits or seizures
CT findings of chronic subdural hematoma?
Hypodensity in subdural space (abnormality is isodense during subacute transition from hyperdense to hypodense)
CT findings of epidural hematoma?
Hyperdensity in epidural space, classically lenticular-shaped and located over the middle meningeal artery (temporal fossa) due to a temporal bone fracture
How does diffuse axonal injury occur?
Occurs when rotational deceleration causes shear-type forces that result in generalized, widespread disruption of axonal fibers and myelin sheaths
CT/MRI findings of diffuse axonal injury?
- CT: At first, may be normal or show small hyperdensities (microhemorrhages) in corpus callosum, centrum semiovale, basal ganglia, or brain stem
- MRI: Multiple small microhemorrhages in deep white matter or subcortical areas and brain stem
Which type of vault fracture has increased risk of infection and requires surgical debridement within 24 h?
Open, depressed
Linear, non-depressed vault fractures typically occur where?
Typically occur over temporal bone, in area of middle meningeal artery (commonest cause of epidural hematoma)
Symptoms and signs of TBI?
- Lose consciousness (usually for seconds or minutes), although some patients with minor injuries have only confusion or amnesia (retrograde amnesia)
- Young children may simply become irritable.
- Seizures, often within the first hour or day.
- After these initial symptoms, patients may be fully awake and alert, or consciousness and function may be altered to some degree, from mild confusion to stupor to coma
Epidural hematoma symptoms?
- Increasing headache
- Decreased level of consciousness
- Focal neurologic deficits (eg, hemiparesis)
- Some patients who have an epidural hematoma lose consciousness, then have a transient lucid interval, and then gradual neurologic deterioration.
Acute subdural hematoma symptoms?
- Headache
- Seizures
- Hemiparesis
- Symptoms of increased ICP
- Pupillary asymmetric, abnormal brain stem reflexes, and coma from brain stem compression due to uncal herniation
Markedly increased ICP classically manifests as a combination of the following (called the Cushing triad):
- Hypertension (usually with increased pulse pressure)
- Bradycardia
- Respiratory depression
Signs of Basal Skull Fracture?
- Battle’s sign (bruised mastoid process)
- Hemotympanum
- Raccoon eyes (periorbital bruising)
- CSF rhinorrhea/otorrhea
Long-term symptoms of TBI?
- Postconcussion syndrome
- A range of cognitive and neuropsychiatric deficits can persist after severe, moderate, and even mild TBI, particularly if structural damage was significant. Common problems include
- Amnesia
- Behavioral changes (eg, agitation, impulsivity, disinhibition, lack of motivation)
- Emotional lability
- Sleep disturbances
- Decreased intellectual function
- Late seizures (> 7 days after the injury)
- Persistent vegetative state can result from a TBI that destroys forebrain cognitive functions but spares the brain stem.
What are the symptoms of postconcussion syndrome
Persistent headache, dizziness, fatigue, difficulty concentrating, variable amnesia, depression, apathy, and anxiety. Commonly smell (and thus taste), sometimes hearing, or rarely vision is altered or lost. Symptoms usually resolve spontaneously over weeks to months.
Symptoms of late seizures from TBI?
Spastic motor impairment, gait and balance disturbances, ataxia, and sensory losses may occur.
Persistent vegetative state can result from a TBI that destroys _____ functions but spares the brain stem.
Forebrain cognitive
Persistent vegetative state symptoms/findings?
The capacity for self-awareness and other mental activity is absent; however, autonomic and motor reflexes are preserved, and sleep-wake cycles are normal. Few patients recover normal neurologic function when a persistent vegetative state lasts for 3 months after injury, and almost none recover after 6 months.
Classification of TBI?
- 14 or 15 is mild TBI
- 9 to 13 is moderate TBI
- 3 to 8 is severe TBI
Definition of mild TBI?
- Transient alteration in mental status that may involve loss of consciousness
- Loss of consciousness (if present) must be less than 30 min, initial GCS must be between 13-15, and post-traumatic amnesia must be less than 24 h
Treatment of minor head injury (GCS 13-15)?
- Close observation over 24-48h
- Wake every hour
- Judicious use of sedatives or pain killers during monitoring period
- Follow Return to Play guidelines
According to the Canadian CT Head Rule; CT Head is only required for patients with minor HI with any one of the following HIGH RISK?
- GCS score <15 at 2h after injury
- Suspected open or depressed skull fracture
- Any sign of basal skull fracture (hemotympanum, “raccoon” eyes, CSF otorrhea/rhinorrhea, Battle’s sign)
- Vomiting >2 episodes
- Age >65 yr
Treatment of moderate (GCS 9-12) and severe head injury (GCS <8)?
- Clear airway and ensure breathing; intubate if necessary
- Secure C-spine
- Maintain adequate BP
- Monitor for clinical deterioration
- Monitor and manage increased ICP if present
Admission required for TBI if:
- Skull fracture (indirect signs of basal skull fracture
- Confusion, impaired consciousness, concussion with >5min amnesia
- Focal neurological signs, extreme H/A, vomiting, seizures
- Unstable spine
- Use of alcohol
- Poor social support
According to the Canadian CT Head Rule; CT Head is only required for patients with minor HI with any one of the following MEDIUM RISK?
- Amnesia before impact >30min (i.e. cannot recall events just before impact)
- Dangerous mechanism (pedestrian struck by MVC, occupant ejected from motor vehicle, fall from height >3 ft or five stairs)
Questions asked on history during assessment of brain/head injury?
- Period of LOC, post-traumatic amnesia, loss of bowel/bladder control, loss of sensation, weakness, type of injury/accident
- In urgent situations, remember “SAMPLE-F”: signs/symptoms, allergies, medications, past medical history, last meal, events leading up to the trauma, and baseline functioning
Physical exam of brain/head injury?
- ABCs
- Vital signs: Shock (not likely due to isolated brain injury, except in infants), Cushing’s response to increasing ICP (bradycardia, HTN, irregular respirations)
- GCS
- Brainstem reflexes (if appropriate)
- Cranial nerve exam
- Motor and sensory exam, including peripheral reflexes
- Spine (pain/tenderness, palpable deformity)
- Sphincter tone and saddle sensation
- Record and repeat neurological exam at regular intervals, as appropriate
Severity of brain/head injury determined by?
- LOC
- GCS <8 intubate, any change in score of 3 or more = serious injury
- Mild TBI = 13-15, moderate = 9-12, severe = 3-8 - pupils: size, anisocoria >1 mm (in patient with altered LOC), response to light
- lateralizing signs (motor/sensory)
- May become subtler with increasing severity of injury
- Reassess frequently
Investigations of brain/head injury?
- Assume C-spine injury until ruled out
- C, T, L spine x-rays
- Labs: ABG, cross and type, CBC, electrolytes, INR/PTT, glucose, toxicology screen
- CT scan head and neck (non-contrast) to exclude intracranial hemorrhage/hematoma
Management of brain/head injury?
- General
- ABCs
- Ensure oxygen delivery to brain through intubation and prevent hypercarbia
- Maintain BP (sBP >90)
- Treat other injuries - Early neurosurgical consultation for acute and subsequent patient management
- Seizure treatment/prophylaxis
- Benzodiazepines, phenytoin, phenobarbital
- Steroids are of no proven value
Management of brain/head injury with suspected raised ICP?
- Intubate
- Calm (sedate) if risk for high airway pressures or agitation
- Paralyze if agitated
- Hyperventilate (100% O2) to a pCO2 of 30-35 mmHg
- Elevate head of bed to 20o
- Adequate BP to ensure good cerebral perfusion
- Diurese with mannitol 1g/kg infused rapidly (contraindicated in shock/renal failure)
Definition of neurologically brain death?
- Irreversible and diffuse brain injury resulting in absence of clinical brain function
- Cardiovascular activity may persist for up to 2wk
Criteria of diagnosis for neurologically brain death?
- Prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug intoxication/poisoning, temperature >32oC, no electrolyte/acid-base/endocrine disturbance
- Absent brainstem reflexes: pupillary light reflex, corneal reflexes, oculocephalic response, caloric responses (e.g. no deviation of eyes to irrigation of each ear with 50 cc of ice water - allow 1 min after injection, 5 min between sides), pharyngeal and tracheal reflexes, cough with tracheal suctioning, absent respiratory drive at PaCO2 >60 mmHg, >20 mmHg rise above baseline, and pH <7.28 (apnea test)
- 2 Evaluations separated by time, usually performed by two specialists (e.g. anesthetist, neurologist, neurosurgeon)
- Confirmatory testing: flat EEG, absent perfusion assessed with cerebral angiogram
Definition of hypothermia?
Hypothermia is defined as a core temperature below 35C, in which the body’s heat loss is greater than heat production
Ddx of hypothermia?
- Decreased heat production
- Endocrine (hypopituitarism, hypothyroidism, adrenal insufficiency)
- Insufficient fuel (hypoglycemia, malnutrition)
- Neuromuscular inactivity (age, impaired shivering) - Impaired thermoregulation
- Central: Metabolic (cirrhosis, uremia), Drug/OD (barbiturates, phenothiazines, tricyclics, insulin), CNS (stroke, trauma, SAH, Parkinsonism, hypothalamic dysfunction, MS)
- Peripheral (spinal cord transection, neuropathy, DM, neuromuscular disease) - Increased heat loss
- Accidental/immersion hypothermia (exposure to cold air, water)
- Vasodilatation (drugs, EtOH, tox, sepsis)
- Skin disorders (burns, exfoliative dermatitis)
- Iatrogenic (cold infusion)
Questions to ask on history for hypothermia?
Concomitant EtOH/other tox, Hx of previous illness, namely thyroid disease, CV/Resp dis- ease, neuromuscular or CNS disease, endocrinologic etiologies such as adrenal insufficiency, and hypopituitarism
Monitors for hypothermia?
ECG, rectal thermometer, Foley catheter, NG tube, monitor metabolic status frequently
Investigations for hypothermia?
- Labs: CBC, electrolytes, ABG, serum glucose, Cr/BUN, Mg2+, Ca2+, amylase, coagulation profile, TSH
- Imaging: CXR (aspiration pneumonia, pulmonary edema are common)
Classification of hypothermia?
- Mild (32-34.9C)
- Moderate (28-31.9C)
- Severe (<28C)
Symptoms of mild hypothermia
Tachypnea, tachycardia, ataxia, dysarthria, shivering
Symptoms of moderate hypothermia
Loss of shivering, dysrhythmias, Osborne (J) waves on ECG, decreased LOC, combative behaviour, muscle rigidity, dilated pupils
Symptoms of severe hypothermia
Coma, hypotension, acidemia, VFib, asystole, flaccidity, apnea
What is passive external re-warming?
Involves covering patient with insulating blanket; body generates heat and re-warms through metabolic process, shivering
Who is passive external re-warming suitable for?
Suitable for most stable patients with core temperature >32.2°C
What is active external re-warming?
Involves use of warming blankets, heating pads – to thorax, bath immersion >40C
What is after drop phenomenon?
Warming of extremities causes vasodilation and movement of cool pooled blood from extremities to core, resulting in a drop in core temperature leading to cardiac arrest
Who is active core re-warming suitable for?
Generally for patients with core temperature <32.2°C, and/or with cardiovascular instability
Re-warming techniques for active core re-warming
- warmed humidified oxygen, IV fluids
- peritoneal dialysis with warm fluids
- gastric/colonic/pleural irrigation with warm fluids
- external circulation (cardiopulmonary bypass machine) is most effective and fastest
What are the re-warming options for hypothermia?
- Passive external re-warming
- Active external re-warming
- Active core re-warming
Definition of frostbite?
Damage to tissues from freezing due to the formation of ice crystals within cells, rupturing the cells and leading to cell death
Classification of frostbite?
- 1st degree
- 2nd degree
- 3rd degree
- 4th degree - extension into subcuticular, osseous, and muscle tissues
Signs and symptoms of first degree frostbite?
- symptoms: initial paresthesia, pruritus
- signs: erythema, edema, hyperemia, no blisters
Signs and symptoms of 2nd degree frostbite?
- symptoms: numbness
- signs: blistering (clear), erythema, edema
Signs and symptoms of 3rd degree frostbite?
- symptoms: pain, burning, throbbing (on thawing); may be painless if severe
- signs: hemorrhagic blisters, skin necrosis, edema, no movement
Management of frostbite?
- Treat for hypothermia: O2, IV fluids, maintenance of body warmth
- Remove wet and constrictive clothing
- Immerse in 40-42C agitated water for 10-30min (very painful; administer adequate analgesia)
- Clean injured area and leave it open to air
- Consider aspiration/debridement of blisters (controversial)
- Debride skin
- Tetanus prophylaxis
- Consider penicillin G as frostbite injury has high risk of infection
- Surgical intervention may be required to release restrictive eschars
- Never allow a thawed area to re-chill/freeze
Definition of near-drowning?
Survival following submersion in a liquid and subsequent distress requiring medical attention
Questions on ask on history for near-drowning?
- Elicit a Hx of the events surrounding the submersion and if resuscitative measures were started.
- Determine the quality of the liquid in which the patient was submerged-mud, sewage, and particulates significantly increases the risk of developing ARDS and pulmonary infections.
- Try to discover the relative temperature of the liquid into which the patient was submerged.
Physical exam for near-drowning?
- ABCs, vitals: watch closely for hypotension
- Respiratory: rales (ARDS, pulmonary edema), decreased breath sounds (pneumothorax)
- CVS: murmurs, dysrhythmias, JVP (CHF, pneumothorax)
- H&N: assess for C-spine injuries
- Neurological: GCS, pupils, focal deficits
Investigations of near-drowning?
- Labs: CBC, electrolytes, ABGs, Cr, BUN, INR, PTT, U/A (drug screen, myoglobin) - >50% have renal dysfunction due to lactic acidosis and hypoperfusion; may develop rhabdomyolysis
- Imaging: CXR (pulmonary edema, pneumothorax) ± C-spine imaging
- ECG
Symptoms of near-drowning?
Anxiety, vomiting, wheezing, and altered consciousness are common. Patients may have respiratory failure with tachypnea, intercostal retractions, or cyanosis. Respiratory symptoms are sometimes delayed for up to 8 hours after submersion.
____ is the major insult in drowning, affecting the brain, heart, and other tissues; respiratory arrest followed by cardiac arrest may occur
Hypoxia
Brain hypoxia may cause cerebral edema and, occasionally, permanent neurologic sequelae
Fluid aspiration, especially with particulate matter or chemicals, may cause ____ or ____ and may impair alveolar secretion of surfactant, resulting in patchy atelectasis.
Chemical pneumonitis
Secondary bacterial pneumonia
Hypothermia can be protective by stimulating the mammalian ____.
Diving reflex
What is the diving reflex?
Slowing the heart rate, and constricting the peripheral arteries, shunting oxygenated blood away from the extremities and the gut to the heart and brain
Treatment of near-drowning?
- ABCs, treat for trauma, shock, hypothermia - rewarm
- Cardiac and O2 monitors, IV access
- Intensive respiratory care: Ventilator assistance if decreased respirations, pCO2 >50 mmHg, or pO2 <60 mmHg on maximum O2. May require intubation for airway protection, ventilation, pulmonary toilet
- Dysrhythmias: usually respond to corrections of hypoxemia, hypothermia, and acidosis
- Vomiting: very common, NG suction to avoid aspiration
- Convulsions: usually respond to O2; if not, diazepam 5-10mg IV slowly
- Bronchospasm: bronchodilators
- Bacterial pneumonia: prophylactic antibiotics not necessary unless contaminated water or hot tub (Pseudomonas)
Always initiate CPR in drowning – induced cardiac arrest even if patient _____; continue CPR until patient is fully rewarmed (restored to 32-35)
Hypothermic
Definition of anaphylaxis?
An exaggerated immune mediated IgE hypersensitivity reaction that leads to systemic histamine release, increased vascular permeability, and vasodilation
Etiology of anaphylaxis?
- Drugs (eg, beta-lactam antibiotics, insulin, streptokinase, allergen extracts)
- Foods (eg, nuts, eggs, seafood)
- Proteins (eg, tetanus antitoxin, blood transfusions)
- Animal venoms
- Latex
Pathophysiology of anaphylaxis?
Interaction of antigen with IgE on basophils and mast cells triggers release of histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction (eg, resulting in bronchoconstriction, vomiting, or diarrhea) and vasodilation with plasma leakage (eg, resulting in urticaria or angioedema).
S/S of anaphylaxis?
- Skin: generalized urticaria (hives), angioedema
- Airway: wheezing, swelling of the throat
- CNS: Anxiety, headache, confusion
- CVS: chest pain, low blood pressure
- GI Tract: N/V, diarrhea, abdominal cramping
Management of a moderate anaphylactic reaction?
- Epinephrine (1:1000) 0.3-0.5 mg (IM in anterolateral thigh)
- Antihistamines: diphenhydramine (Benadryl) 25-50 mg PO/IV
- Salbutamol (Ventolin) 1 cc via MDI
Management of a severe anaphylactic reaction?
- ABCs, may need definitive airway (e.g. ETT) due to airway edema
- Epinephrine (1:1000) 1-10 ug/min IV (or via ETT if no IV access) titrated to desired effect
- Antihistamines: diphenhydramine (Benadryl) 50 mg IV (~1 mg/kg)
- Glucocorticoids: methylprednisolone 125-250 mg IV or prednisone/prednisolone 40-60 mg PO
- Large volumes of crystalloid may be required
