LeFort Fracture

Fracture of the midface involving the base of the skull resulting from high impact injury. May be associated with
dental fracture or other facial fractures.
Type I horizontal maxillary fracture involving the dental alveolar ridge floating plate. Occurs at lower velocity (eg hit).
Loose teeth, dental fractures.
Type II pyramidal pattern fracture involving the pterygoid plate and/or sphenoid bone. Swelling, midface deformity,
periorbital oedema, mobility of upper jaw and nose. Epistaxis, CSF rhinorrhea.
Type III horizontal/transverse fracture with craniofacial dislocation involving the nasal bone, maxillary bone &
zygomatic arch. Face sunken in, craniofacial dissociation, epistaxis, CSF rhinorrhoea and ottorhea,

Coronal view
Fracture of pterygoid plates bilaterally
Le Fort Type II fracture

Traumatic brain injury (TBI) [Tinti pg 1683]

Brain function impairment that results from external force.
Mild GCS 14-15; Moderate 9-13; Severe GCS ≤8
Pathophys: CEREBRAL BLOOD FLOW Autoregulation, cerebral perfusion pressure (CPP), mean arterial pressure (MAP),
and intracranial pressure (ICP) affect cerebral blood flow. CPP = MAP – ICP. Autoregulation adjusts to accommodate
CPPs from 50 to 150 mm Hg in order to maintain local cellular oxygen demands & regional cerebral blood flow. In
brain injury, autoregulation is often impaired, so small drops in blood pressure can decrease brain perfusion causing
cellular hypoxia. Maintain a MAP of ≥80 mm Hg because low BP in the setting of ↑ ICP will result in a low CPP and
brain injury.
Munroe-Kelly doctrine cranium is an enclosed space with a fixed volume. Any changes to the volume of the
intracranial contents (e.g., bleeding) affect the ICP, and an increase in ICP can decrease the CPP. ICP is determined by
the volume of the three intracranial compartments: brain parenchyma (<1300 mL), CSF (100 to 150 mL), and blood
(100 to 150 mL). When one compartment expands, there is compensatory reduction in the volume of another, and/or
the baseline ICP will increase. Elevations in ICP are life threatening and may lead to Cushing reflex (HTN, bradycardia,
and respiratory irregularity). Hypertension is a compensatory attempt to maintain cerebral perfusion.
PRIMARY BRAIN INJURY: Contusions (bruises to brain parenchyma), hematomas (subdural, epidural,
intraparenchymal, intraventricular, and subarachnoid), diffuse axonal injury (stress or damage to axons), direct cellular
damage (neurons, axons, and other supportive cells), loss of the blood–brain barrier, disruption of the neurochemical
homeostasis, and loss of the electrochemical function.
SECONDARY BRAIN INJURY: Secondary neurotoxic cascade is a massive release of neurotransmitters, causes ongoing
damage to the brain and ultimately results in a poorer neurologic outcome than might have occurred based on the
original mechanism.
PECARN Rules [Tinti pg 700]
Used to identify pediatric pts at low risk of intracranial injury with GCS of 14-15 who do not need a CT. If all six
predictor variables are negative, the risk of a clinically important traumatic brain injury is so low that a CT scan is not
necessary.
<2 Normal mental status
Normal behaviour per routine
caregiver
No LOC
No severe mechanism of injury
No non-frontal scalp hematoma
No evidence of skull fracture
2-18 yrs Normal mental status
No LOC
No severe mechanism of injury
No vomiting
No severe headache
No signs of basilar skull fracture
Traumatic Bleeds [Tinti pg 1689]

CT Findings Anatomic Common Cause Symptoms

Location
Epidural Biconvex, Potential space Skull fracture with Immediate LOC with a “lucid” period
Young, rare in football-shaped between skull tear of the middle prior to deterioration (only occurs in
the elderly and hematoma and dura mater meningeal artery about 20%)
those age <2 y
Subdural Crescent- or Space between Acceleration- Acute: rapid LOC, lucid period
More risk in the sickle-shaped dura mater and deceleration with possible
elderly and hematoma arachnoid tearing of the Chronic: altered mental state and
alcoholic bridging veins behavior with gradual decrease in
patients consciousness
Subarachnoid Blood in the Subarachnoid Acceleration- Mild, moderate, or severe traumatic
basilar cisterns deceleration with brain injury with meningeal signs
and hemispheric tearing of the and symptoms
sulci and fissures subarachnoid
vessels
Intracerebral May be normal Usually anterior Severe or Symptoms range from normal to
initially with temporal or penetrating LOC
delayed bleed posterior frontal trauma; shaken
lobe baby syndrome

Syncope (362)
Brief loss of consciousness accompanied by loss of postural tone that resolves without medical intervention.
Pathophys: Cerebral hypoperfusion:

SPINE INJURIES [Tinti pg 1697]

Pathophys: Primary injury from mechanical forces that directly traumatize the spinal cord and vasculature,
characterized by hemorrhage into the cord and formation of edema at the injured site and surrounding region. This
insult sets into motion a series of vascular and chemical processes that lead to secondary injury. Local spinal cord
ischemia ensues secondary to vasospasm and thrombosis of the small arterioles within the gray and white matter.
Extension of edema may further compromise blood flow and increase ischemia. A later tissue degeneration phase
begins within hours of injury

NEXUS Criteria [pg 1710] Canadian C-Spine Rule

• Absence of midline cervical tenderness Assessment
• Absence of focal neurologic deficit Assessment #1:
• Normal level of alertness and consciousness* There are no high-risk factors that
• No evidence of intoxication mandate radiography.
• Absence of painful distracting injury†
Assessment #2:
There are low-risk factors that allow a
safe assessment of range of motion.
Assessment #3:
The patient is able to actively rotate
his/her neck (regardless of pain).
Definitions
High-risk factors include:
Age 65 years or older
A dangerous mechanism of
injury*
The presence of
paresthesias in the
extremities
Low-risk factors include:
Simple rear-end motor
vehicle crashes
Patient able to sit up in the
ED
Patient ambulatory at any
time
Delayed onset of neck pain
Absence of midline cervical
tenderness
Can rotate neck 45 degrees
to the left and to the righ
 Jefferson # burst fracture of the C1 ring due to axial loading (vertical
compression) driving the lateral masses apart and downwards over the dens of
C2, potentially unstable [pg 1701]
This is best seen as outward displacement of the lateral masses on the open-
mouth odontoid radiograph or on CT.
If displacement of both lateral masses (measured as offset from the superior
corner of the C2 vertebral body on each side) is >7 mm when added together,
rupture of the transverse ligament is likely, and the spine is unstable.

Teardop # Extreme hyperflexion causes complete disruption of the spinal

ligaments at the level of injury.
The “teardrop” is the anteroinferior portion of the vertebral body that is
separated and displaced from the vertebral body by the anterior spinal ligament.
“Fanning” of the spinous processes may be present, with or without fracture. A
sagittal fracture through the vertebral body may be seen on CT.
Associated with anterior spinal cord syndrome.

Clay shoveler # is a spinous process avulsion # caused by forceful cervical flexion

combined with contraction of paraspinous muscles.
Most commonly seen in lower cervical and upper thoracic spine.

Chance # vertebral fracture, usually lumbar, involving the posterior

spinous process, pedicles and body. Caused by forced flexion, seen in lap
belt injuries.
Radiographic findings include posterior vertebral wall fracture, increased
height of the posterior vertebra,,minor anterior vertebral compression
and “fanning” of the spinous processes.
 Hangman # disruption of the posterior arch of C2 with bilateral pedicle
fracture and anterior subluxation of the body of C2 on C3, due to
hyperextension.
Traumatic spondilolisthesis
Unstable fracture.
The large spinal canal at C2 means there is usually no neurologic injury.

Cord Syndromes [Tinti pg 1709]

Anterior Cord syndrome due to anterior cord compression causing loss of function in the anterior 2/3 of the spinal
cord from damage to corticospinal & spinothalamic tracts. Leads to ipsilateral loss of voluntary motor function
(paralysis) and loss of pain and temperature sensation below the level of the injury. Potentially reversible, poor
prognosis. Associated with teardrop #.

Central Cord syndrome hyperextension injury or disruption of blood flow to spinal cord causing injury to central
portion corticospinal and spinothalamic tracts. Causes quadriparesis, greater in ULs, some loss of pain and
temperature. Usually seen in older pts with cervical stenosis.

Brown-Séquard syndrome injury due to a hemisection of the spinal cord, usually from penetrating trauma. Ipsilateral
loss of motor (corticospinal), proprioception & vibratory sense (posterior) and contralateral loss of pain and
temperature (spinothalamic tract)

Cauda Equina syndrome injuries to nerve roots at L2 and lower, causing peripheral nerve injuries.
Unilateral radicular pain, absent knee& ankle reflexes. Saddle anaesthesia, bowel and bladder dysfunction, lower limb
motor and sensory loss, ↓reflexes & sciatica.

Reduction techniques for anterior shoulder dislocation

Scapular Manipulation (80% to 100% successful)
 Upright or prone
 In upright position, the patient is sitting up, may rest unaffected shoulder against upright head of bed
 Stand behind patient and use one thumb over tip of scapula and push medially while pushing acromion
inferiorly with the other thumb
 Assistant simultaneously provided traction by grabbing patient’s wrist with one hand and flexed elbow with
other hand and pushing down on elbow
 The reduction may be subtle, without obvious “clunk.”
 Reduced risk of associated fractures
External Rotation Technique
The external rotation technique reduces anterior glenohumeral dislocation by overcoming spasm of the internal
rotators of the humerus, unwinding the joint capsule, and enabling the external rotators of the rotator cuff to pull the
humerus posteriorly.
 Easy and can do alone
 With patient supine, elbow flexed to 90 degrees, elbow held with one hand, and wrist is held with another
hand
 Slowly, have patient allow the arm to fall to the side, externally rotating forearm. The patient pauses with
pain and allows muscles to relax. Over 5 to 10 minutes, the arm externally rotates, and reduction occurs
 Reduction usually occurs with arm externally rotated between 70 to 110 degrees
Cunningham Technique
 Patient is seated with examiner seated in front of patient, and the patient places ipsilateral hand on top of
examiner’s shoulder
 The clinician rests one arm in patient’s elbow crease and uses the other hand to massage the patient’s biceps,
deltoid, and trapezius muscles
 Have patient relax and instruct to pull their shoulder blades together and straighten their back
 Popular technique now since rarely conscious sedation needed
Milch Technique (add Milch technique if external rotation unsuccessful)
  Patient is supine, fingers over the shoulder with thumb in axilla to stabilize
 Arm is externally rotated and then abducted over patient’s head while maintaining external rotation with
simultaneously placing direct pressure over the humeral head
Stimson Technique
 No assistant needed and no need for conscious sedation
 Patient is prone with affected arm hanging off the side of bed with 5 lb (2.3 kg) to 15 lb (6.8 kg) of weight
 Reduction is usually achieved within 30 minutes
Traction Countertraction
 A sheet is wrapped under the axilla, and one assistant provides continuous traction at the wrist or elbow
while the other provides countertraction with the sheet from the opposite side
Spaso Technique
 Patient is supine while examiner grasps wrist or distal forearm and lifts vertically with gentle vertical traction
and external rotation
Fares Technique
 Patient is supine with upper extremity at their side
 The examiner holds patient’s wrist and gently pulls the arm to provide traction
 The arm is abducted while continuously moving arm in anteriorly and posteriorly in small oscillating
movements (about 10 cm)
 If shoulder has not reduced by 90 degrees of abduction, add external reduction
Fulcrum Technique
 Patient is supine or sitting, and a rolled towel or sheet is placed in axilla
 The distal humerus is adducted with simultaneous posterolateral force on the humeral head
 Requires increased force, may have increased complications
Kocher’s and Hippocratic Techniqueoot placed in patient’s axilla before traction) no longer recommended due to
higher risk of complications
Posterior Shoulder Reduction
 The patient is in the supine position. An assistant applies anterior pressure to humeral head while examiner
applies axial traction to the humerus with internal and external rotation of humerus

Back Pain [Tinti pg 1884]

Differential
Mechanical Nonmechanical Visceral disease
1. Acute nonspecific back pain 1. Malignancy 1. AAA
2. Chronic nonspecific back pain 2. Infection
3. Low back pain with Sciatica 3. Inflammatory arthritis
4. Disk herniation
5. Spinal Stenosis
6. Epidural Compression
syndrome
7. Transverse myelitis
8. Spinal infection

RED FLAG FEATURE Possible cause Imaging

Age > 50yrs Fracture, malignancy LS spine Xray
Trauma Fracture LS spine Xray
Fever, IV drug use, recent infection Infection MRI
Unexplained blood loss, Hx of cancer Metastases LS spine Xray
Urinary retention, motor deficits, saddle Cauda equina syndrome MRI
anaesthesia, fecal incontinence
Progressive motor weakness Myelopathy MRI
Failure to improve after 1 month Fracture, malignancy LS spine Xray
Immunosuppression or steroid use Fracture, infection LS spine Xray, MRI or CT
Midline spinal tenderness Fracture, infection, malignancy LS spine Xray

Young-Burgess classification is a classification system for pelvic ring fractures. It takes into account force type,
severity, and direction, as well as injury instability. Three basic mechanistic descriptions are used, each with degrees of
severity.
Anteroposterior compression (APC)
 APC I: stable
 o pubic diastasis <2.5 cm
 APC II: rotationally unstable, vertically stable
o pubic diastasis >2.5 cm
o disruption and diastasis of the anterior part of the sacroiliac joint, with intact posterior sacroiliac joint
ligaments
 APC III: equates to a complete hemipelvis separation (but without vertical displacement); unstable
o pubic diastasis >2.5 cm
o disruption-diastasis of both anterior and posterior sacroiliac joint ligaments with dislocation

Lateral compression (LC). Most common type.

 LC I: stable
o oblique fracture of pubic rami
o ipsilateral anterior compression fracture of the sacral ala
 LC II: rotationally unstable, vertically stable
o fracture of pubic rami
o posterior fracture with dislocation of the ipsilateral iliac wing (crescent fracture)
 LC III: unstable
o ipsilateral lateral compression (LC)
o contralateral anteroposterior compression (APC)

Vertical shear (VS)

Most severe and unstable type with a high association of visceral injuries.
 vertical displacement of hemipelvis, pubic and sacroiliac joint fractures

Combined
Stability depends on the individual components of this injury.
 complex fracture, including a combination of anteroposterior compression (APC), lateral compression (LC), and/or
vertical shear (VS)
Finger

Infected tenosynovitis Flexor tendon sheath infection.

Kanavel signs: Flexor sheath infection are a finger held in slight flexion, fusiform swelling of the affected digit,
tenderness along the flexor tendon sheath, and pain with passive extension of the digit.

Wrist Fractures
Colles Fracture – FOOSH
 extra-articular distal radial metaphysis fracture
 dorsal angulation, Displaced dorsally and proximally
 May have dorsal comminution
 May have ulnar styloid # with injury to triangular fibrocartilonage complex (needs CT)
 Dinner fork deformity
 Median nerve injury = palmar parasthesia
 Unstable if angulation >20o, intra-articular involvement

Smith’s fracture (reverse Colles) -

Barton Fracture - intra-articular distal radius fracture with dorsal displacement/angulation
Reverse Barton Fracture - intra-articular distal radius fracture with volar displacement/angulation
Die-Punch Fracture - fracture of the articular surface with depression of the lunate facet
Chauffer’s Fracture - avulsion fracture of the radial styloid
Distal Radioulnar Joint (DRUJ) disruption- injury to the sigmoid notch of the radius and the lunate facet
Triangular Fibrocartilage Complex (TFCC) tear - damage to the cartilaginous structure on the ulnar aspect of the wrist
Galeazzi Fracture - distal 1/3 radial # with disruption/dislocation of the distal radioulnar joint (DRUJ)
 Concurrent Ulnar Styloid fracture is common
 Caused by FOOSH with flexed elbow or direct blow
Distal Leg Fractures
 Tibial plateau fracture
 Tibial shaft fracture
 Pilon fracture
 Maisonneuve fracture
o Fibula fracture (anywhere from head or as far down as 6cm above ankle joint)
o Deltoid ligament rupture or medial malleolus avulsion fracture
o Injury then directed upward and laterally tearing interosseous membrane and anterior inferior tibiofibular
ligament
o May involve posterior tibiofibular ligament or posterior malleolar fracture
o TTX: Long leg posterior splint with reduction of medial ankle and syndesmotic clear space
 Tibia fracture (peds)
 Ankle fracture
 Tillaux fracture
 Foot and toe fractures

Foot and Toe Fractures

Hindfoot
 Talus fracture
 Calcaneus fracture
Midfoot
 Lisfranc injury
 Navicular fracture
 Cuboid fracture
 Cuneiform fracture
Forefoot
 Fifth metatarsal fracture
 Non-fifth metatarsal fracture
 Toe fracture

Clinical Features
 Examine for ecchymoses, abrasions, or swelling
 Vascular and neurologic assessment
o DP and PT pulses
o 4 sensation distributions: saphenous nerve (medial mal), superficial fib (lat mal), sural nerve (lateral 5th
digit), deep fib (1st web space)
 Note skin integrity and areas of tenderness or
crepitus over ankle
 Range joint passively and actively to evaluate for
stability
 Examine joints above and below the ankle
 Perform anterior drawer test (positive exam
suggests torn ATFL)
 Always palpate entire length of fibula to rule-
out Maisonneuve Fracture (fibulotibialis ligament
tear)
o crossed-leg test to detect syndesmotic injury
 Evaluate integrity of Achilles tendon (Thompson
test)
 Palpate midfoot and base of 5th metatarsal for
tenderness
Compartment Syndrome [Tinti pg 1876]
Ludwig's angina originates as a dental infection of the second or third mandibular molars, including partially erupted
third molars [1]. The infection begins in the subgingival pocket and spreads to the musculature of the floor of the
mouth. It progresses below the mylohyoid line, indicating that it has moved to the sublingual space. As the roots of
the second and third mandibular molars lie below this line, infection of these teeth will predispose to Ludwig's angina.
The infection spreads lingually rather than buccally because the lingual aspect of the tooth socket is thinner. It initially
spreads to the sublingual space and progresses to the submandibular space.

The disease is usually polymicrobial, involving oral flora, both aerobes and anaerobes. The most common organisms
are Staphylococcus, Streptococcus, Peptostreptococcus, Fusobacterium, Bacteroides, and Actinomyces.
Immunocompromised patients are at higher risk of Ludwig's angina.

UROLOGY
Phimosis
Inability to retract the foreskin proximally and posterior to the glans penis
Physiological in newborn, resolves by 5 yrs
Pathological causes include: Poor hygiene, infection, injury
Complications
1. Scarring at tip of penis can occlude the meatus causing
 Foreskin to balloon during urination
 Dribbling of entrapped urine
 Urinary retention
Treatment: topical steroids bd for 4-8 wks
Paraphimosis
True urologic emergency
Inability to reduce the proximal edematous foreskin distally over the glans penis.
If not reduced compromise of arterial supply may lead to necrosis of the glans.
Treatment: Reduce by compressing the glans for several minutes to reduce edema and then slide foreskin over glans.
If not successful use 21 gauge needle to puncture foreskin & compress to drain edema. Dorsal slit as last resort
Complications:
1. Infection
2. Ischemia/Necrosis

Fournier’s gangrene: a form of necrotizing fasciitis, is a rapidly progressive disease that affects the deep and
superficial planes of the perineal and genital region.
DD: Scrotal abscess, Scrotal edema, Epididimoorchitis
Etiology: gram-positive: Group A Streptococci and Staphylococcus aureus and gram-negative bacteria: E.
Coli and Pseudomonas aeruginosa
Bacterial infection involves an initial insult such as a urinary tract infection, perineal abscess, recent surgical
manipulation of the genital or perineal area. Spread of inflammation and infection along fascial planes and adjacent
soft tissue leads to thrombosis of blood vessels, which in turn leads to ischemia and necrosis of the adjacent soft
tissue and fascia.
US: scrotal wall thickening & dirty shadowing suggestive of air in tissues
CT: better evaluation, findings include fascial thickening, subcutaneous air, and fluid collections such as an abscess
Treatment: Piperacillin-tazobactam 4.5 gr IV qid OR Imipenem 1 gr IV od OR Clindamycin 600-900 gr IV tid
Refer to Urology & Admit

Penile Fracture
Urological emergency
Traumatic rupture of the tunica albuginea and one or both of the corpora cavernosa of the erect penis
Clinical Features: Cracking, snapping, or popping sound caused by rupturing of the tunica albuginea and soft tissue
Immediate detumescence (loss of erection)
Pain; varies in intensity depending on severity of the injury
Soft tissue swelling, curving, hematoma of the penis (“eggplant” appearance with intact Bucks fascia)
Butterfly appearance in violated Buck’s fascia with Colles fascia intact
Blood at the urethral meatus, urinary retention, gross hematuria in concomitant urethral injury
Retrograde urethrography to check for urethral injury
Urology referral & Sx treatment
Complications: Abnormal curvature of the penis, Erectile dysfunction, Painful erection, Urethral stenosis
Penile Block
Dorsal penile nerve provides most of the somatosensory innervation to the shaft and glans penis.
Indications: minor painful procedures of the penis, such as paraphimosis reduction, dorsal slit procedure, or zipper
entrapment release.
Using a 25- or 27-gauge needle, inject lidocaine hydrochloride without epinephrine into the base of penis, at the
junction between the penis and the suprapubic skin, off the midline to avoid the superficial dorsal vein. Inject the
lidocaine just deep to the Buck fascia, which is located 3 to 5 mm beneath the skin.
A slight “pop” is usually felt as the needle passes through the fascial layer. Aspirate before injecting the lidocaine,
because the dorsal arteries and veins are within close proximity to the nerve. Depending on the size of the child,
between 1 and 5 mL of lidocaine should be used. Half of the volume is injected at the 10 o’ clock position, with the
other half injected at the 2 o’ clock position.
Another technique involves injecting only once at the midline through the Buck fascia, with injection of the full volume
directed toward each direction after negative aspiration of blood.
Optimal analgesia is achieved after 5 minutes.

Micturition: a spinal reflex modulated by CNS.

RAAS

SIADH
Syndrome of Inappropriate secretion of anti-diuretic hormone (vasopressin) results from abnormally high ADH levels
from the posterior pituitary. Produced in hypothalamus, stored in posterior pituitary. Binds to the V2 receptors in the
kidney tubules in the collecting duct. Unregulated ADH release causes Na + to drop as more excess free water is
retained (antidiuresis). Leads to concentrated urine.
Myocardial Infarction
Acute myocardial ischemia due to imbalance between O2 demand and supply with reduction in myocardial blood flow
due to coronary arterial spasm, microvascular dysfunction, disruption or erosion of atherosclerotic plaques, and
platelet aggregation or thrombus formation. Plaque fissuring and rupture, when plaque rupture occurs, potent
thrombogenic substances activate circulating platelets. This leads to platelet aggregation. Adherent platelets are
strongly thrombogenic.
In stable angina, ischemia occurs only when activity induces O2 demands beyond the supply restrictions imposed by a
partially occluded coronary vessel. Ischemia occurs at a relatively fixed point and changes slowly over time. In this
scenario, the atherosclerotic plaque has not ruptured, and there is little or no superimposed thrombus.
In ACS, atherosclerotic plaque rupture and platelet-rich thrombus develop. Coronary blood flow is reduced suddenly,
and myocardial ischemia occurs. The degree and duration of the O2 supply–demand mismatch determine whether the
patient develops reversible myocardial ischemia without necrosis (unstable angina) or acute myocardial ischemia with
necrosis. More severe and prolonged obstruction increases the likelihood of infarction.
Wellens syndrome (pg 339)
A syndrome characterized by unstable angina in combination with deeply inverted or biphasic T waves in leads V₂-V₃
on ECG. Caused by severe, proximal stenosis of the left anterior descending artery.

Eclampsia
Eclampsia is defined as the new onset of generalized tonic-clonic seizures or coma in a woman with preeclampsia
Pathphys: Abnormal placentation which leads to inadequate invasion of the cytotrophoblasts, and poor remodeling of
the spiral arteries, which reduces the blood supply to the placenta. Abnormal blood supply leads to increased uterine
arterial resistance and vasoconstriction, which ultimately produces placental ischemia and oxidative stress. Free
radicals and cytokines, are released as a direct result of oxidative stress, leading to endothelial damage, affecting
cerebral endothelium. Elevated blood pressure from preeclampsia causes dysfunction of autoregulation of the
cerebral vasculature, which causes hypoperfusion, endothelial damage, or edema.
Ttx IV MgSO4 4-6 gr in 100 mls over 20-30 min then IVI 2 gr/hr for 24 hrs.
Labetalol 20 mg IV – selective ά & non-selective β antagonist
Hydralazine 5 mg IV –arterial vasodilator attaches to receptors in arterial endothelium, NO released and smooth muscle relaxes.
Nifedipine 10 mg PO – Calcium channel agonist
PROMPT DELIVERY

Central Nervous System Control of Breathing

The brain’s connection to respiration relates to two forms of breathing: spontaneous breathing and voluntary control.
These forms of breathing are controlled by mechanisms involving:
 Brainstem respiratory centers
 Central chemoreceptors: respond to changes in the pH (hydrogen ion content) of CSF (cerebrospinal fluid), the
result of arterial paCO2 concentration.
 Peripheral receptors respond to PaO2 (carotid baroreceptors)
 Voluntary control (breath holding, sighing, etc) can override breathing through the cerebral cortex
Respiratory Failure

Type 1 Hypoxemic Type 2 Hypercapneic

Definition Respiratory failure characterized by Respiratory failure characterized hypercapnia
hypoxemia and normocapnia or and normoxemia or hypoxemia on arterial blood
hypocapnia on arterial blood gas analysis gas analysis
PaO2 ↓ (< 60 mmHg) Normal or ↓ (< 80 mm Hg)
PaCO2 Normal or ↓ (< 33 mm Hg) ↑ (> 50 mmHg)
Pathophysiology V/Q mismatch and shunt decrease in alveolar ventilation due to reduction
in overall (minute) ventilation or an increase in
the proportion of dead space ventilation
Causes Cardiogenic pulmonary edema drug overdose, neuromuscular disease, chest
Noncardiogenic pulmonary edema wall abnormalities, and severe airway disorders
Pneumonia (eg, asthma and chronic obstructive pulmonary
Pulmonary haemorrhage disease [COPD])
Pulmonary contusion (flail chest)
Pulmonary arterial hypertension
Clinical Features Tachypnea, dyspnea Hypoventilation
Cyanosis Headache, daytime sleepiness
Pleuritic chest pain Anxiety
Tachycardia, arrhythmia Warm extremities
Confusion, somnolence Papilledema
Asterixis
Coma
Paralytic ileus

Noninvasive positive-pressure ventilation (NIPPV),

Allows the delivery of air or a mixture of oxygen combined with other gases by positive pressure into the lungs
without the use of an endotracheal tube. Positive pressure is beneficial in hypercapneic respiratory failure by
decreasing the work of breathing, allowing a larger tidal volume for a given respiratory effort, and hence improving
alveolar ventilation. In place of the tube is a tight-fitting nasal or facial mask that is attached to a continuous positive
airway pressure (CPAP), a bilevel positive airway pressure (BiPAP) machine or Average volume-assured pressure
support (AVAPS).
Indications Hypercapneic respiratory failure
Hypoxemic respiratory failure
Circulatory failure
Contraindications: The need for intubation
Encephalopathy or altered mental status
Hemodynamic instability
Facial trauma or facial defects
Airway obstruction secondary to a mass
Anticipated need for prolonged mechanical ventilation
Gastrointestinal bleeding
Complications: Ventilator-associated pneumonia,
Barotrauma,
Volutrauma
Gastric insufflation
Reduction in preload to the heart secondary to increased intrathoracic pressure
Sepsis is the life-threatening condition with organ dysfunction caused by dysregulated host response to an infection.
Septic shock is part of sepsis where circulatory abnormalities and cellular metabolism occur. Septic shock is mainly
characterised by hypotension, with the patient still requires a vasopressor to maintain MAP ≥65mmHg, or blood
lactate levels >2mmol/L after fluid resuscitation.

Positive if any 2 criteria are present

PANCREATITIS
Caused by the premature activation of trypsinogen to trypsin within the acinar cell as opposed to in the duct lumen.
This leads to which activates enzymes such as elastase and phospholipases. Early activation of these zymogens leads
to localized tissue damage.
Etiology: Alcohol use, Gallstones, Hypertriglyceridemia, Idiopathic, Drug-induced pancreatitis, Post-procedural (ERCP).
moderate to severe abdominal pain located in the epigastrium with nausea and anorexia, may radiate to back.
Ttx: FLUID RESUS

Meningitis is a serious infection of the meninges in the brain or spinal cord

Etiology
• Otitis media
• Sinusitis
• CSF leak after head trauma or neurosurgery
• Maternal group B streptococcal infection during birth
 Sepsis

Most pathogens that cause meningitis colonize the nasopharynx or the upper airways before entering the CNS via:
1. Hematogenous dissemination
2. Contiguous spread of infections in nose, eyes, and ears
3. Retrograde transport along or within peripheral or cranial nerves
4. Direct infection (e.g., due to trauma or head surgery)

Signs of meningeal irritation

 Neck stiffness
 Kernig sign: pt supine, hip flexed @90, extending knee causes pain
 Brudzinski sign: flexion of the neck causes flexion of hips and knee
Systemic signs of inflammation
 Fever
 Hypotension
 Tachycardia
Signs of increased intracranial pressure: e.g., papilledema (< 5% of cases)
Signs of underlying infections
 Bulging and redness of tympanic membrane: acute otitis media
 Skin manifestations
 Cutaneous petechiae in meningococcal meningitis: suggestive of meningococcemia
 Maculopapular rash in some viral meningitis (e.g., West Nile virus, enterovirus)
 Nonblanching rash: should raise suspicion for meningococcal meningitis or Rocky Mountain spotted
fever (see “Subtypes and variants”)

Workup
Blood cultures (two sets): obtain before starting antibiotic therapy
CBC:Normal/↑ WBC count In severe infections, ↓ WBC count and thrombocytopenia
BMP: Blood glucose is needed to analyze CSF glucose. Common finding: mild electrolyte disturbances (e.g.,
hyponatremia from SIADH). In critically ill patients: possible signs of acute kidney injury
CRP: elevated
Coagulation panel if there is suspicion for disseminated intravascular coagulation (e.g., petechiae, purpura)
Blood gas: metabolic acidosis may be present in critically ill patients
Consider testing for atypical infections

Normal Bacterial Viral Fungal SAH TB

 Opening 7-18 cmH2O >30 N or mild ↑ ↑↑ Increased ↑↑
pressure
Appearance Clear Turbid Clear Cloudy Bloody, Fibrin web
Xanthrochromic
or clear
Predominant Polymorphs Lymphocytes Lymphocytes
cell
Cell count <5 90-1000 50-1000 20-200 10-1000
Gram stain Negative Positive Negative Negative Negative
Glucose (2.8- 2/3 serum ↓↓ <1/2 Normal, >1/2 ↓ Normal ↓↓ <1/2
4.2 mmol/L) plasma plasma, slightly plasma
↓
Glucose 0.6 <0.4 >0.6 0.6
Serum/CSF
ratio
Protein (0.15- >1.5 ↑↑ <1 (Normal) ↑ ↑ 1-5 ↑
0.45 g/L)
Chloride (115- ↓↓ Normal or ↓ ↓↓
130 mmol/L)

Ttx: 3rd gen Cephalosporin + Vancomycin (Glycopeptide).

<1 mth Ampicillin (Penicillase sensitive penicillin) + Gentamycin (glycopeptide)
Corticosteroid: dexamethasone for 2–4 days. Reduces the local and systemic inflammation seen in bacterial meningitis
and improves outcomes. Should be administered before or concomitant to antibiotics for optimal results
 INFECTIOUS DISEASE (pg 1032)
HIV
Cytopathic retrovirus that kills infected cells.
2 major subtypes of HIV; HIV-1 is the predominant subtype worldwide and causes AIDS. HIV-2 causes a similar immune
syndrome, but exists primarily in western Africa and is infrequent in the United States, but its incidence is growing.
HIV virion is a central RNA molecule and a reverse transcriptase protein surrounded by a core protein encased by a
lipid envelope.
It selectively attacks host cells involved in immune function, primarily CD4+ T cells. HIV-encoded RNA uses reverse
transcription to enter into DNA, aided by the enzyme reverse transcriptase. The viral genome integrates into the host
genome, where it may lie dormant or be transcribed and translated to produce virally encoded proteins and new HIV
virions.
As a result of infection, immunologic abnormalities eventually occur, including lymphopenia, qualitative CD4+ T-cell
function defects, and autoimmune phenomena. Defects in cellular immunity ultimately result in a variety of
opportunistic infections and neoplasms.
HIV exists in saliva, urine, cerebrospinal fluid (CSF), pus, brain, tears, alveolar fluid, synovial fluid, and amniotic fluid.
Transmission of HIV occurs through semen, vaginal secretions, blood or blood products, and breast milk, and in utero
by placental transmission.
Stage 1/Acute Retroviral Syndrome acute HIV infection 2-4 wks after infection up to seroconversion: Fever, fatigue,
pharyngitis, rash, headache, weight loss, diarrhoea
Stage 2/Clinical latency no complaints or findings, maybe lymphadenopathy. Towards the end as viral load rises and
CD4 count drops. Infections such as thrush, vulvovaginal candidiasis, herpes zoster
Stage 3/AIDS defining illness or CD cell count <200 cells/mm

•Bacterial infections, multiple or • HIV Encephalopathy • Mycobacterium avium complex or

recurrent*
• Candidiasis of bronchi, trachea, or
lungs
• Candidiasis of esophagus
• Cervical cancer, invasive†
• Coccidioidomycosis, disseminated
or extrapulmonary
• Cryptococcosis, extrapulmonary
• Cryptosporidiosis, chronic
intestinal (>1 month in duration)
• Cytomegalovirus disease (other
than liver, spleen, or nodes), onset
at age >1 month
• Cytomegalovirus retinitis (with
loss of vision)
• Herpes Simplex
• Histoplasmosis, disseminated or
extrapulmonary
• Isosporiasis, chronic intestinal (>1
month in duration)
• Kaposi’s sarcoma
• Lymphoma, Burkitt’s
• Lymphoma, immunoblastic
• Lymphoma, primary, of brain
• Lymphoid interstitial pneumonia
or pulmonary lymphoid hyperplasia
complex*
• Mycobacterium, other species or
unidentified species, disseminated
or extrapulmonary
Mycobacterium kansasii,
disseminated or extrapulmonary
• Mycobacterium tuberculosis of
any site, pulmonary,† disseminated,
or extrapulmonary
• Pneumocystis jirovecii pneumonia
• Pneumonia, recurrent†
• Progressive multifocal
leukoencephalopathy
• Salmonella septicemia, recurrent
• Toxoplasmosis of brain, onset at
age >1 month
• Wasting syndrome

Kaposi’s Sarcoma: firm painless raised brown-black or purples patches

TOXOPLASMIC ENCEPHALITIS: Toxoplasmosis gondii obligate intracellular protozoa.
Unenhanced CT scan, toxoplasmosis typically appears as multiple subcortical lesions with a predilection for the basal
ganglia and corticomedullary junction. Contrast-enhanced CT scan typically shows multiple ring-enhancing lesions with
surrounding areas of edema. Ttx: Pyrimethamine + Sulfadiazine + Leucovorin
Pyrimethamine & Sulfadiazine both inhibit bacterial folic acid synthesis, both bacteriostatic combined are
bacteriocidal.
CRYPTOCCAL MENINGITIS IV Amphotericin B + PO Flocytosine followed by Fluconazole
CMV Ttx Ganciclovir
CNS LYMPHOMA

Antiretroviral Therapy
Nucleoside reverse transcriptase inhibitors (NRTI): Zidovudine, Lamivudine
Mechanism of action
 NRTIs act as nucleoside analogs → competitive blockage of nucleoside binding to reverse transcriptase → inhibition
of formation of 3' to 5' phosphodiester linkages → termination of DNA chain → inhibition of RNA to DNA reverse
transcription
 Activation requires intracellular phosphorylation, so their efficacy is reliant on kinase availability and activity, which
varies depending on cell functionality and activation state.

Nonnucleoside reverse-transcriptase inhibitors (NNRTI): Efavirenz

Mechanism of action
 Noncompetitive inhibitors of viral reverse transcriptase that bind to the reverse transcriptase at a different location
than NRTIs
 NNRTIs do not require intracellular phosphorylation for activation but are instead direct inhibitors.

HIV protease inhibitors (PI): Ritonavir

Mechanism of action:
inhibition of viral HIV-1 protease (encoded by pol gene) → inability to cleave viral mRNA into functional units →
generation of impaired viral proteins → production of immature (noninfectious) virions

Gonorrhea
Gram negative diplococcus Neisseria gonorrhoeae, has an incubation period of 2–7 days.
Usually between 15–24 years of age
Asymptomatic, especially in women
Genitourinary tract infections such as urethritis, cervicitis, pelvic inflammatory disease (PID) and epididymitis.
Purulent vaginal or urethral discharge, dysuria
Epdidymitis (e.g., scrotal pain) or PID (e.g., pelvic pain, dyspareunia).
Extragenitourinary manifestations: proctitis, pharyngitis.
Disseminated disease may manifests with a triad of arthritis, pustular skin lesions, and tenosynovitis.
Diagnostic tests include nucleic acid amplification testing, gram stains, and bacterial cultures from urine or swabs of
the genitourinary tract as well as blood and synovial fluid in disseminated infection.
Treatment Ceftriaxone 250 mg IM (1gr x 1-2 dys in disseminated dz) & Azithromycin 1 gr PO
Complications: hymenal and tubal synechiae that lead to infertility in women.

Chlamydia
Chlamydia trachomatis, obligate intracellular, gram negative bacterium
Lymphogranuloma Venereum caused by specific subtype (Doxycycline)
Men urethritis, epididymitis, proctitis, or Reiter’s syndrome (urethritis, conjunctivitis, and rash).
Women asymptomatic cervicitis. Symptoms include vaginal discharge (mucopurulente), bleeding between menses,
and dysuria. Fitz-Hugh-Curtis Syndrome (peritoneal irritation & perihepatitis)
Primary: Azithromycin 1 g PO x 1 dose OR Doxycycline 100 mg PO bid x 7 days
Secondary: Levofloxacin 500 mg PO x 7 days OR Ofloxacin 300 mg bid x 7 days

Syphilis
Organism: Spirochete bacterium, treponema pallidum
 Primary: single, painless lesion known as the chancre at the site of inoculation about 3 weeks post infection. May
resolve spontaneously.
 Secondary: rash typically involves the palms of the hands and soles of the feet, with lymphadenopathy. Symptoms
occur several weeks after the initial infection
 Tertiary: gummatous lesions and cardiac involvement, including aortic disease that may not appear until after 20
years of syphilis infection.
 Latent: Asymptomatic stage.
 Neurospyhillis: Can occur at any stage. Symptoms include stroke, altered mental status, cranialnerve dysfunction,
and tabes dorsalis
Ttx: Penicillin G benzathine, 2.4 million units IM x 1 dose.

Angioedema is classified as histamine-mediated angioedema and bradykinin-mediated angioedema.

Histamine-mediated angioedema is the most common and is secondary to mast-cells and basophil activation.
Bradykinin-mediated angioedema (hereditary angioedema, acquired C1-inhibitor deficiency and angiotensin-
converting enzyme inhibitor-associated angioedema). Allergic reactions and hives do not trigger this condition. C1-
inhibitor is a regulator of complement and the contact system; if deficient or dysfunctional it causes activation of the
contact system resulting in uncontrolled production of kallikrein leading to proteolysis of high-molecular-weight
kininogen and bradykinin, leading to edema by increasing in vascular permeability. Bradykinin-mediated angioedema
is seen in:
 C1 inhibitor deficiency: Excessive production of bradykinin
 Angiotensin-converting enzyme inhibitor-associated angioedema: Decreased degradation of bradykinin
 Histamine and bradykinin increase localized microvascular permeability.
 NSAID induced: cyclooxygenase 1 inhibitor affects arachnoid acid metabolism, leukotriene/prostaglandin
binding to the receptor or may be IgE mediated.

HEAT EMERGENCIES [Tinti pg 1345]

Pathophys: Heat is generated by cellular metabolism and the mechanical work of skeletal muscle. Heat accumulates from
radiation from the sun and contact with hot objects. Heat is absorbed when the ambient temperature rises above body
temperature. As core temperature rises, the autonomic nervous system is stimulated to promote sweating and cutaneous
vasodilatation.
Heat stroke is triggered by hyperthermia. Heat exhaustion and heat stroke occur when the body’s thermoregulatory
responses are impaired or overwhelmed and are no longer capable of maintain homeostasis. Excessive heat is toxic to
cells, causes a release of inflammatory cytokines, and damage to vascular endothelium. Nearly all cells respond to
sudden heating by producing heat stress proteins. Rising cellular temperature results in denaturation of proteins,
interruption of cellular processes, and cell death. Temperatures of >41.6°C (>106.9°F) can cause cellular injury in
hours. As temperature rises, cellular damage occurs more quickly and extensively. Temperatures >49°C (>120.2°F)
typically result in immediate cell death and tissue necrosis. The enhanced vascular permeability due to damaged
vascular endothelium results in activation of the coagulation cascade and disseminated intravascular coagulation.
There is evidence that secondary endotoxemia triggers a systemic inflammatory response, coagulopathy, and
multiorgan failure
Mec. Of Heat transfer
1. Evaporation: heat loss by vaporization of water or sweat. Becomes ineffective @ humidity ≥75%
 2. Radiation: transfer by electromagnetic waves from warm object to a cooler one, ineffective @ ambient temp
>35oC/95o F
3. Convection: air or liquid passing over surface eg fans, wind, ineffective at ambient >32.2oC & humidity >35%
4. Conduction: exchange between 2 surfaces eg cooling blankets
↑ in body temp = ↑O2 consumption & ↑metabolic rate = hyperpnea & tachycardia
Response to heat stress
Hypothalamus maintains body core temp 36oC-38oC (96.8oF – 100.4oF). Thermal regulation begins to fail <35oC/95oF or
>40oC/104oF
1. Dilation of blood vessels
2. ↑ sweat production (due to cholinergic stimulation)
3. ↓heat production
4. Behavioural heat control
Medications
Anticholinergic agents impair sweating and cardiovascular response to heat.
Diuretics lead to volume depletion and decreased cardiac output.
Phenothiazines have anticholinergic properties and deplete central stores of dopamine, interfering with the
hypothalamic thermoregulatory center.
β-blockers & CCBs decrease CVS response to heat, reduce peripheral blood flow & the ability to sweat.
Sympathomimetics cause cutaneous vasoconstriction & inhibit sweating.
Alcohol inhibits secretion of antidiuretic hormone, leading to dehydration, and blunts the psychological heat-
avoidance response.
Heroin, cocaine & amphetamines disrupt the function of endogenous endorphins & adrenocorticotropic hormones
that are involved in heat adaptation mechanisms.
Amphetamines & cocaine increase muscle activity causing ↑ heat production.
Lysergic acid diethylamide(LSD) and phencyclidine act on the CNS to induce a hypermetabolic state.

Heat Edema: self-limited process manifested by mild swelling of the feet, ankles, and hands that appears within the
first few days of exposure to a hot environment. Heat edema is due to the cutaneous vasodilatation and orthostatic
pooling of interstitial fluid in gravity-dependent extremities.
Prickly Heat: pruritic, maculopapular, and erythematous rash over normally clothed areas of the body, also known as
heat rash. Sweat pores are blocked by macerated stratum corneum and become dilated under pressure, ultimately
rupturing, producing superficial vesicles. Infection with Staphylococcus aureus or methicillin-resistant S. aureus is a
common complication
Heat Cramps: painful, involuntary, spasmodic contractions of skeletal muscles. Occur because person sweating heavily
repace fluids with H2O or other hypotonic solution leading to cramps due to relative deficiency of Na, K or Mg. Self-
limiting, confined to 1 muscle group, Rhabdo is rare.
Ttx: fluid and salt replacement (PO or IV) & rest in a cool environment. For mild cases 0.1% to 0.2% saline solution PO.
Severe symptoms require IV rehydration with normal saline.
Heat Stress/Exhaustion: can result from either H2O and/or Na depletion. Water depletion tends to occur in the elderly
and persons working in hot environments with inadequate water replacement. Salt depletion tends to occur in
nonacclimatized individuals who replace fluid losses with large amounts of hypotonic solutions. Present with muscle
cramps, headache, nausea, orthostasis, normal or ↑ temp <40oC.
Ttx: volume and electrolyte replacement and rest. 1-2 L IV NS, cool until core temp drops to <39oC to prevent
progression to heat stroke.
Heat Stroke: All the symptoms of heat stress, anhidrosis or sweating PLUS neurologic abnormalities and temp >40oC
Ttx: immediate cooling & aggressive support of organ system fxn.
Evaporative cooling
Immersion cooling
Invasive cooling measures: cardiopulmonary bypass, cold water lavage (gastric & urinary)
Cooling blankets, ice packs
Thermal Burns

Physiological Effects of Thermal Burn

•Cell damage occurs at temperatures of >45°C (113°F) owing to denaturation of cellular protein
•Disruption of sodium pump
• Intracellular influx of sodium and water
• Extracellular efflux of potassium
• Depression of myocardial contractility (>60% of body surface area burned)
• Increased systemic vascular resistance
• Metabolic acidosis
• Increase in hematocrit and increased blood viscosity
• Secondary anemia from erythrocyte extravasation and destruction
• Local tissue injury
• Release of histamines, kinins, serotonins, arachidonic acids, and free oxygen radicals

Jackson’s Theory of Thermal Burns

1. zone of coagulation: tissue is irreversibly destroyed with thrombosis of blood vessels
2. zone of stasis: stagnation of the microcirculation, can become progressively more hypoxemic and ischemic if
resuscitation is not adequate
3. zone of hyperemia: there is increased blood flow, minimal damage to the cells and spontaneous recovery is
likely.
Prognosis determined by the severity of the burn, presence of inhalation injury, associated injuries, patient’s age,
comorbid conditions, and acute organ system failure.

Burn Depth Histology/Anatomy Example Healing

Superficial (first degree) Epidermis Sunburn 7d
No blisters, painful
Superficial partial-thickness Epidermis and superficial Hot water scald 14–21 d, no scar
(superficial second degree) dermis
Blisters, very painful
Deep partial-thickness (deep Epidermis and deep dermis, Hot liquid, steam, grease, 3–8 wk, permanent scar
second degree) sweat glands, and hair flame
follicles
Blisters, very painful
Full-thickness (third degree) Entire epidermis and dermis Flame Months, severe scarring, skin
charred, pale, leathery; no grafts necessary
pain
Fourth degree Entire epidermis and dermis, Flame Months, multiple surgeries
as well as bone, fat, and/or usually required
muscle
Complication: Inhalation injury
DD: Chemical burns, Electrical burns, TENS, Sunburn
 Parkland Formula for Fluid Resuscitation
Adults
• LR 4 mL × weight (kg) × % BSA burned* over initial 24 h
• Half over the first 8 h from the time of burn
• Other half over the subsequent 16 h
• Example: 70-kg adult with 40% second- and third-degree burns: 4 mL × 70 kg × 40 = 11,200 mL over 24 h
Children
• LR 3 mL × weight (kg) × % BSA burned* over initial 24 h plus maintenance
• Half over the first 8 h from the time of burn
• Other half over the subsequent 16 h

Maintain UO of 1ml/kg/h

TOXICOLOGY

Iron [Tinti pg 1289]

Pathophys: A potent catalyst for the production of oxidants (eg free radicals), which are GI tract irritants causing
vomiting, diarrhoea, abdominal pain, mucosal ulceration and bleeding soon after a significant ingestion. The mucosal
surface is injured, regulatory enterocyte barrier is compromised, and free iron passes into systemic circulation. Free
iron disrupts cellular processes and induces metabolic acidosis and multi-organ toxicity including hepatotoxicity due to
iron deposition. Inhibition of thrombin formation and the effect of thrombin on fibrinogen leads to coagulopathy.
Vasodilation, negative ionotropic effect, and direct myocardial iron deposition causes myocardial and valvular
dysfunction.

Ttx
Whole-bowel irrigation with a polyethylene glycol solution
Deferoxamine [1 gr IV, 50 mg/kg in kids] is a chelating agent that binds free iron, iron from plasma, and intracellular
iron forming ferrioxamine*, which is renally excreted giving urine a “vin rosé” colour, more typically a brown or rusty
hue. The disappearance of the “vin rosé” colour suggests there is no more free iron available to be complexed with
deferoxamine and excreted. Is indicated in the iron-poisoned patient with systemic toxicity, persistent emesis,
metabolic acidosis, progressive toxicity, or a serum iron level predictive of moderate to severe toxicity.
Exchange transfusion
*haemodialysis and hemofiltration do not remove iron, rather remove the deferoxamine–iron complex in patients with renal failure unable to
excrete it in their urine.

Paraquat [Tinti pg. 1305] LETHAL DOSE 30 mls

Pathophys: A contact herbicide, it is a severe local irritant and devastating systemic toxin. Ingested paraquat is
absorbed rapidly, particularly if the stomach is empty. Plasma concentration peaks within minutes to 2 hours after
ingestion. Paraquat is then distributed to most organs, highest concentrations in kidneys and lungs. It accumulates in
the alveolar cells of the lungs, where it undergoes redox cycling, a process involving repetitive enzyme-mediated
cycling between paraquat and paraquat radicals which consumes NADPH, one of the cell’s key antioxidant defences. A
by-product of this process is a superoxide radical, a highly reactive oxygen species, which can cause direct cellular
damage or react further to form other reactive oxygen species and nitrite radicals. The degradation of cell membranes
causes dysfunction & necrosis.
Lung injury has two phases. An initial destructive phase is characterized by loss of type I and type II alveolar cells,
infiltration by inflammatory cells, and hemorrhage. These changes may be reversible. The later, proliferative phase is
characterized by fibrosis in the interstitium and alveolar spaces.
A lethal dose of the 20% concentrate solution is about 10-20 mL in an adult and 4-5 mL in a child. To reduce the
toxicity of these herbicides in the event of ingestion, products containing these herbicides are often co-formulated
with an emetic, dye, and stenching agent.
 Labs: Electrolytes (altered due to vomiting), ABG (early
alkalosis due to vomiting, then resp & metabolic acidosis)

The SIPP score is calculated by multiplying the paraquat

concentration (mg/L) by the time since poisoning
(hours). A SIPP score less than 10 (the best cut-off)
indicates survival is likely; the higher the score the more
rapidly death may be expected

Ttx Analgesia and supportive care. Do not administer O2

unless the patient is severely hypoxic because added O2
stimulates superoxide radical formation and promotes
oxidative stress. IVF
Remove clothing and decontaminate.
GI decontamination if pt presents within 2 hrs
 Activated charcoal (1 to 2 grams/kg)
 Diatomaceous fuller’s earth (1 to 2 gr/kg in 15%
aqueous susp)
 Bentonite (1 to 2 grams/kg in a 7% aqueous slurry)
Hemoperfusion
Hemodialysis

Salicylate [Tinti pg 1248]

Mechanism of Action
 Analgesic, antipyretic, anti-inflammatory properties due to inhibition of cyclooxygenase enzyme (COX)
 Salicylates cause inhibition of oxidative phosphorylation, increased renal bicarbonate excretion, lipolysis,
leading to metabolic acidosis
 Activation of the medulla within the brainstem results in hyperventilation (tachypnea) resulting in respiratory
alkalosis
 It is these two mechanisms that lead to the mixed respiratory alkalosis/metabolic acidosis
Pathophysiology
 Aspirin is absorbed and hydrolysed to salicylic acid, the majority bound to proteins
 In overdose, salicylic acid conc ↑saturating protein binding site leaving more unbound/free salicylic acid in
circulation
 Unbound salicylic acid can cross cell membranes and this ↑ brain concentration.
 Salicylate is metabolized in the liver, but this rapidly becomes overwhelmed
 The increase in unbound salicylate causing an ↑ in renal clearance
Differential
 Consider toxicologic and non-toxicologic causes
 Infection/Sepsis, renal failure, liver disease, carbon monoxide toxicity, cyanide toxicity, metformin toxicity,
iron toxicity, INH, DKA, Alcoholic Ketoacidosis, Reye’s syndrome, beta-agonist toxicity

Ttx:
IVF,
NaHCO3 for urinary alkalinisation to promote urinary excretion and correct acidosis
Monitor urine output
Haemodialysis in severe toxicity (>300 mg/kg)
Acetaminophen/Paracetamol (Tinti pg 1252)
Acetaminophen is primarily metabolized by the liver.
 In therapeutic doses, about 90% of acetaminophen is conjugated with glucuronide or sulfate to nontoxic
metabolites, while about 5% is oxidized by cytochrome P-450 to a toxic metabolite, N-acetyl-p-
benzoquinoneimine (NAPQI).
 Hepatic stores of glutathione rapidly combine with NAPQI to form nontoxic metabolites.
 In APAP overdose, normal glucuronide and sulfate conjugation is overwhelmed and a large amount of NAPQI
is produced.
 When NAPQI formation exceeds glutathione stores, free NAPQI binds to cellular proteins causing
hepatotoxicity (centrilobular or zone III).
 High-risk patients: Patients with decreased glutathione stores (alcoholics, malnourished) and those on
cytochrome P-450–inducing medications (INH, anticonvulsants) may have increased risk of hepatotoxicity.

Rumack-Matthew Nomogram used during the 4 to 24 hr window for a single ingestion.

DD: alcohol-related hepatitis, other drug- or toxin-induced hepatitis, viral hepatitis, hepatobiliary disease, Reye's
syndrome, and ischemic hepatitis ("shock liver").

Acetylcysteine In early acetaminophen poisoning (<8 hours after ingestion), acetylcysteine averts toxicity by
preventing the binding of NAPQI to hepatic macromolecules. Acetylcysteine may do this by acting as a glutathione
precursor or substitute, or a sulfate precursor, or it may directly reduce NAPQI back to acetaminophen

Tranexamic acid is an antifibrinolytic agent that reduces blood loss after surgery and may reduce blood loss after
traumatic injury. It prevents cleavage of plasmin and degradation of fibrin.

PALS

Management of Respiratory Emergencies Flowchart

 Airway positioning
 Suction as needed
 Oxygen
 Pulse oximetry
 ECG monitor (as indicated)
 BLS as indicated
Treat Underlying Causes: Treating a reversible underlying cause for the bradycardia could prove effective in certain
situations. The two most common reversible causes are hypoxia and increased vagal tone. You can treat the following
reversible causes of bradycardia by the following:
o Hypoxia: Provide O2 in high concentration.
o Hydrogen ion (acidosis): Provide ventilation and consider sodium bicarbonate in severe cases.
o Hyperkalemia: Restore potassium concentration to normal.
o Hypothermia: Warm the patient.
o Heart block: Consider atropine, chronotropic drugs and/or electrical pacing.
o Toxins/Poisons: Treat with specific antidote.
o Head Trauma: Provide oxygenation and ventilation and obtain expert assistance.

PROCEDURES
PERICARDIOCENTESIS

STEP 1. Monitor the patient’s vital signs and electrocardiogram (ECG) before, during, and after.

STEP 2. Use ultrasound to identify the effusion.

STEP 3. Surgically prepare the xiphoid and subxiphoid areas, if time allows.

STEP 4. Locally anesthetize the puncture site, if necessary.

STEP 5. Using a 16- to 18-gauge, 6-in. (15-cm) or longer over-the-needle catheter, attach a 35-mL empty syringe with a
threeway stopcock.

STEP 6. Assess the patient for any mediastinal shift that may have caused the heart to shift significantly.

STEP 7. Puncture the skin 1 to 2 cm inferior to the left of the xiphochondral junction, at a 45-degree

angle to the skin.

STEP 8. Carefully advance the needle cephalad and aim toward the tip of the left scapula. Follow the needle with the
ultrasound.

STEP 9. Advance the catheter over the needle. Remove the needle.

STEP 10. When the catheter tip enters the bloodfilled pericardial sac, withdraw as much non-clotted blood as possible.

STEP 11. After aspiration is completed, remove the syringe and attach a three-way stopcock, leaving the stopcock
closed. The plastic pericardiocentesis catheter can be sutured or taped in place and covered with a small dressing to
allow for continued decompression en route to surgery or transfer to another care facility.

STEP 12. If cardiac tamponade symptoms persist, the stopcock may be opened and the pericardial sac reaspirated.
This process may be repeated as the symptoms of tamponade recur, before definitive treatment.