• Physiologic score
• Based on GCS , SBP and RR
• High number indicates improved function (0-12)
• RTS <12 - identified 97.2% of fatally injured patients

• Anatomic score
• divides body into 6 regions (thorax, abdomen, visceral pelvis, head and neck, bony pelvis and extremeties, external structures)
• Death likely when ISS >15

Trauma and Injury Severity Score

• Incorporates patients age and ISS - predicts chance of survivale

Primary Injury: Secondary to disruptive forces and mechanism of initial incident

Secondary injury: Cerebral hypoxia due to impaired oxygenation or cerberal blood flow

• Maintenane of airway/ventilation
• Maintenance of cerberal perfusion pressure --> Avoid secondary brain injury (CPP = MAP-ICP)

1. ICP control (Elevate bed 30 degrees, no tight tapes, mannitol 0.5-1g/kg), hypocarbia (in immediate life threatening - reduced CBF and ICP through vasoconstriction but may reduce CPP to point of secondary brain injury)
   
2. Seizure prevention - phenytoin 20mg/kg (first week)
   
3. Antibiotics - compound fractures - flucloxacillin 1g Q6h
   
4. CRASH study - no steroids
5. Therapeutic hypothermia
   

• Associated with fracture of the temporal bone and injury to undelrying middle meningeal artery
• Causes a rise in ICP and eventually uncal herniation
• Convex appearance on CT

• Usually venous - slowly enlarging
• Acute, subacute or chronic

• GCS <15
• Heat trauma on anticoagulation
• GCS of 15 with LOC/amnesia + any of following (Age >60, vomiting, abnormal mental status, evidence of skull #)
• GCS 15 plus any of (headache, isolated LOC, traum above clavicles, deficit in short term memory, dangerous mechanism, alcohol)

• Minor HI - witnessed LOC, definite amnesia or witnessed disorientation in patient with GCS 13-15 + 1 of
• High risk
• GCS <15 2 hours post injury
• Suspected open or depressed skull #
• Any sign of basal skull # - haemotypmanum, racoon eyes, battles signs, CSF otorrhoea/rhinorrhea
• vomiting >2 episodes
• Age >65

• History (LOC >5min, Amnesia >5min, abnormal drowsiness, >2 vomits, suspicion of NAI, any seizure in non-epileptic)

• Examination (GCS <14 or 15 if <1, suspicion of penetrating injury, suspicion of depressed skull #, tense fontanelle, signs of BOS #, any focal neurological deficit, presence of swelling or laceration >5cm in infants)

• Mechanism (high speed MVA >60km/hr, fall >3m, high speed projectile)

• No motor or autonomic information transmitted below damaged area, and ascending sensory stimuli from below damaged spinal segments are blocked
• Total flaccid paralysis, total anaesthesia, total analgesia and usually areflexia
• Sacral sparing - incomplete injury - tracts to sacral areas are on the outermost parts of the spinal cord

• Hyperextension injury
• transmission in the outer rim of the spinal cord is intact
• Motor function: Weakness in both upper and lower limbs (Upper > lower)
• Sensation: Sensory loss in both upper and lower limbs (upper >lower)

• Result of flexion-rotation or vertical compression injuries
• Region supplied by the anterior spinal artery is damaged
• Motor loss below the level of the injured segments
• Spinothalamic transmission is impaired - analgesia, loss of temperature sensation and coarse touch
• Dorsal columns are intact - preservation of joint position, vibration sense and fine touch

• One side of cord affected
• Ipsilateral: Motor function, light touch, joint position, sense and vibration
• Contralateral: Spinothalamic - pain and temperature

• Impaired or disrupted proprioception, vibration and fine touch sensation

• Dorsal Columns: Vibration, light touch, proprioception. Decussate high
• Spinothalamic: Anterior, Pain, temperature. Decussate at level of entry
• Corticospinal: Motor function, Decussate at medulla.

Upper limbs travel centrally

Lower limbs travel peripherally

• Anaesthesia, paralysis below level of injury
• Worse prognosis then incomplete
• Acutely FLACID paralysis - spinal shock
• Followed by Hyper-reflexia
• Autonomic effects - Bradycardia, hypotension, urinary retention, poor thermoregulation

The whole of the sympathetic nervous system and pelvic parasympathetic outflow is transmitted in the spinal cord

• Cardiovascular (Symathetic denervation - relaxation of vasomotor tone - vasodilation, dry extremeties, penile engorgement, hypotension, bradycardia - due to unopposed vagal nerve)
• GIT (paralytic ileus - self limiting, aspiration of stomach contents - paralysis LES)
• Respiratory (thoracic and abdominal wall paralysis - unable to clear airways)
• Urinary (urinary retention)
• Thermoregulatory effects (Inability to shiver or sweat)

• C1 atlas blow out fracture of the ring
• hyperextension or compression

• Bilateral neural arch fracture of C2 (axis)
• Hyperextension injury
• Prevertebral soft tissue swelling
• Anterior sublaxation of C2 on C3

• <6mm at C3 (<7mm at C2 regardless of age)
  
• < 14mm C6 (<15 yo) and <21mm (adults) OR <1 vertebral body

3 x 7 = 21

• The anterior and all of the posterior elements are disrupted
• There is >3mm overriding of the vertebral body above the vertebral body below
• The angle between the 2 vertebrae is >11 degrees
• The height of the anterior border of a vertebral body is <2/3rds of the posterior border

• Anterior column: Anterior longitudinal ligament, anterior part of vertebral body
• Middle column: Posterior part of vertebral body, posterior longitudinal ligament
• Posterior column: All bony and ligamentous structures posterior to posterior longitudinal ligament

Fractures of anterior column stable

Middle and posterior unstable

• No Disturbed conscious state (head injury, intoxication)
• No neurological motor or sensory signs
• No Midline cervical tenderness
• No major distracting injuries

• GCS 15, stable
• Any high risk factors - Age >65, dangerous mechanims (fall from > 1m or 5 stairs, axial load to the head, high speed MVA, rollover, collision involving a motorised recreational vehicle, bicycle collision), paraesthesia
• Low risk factors that allows safe ROM assessment -  (simple rear end MVA, sitting position in ED, ambulatory at any time, delayed neck pain onset, no midline c-spine tenderness)
• Able to rotate neck actively

• Violation of platysma signifides significant injury to vital underlying structures
• If wound traverses midline of neck - likelihood of signficant injury doubles
• Routine C-spine immobilisation not recommended
• Anterior Triangle - 3 zones
• zone 1: Between clavicles and inferior rim of cricoid cartilate
• Zone 2: Superior edge of cricoid to angle of mandible
• Zone 3: extents from angle of mandible to BOS
• Laryngotraceal injury - dyspnoea, stridor, cyanosis, air bubbling at site, pneumomediastinum, haemoptysis, voice change
• Vascular injury - shock, CVA, expanding haematoma, airway compression
• Nerve injury - spinal cord, recurrent laryngeal nerve
• CN transection, VII (unilateral mouth droop), XI (inability to shrug shoulders), XII (tongue deviation)
• GIT - Oesophageal injury
• Do not RSI unless complete airway obstruction --> Transfer to OT
• No hard signs neck injury + injury through platysma - CTA neck and surgical referral

•  Expanding pulsatile haematoma
• Shock
• Air bubbling through wounds
• Voice or airway disturbance
• Active bleeding
• Haemoptysis/haematemesis
• Thrill/Bruit
• Neurological deficit

Blow Out Fractures

Definition, Indications for surgery, Contraindications for surgery

• Fracture of the orbital floor without fracture of the orbital margin
• Minimal displacement, no entrapment, no diplopia - outpatient
• Indications for surgery - acute enophthalmos, hypopthalmos, muscular entrapement with mechanical gaze restriction
• Contraindications (as soft tissue of eye may be aggravated by surgery) - hyphaemia, retinal tears, globe perforation

Ruptured Hemidiaphragm

Associations and Radiological findings

• High-velocity injuries with lateral torso trauma or thoracoabdominal crush injuries
• Lateral rib #, penetrating LUQ wounds, # pelvis
• Classical radiological findings - Viscera in thoracic cavity, NGT coiled in the thoracic cavity, marked hemi-dipahragm elevation

Crush Syndrome

Presentation & Ix

Characterised by major shock and renal failure after a crushing injury of skeletal muscle

Pathophysiology

• Reperfusion injury that appears after the reelase of the crushing pressure - muscle breakdown products like myoglobin, potassium and phosphorus along with cytokines released into the blood stream - systemic effects of shock
• Breakdown products of myoglobin are thought to deposit in kidneys and cause renal failure
• Immediate: muscle cells may burst releasing K+, H+, myoglobin, oxygen free radicals and phosphate ions --> Acute renal injury
• Release of crushed tissue releases all above into systemic circulation
• Pre-hospital fluids ++ important
• Clinically: Tense, hard tender muscles, dark urine (myoglobin)
• Ix: ECG (K+), Bloods (Cr, CK, acid base)
• Early death - arryhtmias
• 3-5 days - renal failure, coagulopathy, haemorrhage, sepsis

Crush Syndrome

Treatment

• Stabilising cardiac milieu against K+
• Aggressive volume therapy to prevent shock and renal failure
• Enhance haem protein elimimination
• Trapped patients should have aggressive fluid loading before extraction +/- calcium gluconate
• Severe crush injury 12L fluid/48 hours
• Once urine flow is established - alkaline mannitol diuresis (2mL/Kg/hr output, increases renal tubular blood flow, renal vasodilator, free radical scavenger)
• Evidence supporting use of other IV tx (apart from IVF) is in animals and inconsistent. Mannitol (acts by osmosis to enhance urine production). Bicarb (added to IVF may alleiate acidosis and make urine more alkaline to prevent cast formation in kidneys (limited evidence)
  
• Urine pH >5 - myoglobin 50% soluble (bicarbonate 50mmol/hr after 3L normal saline)
• Correct Electrolytes
  
• Dialysis - oligoanuric, refractory hyperkalaemia or acidosis, fluid overload and pulmonary oedema
• Other complications - compartment syndrome
• DIC - generally resolves when underlying causes are treated, but give FFP or platelets if levels dip enough
  

• Widenend mediastinum >6cm erect PA, >8cm in supine AP
• Deviation of the oesophagus/NGT to R of T4 spinous process
• Obliteration of the aortopulmonary window
• Deviation of the trachea to the R of T4 spinous process
• Depression of the L main bronchus to below 40 degrees from the horizontal
• Increased R paratracheal stripe (>4mm)
• Increased L paravertebral stripe (>5mm)
• Left apical cap

• Life-threatening multi-organ syndrome affecting the lungs, brain, CVS and skin
• 6-48 hours post long bone fracture (also caused by closed cardiac massage, burns, liver injury, BMT, lipo)
• Clinically: Hypoxaemia, CXR changes, skin petechiae, ALOC
• Treatment: Oxygen, haemodynamic, prophylaxis for DVT, PUD
• Self limiting
• Early fixation of # help prevent
• intramedullary reaming and nails increase risk

Neuropraxia: Transient change in conduction. Following chrush or contusion or stretching of nerve. Complete return of function in 8 weeks

Axonotmesis: Complete denervation with an intact nerve sheath. Regeneration over months. Result of blunt trauma

Neurotmesis: complete division of a nerve and its sheath. Needs surgical repair

Pelvic Trauma

Young Burgess Classification (mechanism + stability)

Tile Classification (stability)

• Lateral compression (LC): usually stable, pedestrial struck by car. Common features is transverse pubic rami #. LC1 (pubic rami # -stable). LC2 (pubic rami + sacral, iliac, SI injury). LC3 (LC2 + APC injury to contralateral pelvis)
• AP compression (APC): Anterior forces applied directly to pelvis, head on MVA. Unstable fractures. (APC 1 widened pubic symphysis <2.5cm, APC 2 pubic sympysis >2.5cm, torn anterior sacral ligaments, APC 3 Hemipelvis separation)
• Vertical shear fractures (VS): Fall from height, unstable. Pubic rami # + displacement of SIJ vertically

• A: Rotationally and vertically stable (eg pubic rami , pubic symph diastasis <2.5cm). Do not involve the pelvic ring
  
• B:Rotationally unstable, vertically stable (eg pubic diastasis >2.5cm + widened SI, or pubic symphysis overriding)
• C: Rotationally and vertically unstable (disruption of SI joints)

Pelvic Trauma

Importance

Associated Injuries

• Associated with high energy mechanisms, majorhaemorrhage which can be difficult to control, other major injuries (intra-abdominal 28%, hollow viscus injury 13%, rectal injury 5%), High mortality and morbidity
  
• Vascular/Haemorrhagic shock
• GIT - especially rectal injury
• Genitourinary - urethral, bladder, prostate
• Spinal, neural
• Abdominal injury marker of high energy mechanism
• Fat embolisation
• ARDS
• VTE
• Abdominal compartment syndrome
• Late Cx - Infection, failure, disability and immobility, incontinence, sexual dysfunction, dystocia following pregnancy
  

Pelvic Trauma

Management

• If Haemodynamicaly unstable (most bleeding venous) - Minimum volume resus, pelvic binder, FAST +ve - red blanket
• Pelvic packing +/- ex fix
• If FAST -ve argument for angiography + embolisation (although if unstable preference for OT then angio)
• Haemodynamically stable - CTA to define injury and plan therapy

• Indirect trauma is most likely to cause placental abruption (placenta seperates from underlying decidua)
• Gestational age (>22weeks) is main determinant for fetal viability
• Primary survey - intubation may be difficult due to aspiration risk, breast enlargement and cervical trauma. Should be placed in left lateral position.
• Secondary survey - obstetric exam (fundal height, contractions), FHR, Fetal movements, Pelvic exam by obstetrician
• Ix - Kleihauer-Betke test, c-spine, CXR, PXR, USS, CTG
  
• Possible injuries: Pelvic #, Placental abruption, uterine rupture, fetomaternal haemorrhage

• Maternal resuscitation is the best method of fetal resuscitation
• Adequate oxygenation, proper positioning, aggressive fluid replacement
• NGT inserted to reduce risk of aspiration
• Haemodynamic instability --> labarotomy
• Urgent obstetric review (vaginal bleeding, abdo tenderness, hypotension, absent FHR, fetal distress, amniotic fluid leak)
• Premature labour - salbutamol, magnesium
• DIC due to placental abruption, fetal death
• Anti-D immunoglobulin
• Post mortem c-section within 4 minutes of mother arresting

• More prone to hypothermia
• More prone to multiple injuries
• Hypotension is a late sign
• HI more common as child's head accounts for larger proportion
• Fulcrum at C1-2 unlike C4-C7
• Compliant chest walls - may not show external evidence of trauma
• Predisposed to abdominal injury (larger solid organs, less protective abdominal wall, horizontal diaphgram hence lower lying and more anterior spleen and liver, flexible rib cage allows compression of solid organs)

• Mandatory reporting if a reasonable suspicion exists
• Parent's history of injury is inconsistnet with childs developmental stage and/or medical findings
• Physical signs of injury in a non-ambulant child
• Injury or suspected injury in context of family violence
• Any disclosure of abuse or neglect by a child or parent
• Any observation of abuse or neglect witnessed by staff
• Concerns about Factitious illness
• Bruising (<6mo, bite marks >3cm, instrument outlines or slap marks, bruising behind or on pinnae, grab marks on chest/shoulders)
• Burns (forced immersion pattern-spared flexures, instrumental outlines)
• Skeletal injuries (any #<12 months, rib #, metaphyseal/epiphyseal #, multiple or bilateral #, # of varying age)
• Head Injuries (depressed, basilar or bilateral in fall <1.2m, ICH with hx of minor trauma, retinal haemorrhages except in MVA)
• Genital injury (vaginal trauma without accomanying exernal damage, penile bruising, STDs)

• Bullshit story
• Behaviour (parent/child interaction)
• Background (drugs, SES factors etc)
• Burns
• Bones
• Brain (shaken baby)
• Bottom and genitals
• Broken Frenulum
• Bruises
• Bites
• Blunt abdominal trauma

• S: Spine, Scapula, Sternum
• H: Humerus (except supracondylar), Hand (non ambulant), Head
• M: Metaphyseal corner/bucket handle # (shaking), multiple #
• F: Foot (non ambulatory), Femur (non ambulatory), Fractured ribs

• Peritonism
• Free air
• Evisceration
• Penetrating abdominal trauma + hypotension
• Gunshot wound traversing peritoneum or retroperitoneum
• GI bleeding following penetrating trauma
• Blunt abdominal trauma + hypotension with postive FAST scan, positive DPL or peritonism

FAST Scan

PROS and CONS

• Pros - Quick to perform with immediate results, repeatable, patients doesn't have to leave ED, Sn 96% in detecting >800mL blood
• Cons - Requires >250mL free fluid, operator dependent, doesn't specify anatomical structure injured, does not distinguish other causes of intraperitoneal fluid (ascites, residual fluid after DPL), doesn't look at solid organs, hollow visci or retroperitoneal structures, can be technically difficult in obese patients or those with lots of gas

• PROS - Highly sensitive for intraperitoneal heamorrhage, rapid, performed at bedside
• CONS - invasive, doesn't specify anatomical structures injured, false positives may result from trauma during the procedure, rarely performed as practioners deskilled, residual volume following DPL makes FAST unreliable, modified technique if pregnant, pelvic # or midline scarring

• PROS - identifies specific anatomical structures injured, allows grading of severity, concurrent imaging of other body compartments, images retroperitoneal structures, imaging of spine
• CONS - Patient leaves ED, patient transfers time consuming, requires IV contrast, radiation exposure, less sensitive with pancreatic, diaphgragmatic and hollow viscus injuries, poor access to patient during scan

• Hyperflexion of spine - associated with car accidents when occupant is restrained with a lap belt
• Transverse fracture through a vertebral body and neural arch
• Usually occuring at the thoracolumbar junction

Resuscitation

• ABC
• D - Detect and correct - seizures (benzo), Hypoglycaemia (50ml 50% dextrose), Hyper/Hypothermia (>39.5 paralysis), Emergency antidote administration)

R - Risk Assessment

• Agent
• Doses
• Time since Ingestion
• Clinical features and ingestion
• Patient factors

S - Supportive care and monitoring

• Document - expected clinical course, potential complications, type of observation and monitoring, endpoints that trigger notification, management plans ,need for RR

I - Investigations

• Screening - Paracetamol, ECG
• Diagnose Complications - eLFT, ABG
• Exclude differential diagnosis - CT/LP
  

D - Decontamination

• Induced emesis
• Gastric lavage (CI corrosive ingestions, hydrocarbons)
• Activated Charcoal (adsorbing toxins and enhancing toxic elimination). Agents not bound (hydrocarbons & alcohol, metals, corrosives). 50g or 1g/Kg
• Whole bowel irrigation (sustained release, enteric coated, agents that don't bind charcoal) --> Iron overdose, span K, SR verapamil or diltiazem, aresenic, lead

E - Elimination - MDAC, Urinary alkalisation, haemodialysis, charcoal haemoperfusion

A -Antidotes

D - Disposition

Activated Charcoal

Mechanism

Drugs Effective on

Drugs Not Effective on

• Adsorbing a wide range of toxins
• Enhancing toxic elimination - creates a concentration gradient between bowel and circulation

Indications

• Likely that toxin remains in the GIT
• Potential benefits outweigh the risks
• Toxin absorbed by charcoal
• Further absorption may result in clinical deterioration

Complications

• Pulmonary aspiration
• Direct administration into lung via misplaced NGT
• Impaired absorption of subsequently administered oral antidotes
• Corneal abrasions
• Bowel Perforation

Dose

• 50g (Adults), 1g/Kg

Agents Poorly Bound

• Hydrocarbons & alcohol (ethanol, isopropyl alcohol, ethylene glycol, methanol)
• Metals (lithium, iron, K, Lead, arsenic, mercury)
• Corrosives (Acids, Alkalis)

Drugs Bound

• Carbamazepine
• Quinine
• Theophylline
• Dapsone

• Promotes ionisation of highly acidic drugs and prevents reabsorption across renal tubular epithelium

Drugs

• Filtered at glomerulus
• Small Vd
• Weak Acid
• Salicylate

CI: Fluid Overload

Complications

• Alkalaemia
• Hypokalaemia

Technique

• Correct hypokalaemia
• Give 1-2mmol/Kg NaHCO3 IV bolus
• Infusion of 100mmol soidum bicarb in 1L of 5% dextrose at 250ml/hr
• Aim pH >7.5

• Toxic alcohol poisoning
• Theophylline
• Severe salicylate intoxication
• Severe chronic lithium intoxication
• Phenobarbitone coma
• Metformin Lactic Acidosis
• Massive valproate overdose
• Massive carbamazepine overdose
• Potassium salt overdose

Calculated osmolality (mOsmol/Kg) = 2xNa (mmol/L) + Urea (mmol/L) + glucose (mmol/L) + ethanol (mmol/L)

Osmolar gap = Measured osmolality - Calculated osmolality

Normal Osmolar Gap <10

In suspected toxic alcohol ingestions (ingestions or HAGMA), high osmolality and osmolar gap support the diagnosis

Elevated osmolality and osmolar gap suggest the presence of unmeasured osmotically active compounds

• Acetone
• Ethanol
• Ehtylene glycol
• Glycerol
• Glycine
• Isopropyl alcohol
• Mannitol
• Methanol
• Propylene glycol

Non toxicological conditions

• Alcholic ketoacidosis
• CKD
• DKA
  Hyperlipidemia
• Hyperproteinemia
• Massive hypermagnesemia
• Severe lactic acidosis
• Shock
• Trauma and burns

What is the pH - Primary acid-base disturbance

• Acidaemia if pH <7.40
• Alkalaemia if pH >7.44

Determine whether the primary process is respiratory, metabolic or both

• PaCO2 35-45
• HCO3 22-26

Check the degree of compensation - Determine if secondary process

If Metabolic acidosis

• Calculate the Anion Gap: (Na+ + K+ ) - (Cl- + HCO3-) = 12+/- 4
• Calculate the Osmolar Gap >10
  
• Look at Lactate

Delta Gap - Determine if there is a 1:1 relationship between anions in the blood

• A metabolic disturbance is suspected but not detected
• Anion and non anion gap acidosis are suspected to co-exist

Respiratory Acidosis: Acute PaCO2:HCO3 10:1, Chronic 10:3

Respiratory Alkalosis: PaCO2:HCO3 Acute 10:2, Chronic 10:5

Metabolic Acidosis: PaCO2 = 1.5 x HCO3 + 8

Metabolic Alkalosis: PaCO2 = 0.7 x HCO3 + 21

Chronic respiratory alkalosis can have full compensation

Type A: Anaerobic Metabolism/Tissue Hypoperfusion

• Shock
• Anaemia
• Haemorrhage
• SMA occlussion
  

Type B1:Diseases - increased production, decreased clearance (Liver disease, myopathy, MELAS)

Type B2: Drugs - metformin, B-agonists

Type B3: Deficits - Thiamine, Inborn errors of metabolism

Type D: Bacteria

Methanol, Metformin

Uraemia

Diabetic Ketoacidosis (starvation, alcohol)

Propylene glycol, paraldehyde, paracetamol

Isoniazide, iron

Lactate

Ethanol, ethylene glycol
Salicylates

Cyanide, carbon monoxide

Toluene

Clinical features

• Respiratory: Hyperventilation, shift oxygen-Hb curve to right
• Cardiovascular: Myocardial depression, tissue catecholamine release, pulmonary vasoconstriction, hyperkalaemia

Gastrointestinal loss of bicarbonate

• Diarrhoea
• Urinary diversion
• Small bowel/pancreatic fistula

Renal loss of bicarbonate

• RTA 1,2,4
• Recovery phase ketoacidosis
• Renal insufficiency

Acidifying substances

• HCl
• Cl
• Lysine
• Arginine
• Sulphur
• Carbonic anydrase inhibitors

Ureteric diversion
Small bowel fistula
Extra chloride (resus) or HCl ingestion
DKA (resolving)
Carbonic anhydrase inhibitors
Addisons (type IV RTA)
Renal tubular acidosis (1,2,4)

Pancreatic fistula

Increase unmeasured cations - Li, Ca2+, Mg2+, K+, IgG

Decrease unmeasured cations - Decreased albumin, decreased PO4

Chloride Over Estimation - Bromide, Iodide, Cholesterol

Stimulated Respiratory Drive

• CNS: CVA, ICH, psychogenic
• Hypermetabolic: TFT, pregnancy, sepsis, anxiety, pain, DKA, salicylates
• Environmental: Hypethermia
• Drugs: Aspirin, ammonia, progesterone

Hypoxaemia Induced

• Pneumonia, PE, Asthma
• Congenital Heart Disease
• Chronic altitude compensation
• Early in altitude acclimitisation

Compensation for metabolic acidosis

Hyperventilation removes CO2 - cerebral acidosis - Increased ventilation

Clinically: Decreased Ca2+, K+, PO4, H+ binding, Increase Ca2+ binding - hypocalcaemia - tetany - carpopedal spasm, shift oxgen curve to left

Decreased Respiratory Drive

• CNS: CVA, tumour, infection, haemorrhage
• Drugs: Narcotics, sedatives

Decreased Chest Wall Movement

• Neurological: NM disorders, Guillain Barre, MG, demyelinating disorders, tetanus
• Toxicity: Muscle relaxants, organosphosphates, fentanyl
• Respiratory: Trauma, tension pneumothorax, pleural effusion, upper airway obstruction
• Equipement: Increase dead space

Obstructive Pulmonary Disease

• Asthma, COPD, Pneumonia

Clinical: Vasodilation, sweaty, Increased HR, mydriasis, asterixis, confusion, ALOC

Renal compensation slow --> Hyperventilate

GIT excess acid loss

• Vomting, diarrhoea, NGT drainage, ileostomy, dehydration

Renal exccess acid loss

• Bartters, Gitelmans, Diuretics (Decreased H+, K+, Cl-)

Overdose of Base

• Antacid, laxatives, milk alkali syndrome
• Massive Hartmann's transfusion
• Iatrogenic use HCO3

Endocrine

• Cushing, steroid excess, hyperaldosteronism

Clinical: Shift O2 curve to L, decrease K+, Ca2+, Cl, dizzy, lightheaded, chest tightness, anxiety, dysphasia, laryngospasm

Is PaO2 Normal?

Is arterial oxygen saturation as expected for PaO2

A-a Gradient

• Expected = (age/4) + 4
• PAO2 = FiO2 (760-47) - PaCO2 x 1.25

Is Oxygen Content Adequate

• (Hb x 1.39 x HbO2 sat) + (0.0031 PaO2)

Is Oxygen Delivery adequate

• pH, Temp, 2.3DPG
• Shift of curve to the L increases affinity to Hb

Anion Gap: (Na + K) - (Cl + HCO3) = 12+/-4

Delta Gap: (AG-12)/(24-HCO3)

• <0.4 NAGMA
• 0.4-0.8 NAGMA + HAGMA
• 1 HAGMA
• >2 Concurrent processes

A-a Gradient: PAO2 = FiO2(760-47) - PaCO2 x 1.25 - PaO2

Expected A-a = (age/4) + 4

Corrected Na+ = Na+ + (glucose -5)/3

Corrected K+: For every 0.1 change in pH K+ changes by 0.5

Urea: CR >100 pre-renal, <50 intra-renal

OSMc = 2 x Na+ + glucose + urea

Tox - Fast Sodium Channel Blockade

Results

Causes

A large terminal R wave in aVR or increased R:S indicates slow rightward conduction and is characteristic of fast sodium channel blockade

• Slowed sodium influx during pahse 0 of cardiac AP
• Widened QRS
• RAD of the terminal QRS (Terminal R waves >3mm AVR, R/S ratio >0.7 in AVR)
• Bradycardia
• VT and VF

TCA Major Toxicity

• QRS >100ms - seizures
• QRS >160ms - Ventricular Dysrhythmias
• RAD of terminal QRS

Drugs

• TCA
• Class 1A antidysrhythmic agents
• Local anaesthetics
• Phenothiazines
• Amantadine
• Carbamazepine
• Chloroquine
• Diltiazem
• Hydroxychloroquine
• Propranolol
• Quinine

• Prolonged QTc
• Torsades de pointes
• Antipsychotic agents
• Class 1a antidysrrhytmics
• Class 1c antidysrhythmics
• Class III antidysrrhtymics
• TCA
• Antidepressants
• Antihistamines
• Chloroquine
• Hydroxychloroquine
• Quinine
• Macrolides - Erythromycin

Anticholinergic

Causes

Features

Complications

Due to competitive inhibition of central adn peripheral acetylcholine muscarinic blockage. Dry as a bone, Red as a beet, hot as a hare, mad as a hatter

Causes

• Antihistamines - cyproheptadine, doxylamine, pheniramine
• Antiparkinsonian drugs - amantadine, benztropine
• Antitussives - Dextromethorphan
• Antipsychotic agents - chlorpromazine, droperidol, haloperidol
• Atypical antipsychotic agents - Olanzapine, Quetiapine
• Anticonuvlsants - Carbamazepine
• Motion sickness agents
• Antimuscarinic - atropine, glycopyrolate, hyoscyamine
• Topical ophthalmological agents
• Urinary antispasmodic agents
  
• Plant poisoning

Features

• Central: Agitated derlium, fluctuating mental status, confusion, restlessenss, fidgeting, visual hallucinations, picking at objects, mummbling, disurptive behaviour, tremor, myoclonus, coma, seizures
• Peripheral: Mydriasis, Dry Mucous Membranes, Urinary retention, Tachycardia, Hypethermia, Ileus, flushing, dry skin
  

Sympathomimetic and anticholinergic syndromes can present similarly, hard to distinguish. Main difference is anticholinergic has dry skin, sympathomimmetic diaphoretic and more likely to be hypertensive

Complications

• Dehydration
• Hyperthermia
• Rhabdomyolysis
• Pre-renal failure
• Pulmonary aspiration and atelectasis
  

Anticholinergic

Management

Resuscitation

Risk Assessment

• Usually manifests within first few hours
• May persist up to 5 days

Supportive Care

• Manage in a quiet, will lit area, 1:1 nursing
  
• IVF
• IDC

Investigations

• ECG
• Paracetamol
• Electrolytes, renal function
• CK

Decontamination - Risk benefit

Enhanced Elimination - Risk benefit

Antidotes

• Physostigmine - centrally acting acetylcholinesterase inhibitor. In delerium difficult to control with benzos. Remember risk of cholinergic crisis
  

Serotonin Syndrome

Causes

Features

Causes

• Amphetamines - ecstasy
  
• Antihistamines
• MAOIs
• SNRIs
• SSRIs
• TCA
• Analgesics and antitussives - tramadol
  
• St Johns Wort
• Lithium
• Tryptophan
  

Features

• Mental status changes: Apprehension, anxiety, agitation, psychomotor acceleration and delirium, confusion
• Autonomic stimulation: Mydriasis, sweating, tachycardia, flushing, HTN, hyperthermia
• Neuromuscular excitation: Clonus (ocular and ankle), Hyper-reflexia, Increased tone (LL>UL), Myoclonus, rigidity, tremor
• In severe, without intervention can progress to rhabdomyolysis, renal failure, DIC and death
• Onset within 8 hours

DDX: NMS, Anticholinergic syndrome, malignant hyperthermia, CNS infections, intoxication with salicylates, theophylline, nicotine or sympathomimetics.

Serotonin Syndrome

Management

Resuscitation

• If recurrent seizures, T>39.5 or severe rigidity --> RSI
• Titrated benzodiazepines to achieve gentle sedation
• If refractory HTN - vasodilator GTN, SNP

Risk Assessment

Investigations

• ECG
• Paracetamol
• CK, renal function, Tn

Supportive Care

Antidote

• Only in mild cases and if benzodiazepines not working
• Cryptoheptadine 8mg PO
• Chlorpromazine 25-100mg in 100ml Nsaline
• Olanzapine 10mg SL

Disposition

Causes

• Organophosphates
• Carbamates

Features

• Bradycardia or Tachycardia
• Hypo or HTN
• Miosis or Mydriasis
• Sweating
• Increased bronchial secretions
• Bronchoconstriction
• Hypersalivation
• GI hyperactivity
• Muscle weakness
• Fasciculations

Cholingeric Syndrome

Causes

Symptoms

Causes

• Acetylcholinesterase enzyme inhibition (Organophosphates, carbamate insecticides, chemical warfare nerve agent, dementia agents, MG agents - neostigmine, physostemine, pyridostigmine)
• Direct agonist action (Muscarinic agents - acetylcholine, bethanechol, pilocarphine), (Nicotinic agents - tobacco, gum, patches, mushrooms)

Clinical features

• CNS - agitation, central respiratory depression, coma, confusion, lethargy, seizures
• Neuromuscular - fasciculation, muscle weakness
• Parasympathetic muscarinic effects - abdominal cramping, bradycardia, bronchoconstriction, bronchorrhoea, diarrhoea, lacrimation, miosis, salivation, urinary incontinence, vomiting
• Sympathetic nicotinic effects - HTN, mydriasis, sweating, tachycardia
• Death is from respiratory failure from excessive respiratory secretions and weakness of ventilator muscles

Cholinergic Syndrome

Management

Resuscitation

• Decontaminate the patient and PPE but should not delay resus
• Early control of pulmonary scretions and oxygen
• Atropine if any signs of muscarinic excess - start at 1.2mg and double dose every 5 minutes
• Seizures - benzodiazpeines

Risk Assessment

Supportive Care

• Insecticide poisoning - well ventilated room
• IVF
• IDC

Investigations

• ECG
• Paracetamol
• CXR
• ABG
• Electrolytes and renal function

Decontamination - risk benefit

Enhanced Elimination - risk benefit

Antidotes

• Atropine
• Pralidozine for organophosphates

Neuroleptic Malignant Syndrome

Diagnostic Criteria

Features

Characterised by neuromuscular rigidity, altered mental status, autonomic instability

Causes: Dopamine antagonists - haloperidol, thioridazine

Clinical Features

• CNS: Confusion, Delirium, Stupor, Coma
• Autonomic Instability: Hyperthermia, Tachycardia, HTN, Respiratory irregularities, cardiac dyrhythmias
• Neuromuscular: Lead pipe rigidity, generalised bradykinesia or akinesia, mutism and starring, dystonia and abnormal postures, abnormal involuntary movements, incontinence, chest wall rigidity may impede ventilation. Bradyreflexia differentiates from serotonin with hyperreflexia
  

Diagnostic Criteria

The development of severe muscle rigidity and elevetated temperature associated with the use of antipsychotic medications. + 2 Or more of the following

• Diaphoresis
• HTN
• Tachycardia
• Incontinence
• Dyspahgia
• Mutism
• Tremor
• Changes in LOC
• Leukocytosis
• Elevated CK

DDX: Serotonin syndrome, encephalitis, metabolic encephalopathy, malignant hyperthermia, anticholinergic syndrome, sympathomimmetic syndrome

Neuroleptic Malignant Syndrome

Investigations

Risk Factors

Investigations

• Leukocytosis up to 40
• alterations of hepatic and renal function
• Metabolic acidosis
• Hypocalcaemia
• Hypomagnasaemia
• Decreased Serum iron
• Normal CT and MRI
• CSF - elevated protein
• EEG - generalised slowing

Risk Factors

• High dose of neuroleptic agent
• Increased dose of neuroleptic agent within previous 5 days
• Large magnitude dose increase
• Parenteral administration
• Simultaneous use of 2 or more neuroleptic agents
• Use of haloperidol or depot fluphenazine
• Young age
• Male sex
• Psychiatric co-morbidity
• Genetic factors
• Pre-existing organic brain disorder
• Dehydration
• High CK levels
• Pre-existing medical disorders - trauma, infection, malnutrition, premenstrual pahse, thyrotoxicosis

Complications

• Respiratory failure
• Dehydration
• Renal Failure
• MOF
• Thromboembolism
• residual catatonia and parkinsonian symptoms

Neuroleptic Malignant Syndrome

Management

Resuscitation

• Intubate if T >39.5
• Detect and correct hypoglycaemia
  
• IV benzos are controversial - bromocriptine preferred
• HTN and tachycardia - GTN, SNP

Supportive Care

• Cease causative agent
• IVF
• Monitor T

Investigations

• Screening - ECG, paracetamol
• Detect complications - CK, UEG, LFT, Blood gas
• Exclude DDx - CT/MRI head/LP
  

Decontamination

Enhanced Elimination

Antidote

• Bromocriptine - dopamine agonist, PO or NGT, 2.5mg TDS. Continued for 1-2 weeks
• Dantrolene - If severe muscle rigidity and fever. IV 2-3mg/Kg
• ECT - Increase central dopaminergic activity

• Phenelzine, Moclobemide
• MAO metabolise serotonin, NA, dopamine --> accumulation of serotonin, adrenaline, NA, dopamine
• Clinical features - Serotonin syndrome, Tyramine reaction (headache, HTN, sweating, agitation, mydriasis, chest pain)
• Manage - as per serotonin syndrome

SSRIs

SE

Which Cause QTC prolongation

• citalopram, escitalopram, fluoxetine, paroxetine, sertraline
• Serotonin Toxicity for all apart from citalopram and escitalopram
• Coma indicates co-ingestion
• QTC prolongation - Citalopram and Escitalopram
• Decontamination if >600mg citalopral - charcoal
• Disposition - >600mg citalopram observe for 8 hours, >1g 13 hours, all other patients 6 hours

TCA

(Amitryptiline, Clomipramine, dotheipin, imipramine, nortryptyline)

Mechanism

Summary

• Self poisoning leads to rapid onset of CNS and cardiovascular toxicity
• Prompt intubation, hyperventilation and sodium bicarbonate at first evidence of severe toxicity are life saving

Toxic Mechanism

• NA and serotonin reuptake inhibitors
• GABAa receptor blockers
• Myocardial toxicity due to blockade of inactivated fast Na channels
• Reversible inhibition of K channels and direct myocardial depression

TCA

Clinical Features

• Rapid deterioration in clinical status within 1-2 hours
• CNS: sedation and coma preceede cardiovascular signs, seizures, delirium secondary to anticholinergic is obscured by coma
• Cardiovascular: Tachy, mild HTN, hypotension due to alpha blocking and decreased contractility, broad complex dysryhtmias, broad complex bradycardia pre-arrest.
• Anti-cholinergic effects: agitation, delirium, mydriasis, dry warm flushed skin, urinary retention, myoclonic jerks

TCA

ECG Changes

•  Prolongation of PR and QRS intervals (fast Na channel blockade). QRS >100ms seizures, >160ms VT.
• Large terminal R wave in aVR
• Increased R/S ratio >0.7 in aVR
• QT prolongation (secondary to K+ channel blockade)

TCA

Management

Resuscitation

• Early life threats - Coma, Respiratory acidosis, seizures, cardiac dysrhythmias, cardiac arrest
• A - If CNS depression GCS <12, arryhtmias, seizures - prompt intubation and hyperventilation
• B - Hyperventilate - pH 7.5-7.55
• C - Hypotension - IVF, sodium bicarbonate 100mol (2mmol/Kg) every 2-3 minutes with end point narrow QRS, pH 7.5, inotropes - NA 0.1mcg/Kg/min titrate to MAP 65
  
• Ventricular dysrhythmias - cardioversion unlikely to be successful. Sodium Bicarbonate 100mmol, lignocaine 1.5mg/Kg when pH >7.5. Type 1a antiarryhtmic agents, amiodarone and b-blockers are CI
• Exclude hypoglycaemia
  

Risk Assessment

• Ingestion >10mg/Kg is potentially life threatening
• Onset within 2 hours of ingestion
• Seizures and myoclonus are more common with dothiepin

Supportive Care

• Continous cardiac monitoring
• Sedation
  

Investigations

• ECG

Decontamination

• Activated Charcoal if Ingestions >10mg/Kg and only if intubated

Enhanced Elimination - Nil

Antidotes - Sodium Bicarbonate

Disposition

• If asymptomatic, normal ECG, normal vitals at 12 hours- medically clear
• Minor ECG changes - cardiac monitoring, serial ECG until normal
• Severe Toxicity - ICU
• If arrested continue resus until intubated, hyperventialted + HCO3 to pH 7.55
• Good outcomes after prolonged arrest
  

• Potent selective serotonin and NA reuptake inhibitors. Also Na+ blocking activity in high doses
• Venlafaxine frequently causes seizures and in very large ingestions cardiovascular toxicity
• Onset of seizures may be delayed 16 hours
• High risk of serotonin syndrome if other serotonergic agents are co-ingested
• Massive ingstions >7g - cardiovascular effects
• Clinical Features: Dysphoria, anxiety, mydriasis, sweating, tremour, clonus, tachycardia, HTN common and may herald onset of seizures. Rhabdomyolysis following severe ingestions. Prolongation of QT/QRS/Dysryhtmias with largest overdoses
  
• Management: Early prophylactic dose of IV benzo will prevent seizures
• Decontamination - Charcoal in patients who are alert, within 2 hours and >4.5g. If >7g or ALOC - ETT and give via NGT
• Enhanced Elimination - Nil
• Antidotes - Nil
• Disposition - must be observed 16 hours. Cardiac monitoring for 6 hours. Can discontinue if ingestion <4.5g and normal ECG. >4.5g cardiac monitoring for 12 hours.

• Competitive inhibition of COX 1 and 2 with blockage of prostaglandin synthesis --> directly irritant to GIT, renal glomerular vasoconstriction. Inhibition of TXA2 - prolonged bleeding time. Overdose with any NSAID unless ingestion is massive is benign
• Management is symptomatic and supportive
• Massive overdose (ibuprofen >300mg/Kg)  is associated with severe MOF, shock, coma, seizure, ARF and metabolic acidosis
• Overdose of any amount of Mefenamic acid is commonly associaed with self limiting seizures
• VBG shows HAGMA
  
• Decontamination CI following mefenamic overdose due to risk of seizure
• Disposition - Clear for discharge if asymptomatic with normal vitals at 4 hours

• CNS and respiratory depression
• Death is due to respiratory failure
• Leading cause of death by poisoning in children - single tablet can cause respiratory arrest
• Agonist activity at mu: euphoria, analgesia, dependence, sedation, respiratory depression
• Dopamine: N&V
• Clinical features: CNS depression, respiratory depression, miosis, hypothermia, skin necrosis, compartment syndrome, rhabdomyolysis, hypoxic brain injury
• Antidote - Naloxone
• Special case: Dextroproppxyphene (cough syrup) - CNS depression, seizures, cardiac dysrhythmias

Acute Paracetamol Poisoning

• Elevated production of NADPQI leads to depletion of glutathione stores --> NADPQI binds to other proteins causing hepatocyte injury
• Threshold dose >150mg/Kg (200mg in children) or >10g
• Plot paracetamol level on Prescott nomogram at 4-15 hours
• >8<24 hours - serum paracetamol + LFTS
• >24 hours - paracetamol, eLFTs, glucose, coags
• Survival is 100% when NAC is commenced within 8 hours of overdose
• Patient who presents >24 hours post ingestion with normal hepatic transaminases and no paracetamol level - little risk of developing hepatotoxicity
• Antidote: NAC infusion (150mg/kg 200ml 5% dextrose over 15 min, 50mg/kg in 500ml 5% dextrose 4 hours, 100mg/Kg in 1L 5% over 16 hours)
• If present <8 hours start after level - no further Ix required
• If >8 hours - start NAC immediately, cease if paracetamol <treatment level or ALT normal after 20 hour infusion
• >24 hours - start NAC, if ALT normal can cease or continue until ALT falling
• If ALT >1000 check coags, glucose

• INR >3 at 48 hours or >4.5 at any time
• Oliguria or Cr >200
• Acidosis with pH <7.3 after resuscitation
• Severe hypotension with SBP <80mmHg
• Hypoglycaemia
• Severe thrombocytopaenia
• Encephalopathy of any degree

• Staggered dosing with >4g/day or 60mg/Kg/day in children
• The decision to treat is based on estimation of dose in conjunction with biochemical testing

Risk assessment

• 10g or >200mg/Kg over a single 24 hour period
• 6g or 150mg/Kg/24 hours for the preceeding 48 hours or longer
• >100mg/Kg or 4g/24 hours in patients with risk factors (alcoholism, isoniazid, prolonged fasting)
• Children >200mg/Kg in 24 hours, >150mg/Kg each 24 hours for 48 hours, 100mg/Kg per 24 hours for 72 hours

Investigation and Management

• ALT or AST <50 and paracetamol <20 NAD
• ALT or AST >50 and paraetamol >10 - NAC
• NAC if clinical features of heaptitis
• NAC for 8 hours then repeat ALT/AST if ongoing rise NAC continued at 100mg/Kg for 16 hours until patient is clinically well and ALT and INR are falling
• Falling or static serum AST/ALT suggest a resolving injury and NAC may be ceased

Salicylates

Summary

• Classical symptoms of vomiting, tinnitus, hyperventilation, respiratory alkalosis and metabolic acidosis
• <150mg/Kg minimal symptoms
• >300mg/Kg severe intoxication
• >500mg potentially lethal
  

• Urinary alkalization and haemodialysis are highly effective methods of enhancing elimination
• Chronic intoxication prsents with non specific clinical features - confusion, delerium, dehydration, fever, unexplained metabolic acidosis. Cerebral and pulmonary oedema are more common than in acute
  

Salicylates

Mechanism

• Irreversible inhibition of cox enzymes resulting in decreased prostaglandin synthesis
• Stimulation of respiratory center --> hyperventilation --> respiratory alkalosis
• Uncoupling of oxidative phosphorylation - accumulation of lactic acid --> metabolic acidosis
• Promotion of fatty acid metabolism and generation of keton bodies --> metabolic acidosis

• Progressive over hours, may not be evident until 6-12 hours post ingestion
• GIT: Nausea and vomiting
• CNS: Tinnitus, decreased hearing, vertigo, CNS stimulation, agitation, seizures, cerebral oedema, death
• Acid Base disturbance: Respiratory alkalosis, HAGMA - acidaemia occurs late and indicated immiment demise without intervention
• Hyperthermia, hyper/hypoglycaemia, hypokalaemia

Consider Salicylate toxicity and order a serum salicylate in any elderly patient with ALOC and metabolic acidosis

Salicylates

Management

Investigations

• ECG, Paracetamol
• Salicylate level - therapeutic range is 1.1-1.2mmol/L. Poor correlation between levels adn severity. Serial levels every 2-4 hours to identidy ongoing or delayed absorption from tablet bezoar
• ABG

Decontamination

• Activated charcoal 50g up to 8 hours following acute overdose of >150mg/Kg
• second dose after 4 hours if salicylate level continues to rise

Enhaced Elimination

• Urinary alkalisation - sodium bicarbonate to alkalinise urine and prevent redistribution to CNS - pH >7.4 at all times. If intubated can achieve this by hyperventilation. If not intubated soidum bicarbonate 2mmol/Kg/IV. Maintained unil definitive care with haemodialysis.
• Urinary alkalisation - correct hypokalaemia, give 102mmol/Kg sodium bicarbonate IV bolus, commence infusion of 100mmol in 1L 5% dextrose at 250ml/hr. Add 20mmol KCL to maintain normokalaemia. Monitor serum K and bicarb Q4h. Regularly dipstick urine and aim for pH>7.5
• Haemodialysis if - urinary alkalisation not possible, serum salicylate levels rising >4.4 despite decontamination and urinary alkalisation, severe toxicity

Salicylates

Enhanced Elimination

Urinary Alkalisation

• sodium bicarbonate to alkalinise urine and prevent redistribution to CNS - pH >7.4 at all times. If intubated can achieve this by hyperventilation. If not intubated soidum bicarbonate 2mmol/Kg/IV. Maintained unil definitive care with haemodialysis.

• Urinary alkalisation - Correct hypokalaemia
• give 102mmol/Kg sodium bicarbonate IV bolus
• commence infusion of 100mmol in 1L 5% dextrose at 250ml/hr.
• Add 20mmol KCL to maintain normokalaemia.
• Monitor serum K and bicarb Q4h.
• Regularly dipstick urine and aim for pH>7.5

Haemodialysis

• Urinary alkalisation not possible
• Serum salicylate levels rising >4.4 despite decontamination and urinary alkalisation
• Severe toxicity as evidenced by ALOC, acaeidemia or renal failure
• Very high serum salicylate levels - Acute >7.2, Chronic >4.4

Down regulation of neuro-inhibitory GABA and NMDA excess

Autonomic excitation

• Occurs within hours of cessation and peaks at 24-28 hours
• Tremor
• Anxiety and agitation
• Sweating
• Tachycardia
• HTN
• Nausea and vomiting
• Hyperthermia

Neuro-excitation

• Occurs within 12-48 hours
• Hyperreflexia
• Nightmares
• Hallucinations (visual, tactile)
• Seizures

Delirium Tremens

• Mortality approached 8%
• Associated with medical co-morbidities and delayed presentation
• Hallucinations
• Confusion, disorientation and clouding of consciousness
• Autonomic hyperactivity
• Respiratory and cardiovascular collapse
• Death

Co-morbidities

• Wernicke's encephalopathy
• Dehdyration
• Electrolyte abnormalities
• Alcoholic gastritis
• Pancreatitis
• Alcoholic liver disease and heaptic encephalopathy
• Subdural haemorrhage
• Alcholic ketoacidosis

Amphetamines

Toxic Mechanisms

Clinical Features

Metamphetamines: Ice, speed

MDMA - ecstasy

Toxic Mechanisms

• Structurally related to adrenaline
• Enhance catecholamine release and block their uptake
• Inhibition of MAO
• CNS and peripheral NA, DA, and serotenergic stimulation
• NMDA induces SIADH leading to profound hyponatraemia, coma and convulsions

Clinical features

• CNS: euphoria, anxiety, agitation, paranoid psychosis with visual and tactile hallucinations, hypthermia, rigidity and myoclonic movements, seizures
• Cardiovascular: Tachycardia, HTN, dysrhythmias, ACS, acute cardiomyopathy, APO, hamoptysis
• Peripheral sympathomimetic: Mydriasis, sweating and tremor

Medical Complications

• Rhabdomyolysis, dehydration and renal failure
• Hyponatraemia and cerebral oedema following MDMA ingestion due to SIADH and water ingestion
• Aortic and carotid artery disection
• SAH and ICH
• Ischaemic colitis

Amphetamine

Management

Resuscitation

• Immediately treat HTN, seizures, hyperthermia, hyponatraemia
• Benzodiazepines - if refractory
• Phentolamine 1mg every 5 minutes/GTN
• Beta-blockers are contraindicated - unopposed alpha adn vasoconstriction
• Seizures - IV diazepam
• Hyperthermia >39.5 - Intubate and rapid external cooling
• Hyponatramia - if <120 immediate correction with hypertonic saline 3% 4mL/Kg over 30 minutes and repeat Na. Maintain Na>120 until SIADH resolves

Investigations

• ECG, BSL, paracetamol
• eLFTs - Na, renail failure
• ECG, CK, Tn - MI, ACS, rhabdomyolysis
• CXR - aortic dissection and aspiration

No decontamination, enhanced elimination, antidotes

Cocaine

Clinical Features

Powerful sympatomimetic and LA properties

Toxic Mechanism

• Sympathomimetic: blockade of presynaptic catecholamine reuptake and can result in vascualr dissection, ICH and acute cardiomyopathy
• Vasospastic
• Sodium channel blockade (LA) - ventricular dysrythmias

Clinical Features

• CNS: euphoria, anxiety, dysphoria, agitation, aggression, paranaoid psychosis with visual and tactile hallucinations, hyperthermia, rigidity,myoclonic movements, seizures
• Cardiovascular: Tachycardia, HTN, arrythmias and cardiac conduction abnormalities, ACS - vasospastic and/or coronary thrombotic, QT prolongation, APO
• Peripheral sympathomimetic: Hypethermia, muscle fasciculation, mydriasis, sweating and tremor

Complications

• Hyperthermia induced rhabdomyolysis, renal failure and cerebral oedema
• Aortic and carotid dissection
• SAH, ICH
• Ischaemic colitis
• Pneumothorax
• Pneumomediastinum

Cocaine

Management

Resuscitation

• Immediate intervention: dysrythmias including VT, HTN, hyperthermia, seizures, severe agitation
• VT: IV bolus 50-100mmol sodium bicarbonate, if refractory lignocaine 1.5mg/Kg IV followed by an infusion of 2mg/min
• ACS- normal management except beta blockers. Thrombolytics are CI in severe HTN, seizures, ICH or aortic dissection
• Sinus tachy and HTN - benzodiazepines
• Refractory HTN - same as amphetamines
• Hyperthermia -same as amphetamines

Risk assessment

• Ingestion >1g potentially lethal
• Pregnancy - teratogenic

Investigations

• ECG, BSL, paracetamol
• eLFTs - renal failure and hyponatraemia
• ECG, CK, Tn - MI, infarction, ACS, QT prolongation, rhabdomyolysis. Brugada type pattern. The sensitivity of ECG for detection MI is lower in cocaine
• CXR - aortic dissection, pulmonary aspiration
• CT head - ICH

Disposition

• Well and asymptomatic @4 hours with normal ECG can be discharged
  
  

Clinical Features

• Symptoms may begin within 6 hours of the last heroin use, peak at 36-48 hours and resolve within 1 week
• methadone symptoms onset may be delayed 2-3 days
• Intense cravings
• Dysphoria
• Autonomic hyperactivity
• Gastrointestinal disturbance
• Anxiety, restlessness, insomnia
• Yawning
• Lacrimation, salivation, rhinorrhoea
• Anorexia, nausea and vomiting
• Abdominal cramps and diarrhoea
• Mydriasis
• Piloerection
• Diaphoresis
• Flushing
• Myalgia and arthralgia
• HTN and tachcardia
• ALOC, delirium, hyperthermia and seizures do not occur

Management

• Administration of opioids
• Opioid replacement therapy: Methadone, buprenorphine
• Antagonist detoxification: Naltrexone
• Symptomatic treatment

In excessive doses causes rapid onset of CNS and respiratory depression, myoclonic jerking and bradycardia

Mechanism

• Short chain acid that occurs naturally in the brain, breakdown product of GABA and may be a neurotransmiter itself
• Duration of effects is 4-6 hours

Clinical Features

• Recreational doses: rapid onset of euphoria and drowsiness, enhances sexual desire, performance and orgasm
• Overdose: Euphoria followed by coma
• Patient can be roused by external stimulus
• Sudden recovery within 2-3 hours
• Coma lasting >6 hours indicates alternative diagnosis (co-ingestion or complication)

All volatile liquids and well absorbed via inhalational route

Distributed to lipid rich organs and excreted by the lungs

Acute use

• Patients are euphoric, disinhibited and lethargic and ataxia with slurred speech and inappropriate affect
• Confusion, depressed LOC, seizures and coma
• Aspiration adn chemicla penumonitis
• Sudden death with butane and propane

Chronic Use

• Persistent neurotoxicity characterised by strucutral and functional brain abnormalities
• NAGMA due to distal renal tubular acidosis
• Hyperchloramia
• Hypokalaemia

Management

• Resuscitation
• IV benzo
• Sodium Bicarbonate
• Management of hypokalaemia

Enhanced Elimination

Summary

Aliphatic: Essential oils (eucalyptus), kerosene, petroleum, turpentine

Aromatic: Benzene, Toluene, Xylene

Halogenated: Carbone tetrachloride

MOA: Unclear, disruption of lung surfactant - chemical pneumonitis

Clinical Features: Whether ingested or inhaled can caused rapid onset of CNS depression, seizures and cardiac dysrythmias. Aspiration can lead to chemical pneumonitis

Risk assessment

• CNS depression and seizures major risk
• 1-2ml/Kg of solvent usually required to caused significant toxicity
• 10mL of eucalyptus oil causes significant toxicity

Decontamination

• Remova patient from exposure, remove clothing and wash skin
• Activated charcoal does not bind hydrocarbons
• Gastrointestinal decontamination is contraindicated due to risk of hydrocarbon aspiration

Disposition

• Asymptomatic with normal vitals at 6 hours - fit for discharge

Found in car wheel cleaners, rust removing solution and preparations for glass etching

Mechanism

• Fluoride ions bind with calcium and magnesium as well as interfering with cellular K channel --> Hypocacalcaemia, hypomagnaesemia, hyperkalaemia

Clinical features

• Dermal Exposure: Not immediately painful, gradual onset of severe, deep unremitting pain, blistering and tissue loss
• Inhalational exposure: Mucosal irritation, delayed onset of dyspnoea, cough and wheeze, non-cardiac pulmonary oedema
• Ingestions: Low concentrations <20% are minimally corrosive. Cardiac arrest from systemic fluoroses may occur without warning 30min to 6 hours post ingestions.
• Systemic Effects: Tetany, QT prolongation, ventricular arrhythmias, cardiac arrest

Risk assessment

• Any dermal exposure may lead to delayed severe pain and tissue injury

Investigations

• Serial ECG: Degree of QT prolongation is a useful marker of hypocalcaemia
• Serum or ionised calcium
• Endoscopy - corrosive injury

Management

• ABC
• IV calcium drawn up and available
• Ventricular dysrhythmias: ALS, intubate and hyperventilate, calcium gluconate 10% 60mL or Calcium chloride 10% 20mL adn repeat every 5 minutes. Soidum bicarbonate 100mmol, magnesium sulfate 10mmol.

Decontamination

• Dermal exposure: remove clothing, irrigate with water
• Ingestions: Do not induce vomiting
• Occular: irrigate

Enhanced Elimination - Nil

Antidotes

• Calcium
• Calcium gluconate gel to dermal exposure
• If pain is refractory SC or regional calcium infusion
• Do not give calcium chloride by SC injection, regional, IV infusion or arterial infusion

Disposition

• All patients at risk of systemic flurosis need monitoring for 12 hours in an environment equiped to detect and manage cardiovascular collapse. Need normal ECG without calcium administration for discharge

Local anaesthetic is CI as relief of pain is used as an end point to determine adequacy of calcium

Clinical Features/Risk Assessment

• <30ml dilute (3%) solute - mild GI effects
• >30ml  (3%) - more severe GI corrosive effects. May cause gas embolism from release of O2
• Concentrated (10%) ingestion - Life threatening GI/airway corrosion, life threatening gas embolism/rupture of GI tract

Investigations

• FBC, UEG, ABG
• Consisder CXR, AXR, CT abdo/Chest (perforation), CT head (gas embolism), endoscopy (GI symptoms)

Treatment

• Standard resus + supportive care
• Early airway management if upper airway oedema/obstruction
• Hyperbaric therapy for gas embolism (particularly CNS embolism with neurology)
• NGT - relieve gaseous distention of stomach

Decontamination

• Remove clothes and wash

• Potent psychoactive compound
• Pscychedelic effects are mediated through serotonergic systems - agonist at 5HT2 receptor
• Physiologic effects - sympathomimmetic

Management: Supportive, benzo

Ethanol

Mechanisms

Toxic Mechanisms

• Augmentation of GABA receptor
• Dose dependent cardiovascular depression
• Impairs gluconeogenesis - Hypoglycaemia

Deliberate self poisoning is lethal without timely intervention

Toxic Mechanisms

• CNS effects similar to those of ethanol
• Important effects are due to metabolites
• Severe HAGMA secondary to accumulation of glycolic acid and lactate
• Calcium oxalate crystals in tissues including renal tubules, myocardium, muscles and brain --> hypocalcaemia
• Acute renal failure due to nephrotoxic effects of both glycolic acid and calcium oxalate
• Rapidly absorbed - peak concentration 1-4 hours
• Ethanl competitively inhibits ADH preventing metabolism of EG and hence has to be eliminated exclusively by the kidney

Clinical Features

• CNS, cardiopulmonary and renal
• Initial clinical features similar to ethanol
• Progressively severe features over 4-12 hours - dyspnoea, tachypnoea, tachcyardia, HTN, decreased LOC, shock, coma, seizures and death
• Flank pain and oliguria - ARF
• late cranial neuropathies - CN II, V, VII, IX, X, XII, 5-10 days later

Investigations

• Screening
• eLFTS, lactate, serum osmolality, ABG - elevated osmolar gap, HAGMA, hyperlactaemia, Hypocalcaemia, rising Cr
• Breath or serum ethanol level to determine co-ingestions
• Serum EG level
• Urinary MCS - calcium oxalate crystals

Risk assessment

• Ingestion >1ml/Kg is potentially lethal
• Unintentional ingestions of less then a mouthful is benign
• Co-ingestion of ethanol complicates risk assessment
• Dermal and inhalational exposure does not lead to intoxication

Ethylene Glycol

Management

Resuscitation

• ABC
• Acidaemia with degree of respiratory compensation -> Intubation and maintain hyperventilation to avoid exacerbating acidosis
• Bolus IV sodium Bicarbonate 1-2mmol/Kg
• Seizures - IV benzo
• Detect and treat hypoglycaemia, hyperkalaemia and hypomagnaesemia
• Correct hypocalcaemia only if refractory seizures or prolonged QT

Nil Decontamination

Enhanced Elimination

• Haemodialysis is the definitive management. EG half life is decreased to 2.5-3.5 hours
• Indications
• History of large EG ingestions with osmolar gap >10
• Acidaemia with pH <7.25
• ARF
• Ethylene glycol levels >8mmol/L

Antidotes

• Ethanol and fomepizole are temporizing
• Ethanol competitively blocks formation of toxic metabolites by having a greater affinity for ADH
• Oral, NG or IV

Disposition

• Adult patients, well, negative breath test for ethanol and normal bicarbonate 4 hours post accidental ingestion fit for discharge
• Admit all symptomatic patients

• CNS effects Identical to ethanol but more potent and no HAGMA and no antidotes

Toxic Mechanism

• Production and accumulation of formic acid - HAGMA and direct cellular toxicity
• Retinal injury and oedema - blindness
• Brain - subcortical white matter haemorrhages and putamental oedema
• Late hyperlactaemia due to inhibition of cellular oxidative mechanisms

Clinical Features

• Mild CNS depression
• Headache, dizziness, vertigo, dyspnoea, blurred vision, photophobia
• Tachypnoea, drowsiness, blindness
• Coma and seizures, cerebral oedema, papilloedema
• Extrapyramidal movement disorders

Management  - Same as Ethylene Glycol

Risk Assessment

• Ingestion >0.5mL/Kg is potentially lethal

Investigations

• Serum methanol levels
• CT brain: Demonstrates characteristic injury to the basal ganglion

Haemodialysis

• Any patient who fulfils criterial for ADH blockade
• Acidaemia with pH <7.3
• Visual Symptoms
• Renal Failure
• Deterioration
• Methanol level >16mmol/L

Antidote

• Same as ethylene glycol

Patients without obvious bite marks and symptoms can be envenomed

Pre-Hospital

• First Aid: PIB (over the entire limb, immobilisation of the limb, immobilisation of the whole patient in attempt to delay lymphatic spread of venom). Do not wash wound.
• PIB is not removed until patient has been fully assessed or antivenom administration has commenced

Hospital Resuscitation: Potential early lfe threats

• Hypotension (brown snake, taipan, tiger)
• Respiratory failure secondary to paralysis (death adder, taipan, tiger, rarely brown)
• Seizures (taipan)
• Severe venom induced consumptive coagulopathy (VICC) - (brown, taipan, tiger)

Determine if patient has been envenomed

• Assessment is performed serially over at least 12 hours and is based upon
• History - Geographic, apperance of snake, use of PIB, early symptoms
• Physical examination - bleeding, neurotoxicity, rhabdomyolysis
• Laboratory investigations - FBC, U&E, CK, coags
• Serial physical exams and invstigations pefurmed until envenoming is diagnosed or 12 hours have expired
• If the patient remains well and initial laboratory studies are normal the PIB is removed. It is immediately reapplied if deterioration.
• Upon removal of PIB patient is observed and examined at 1,6 and 12 hours

SVDK

Indications for polyvalent venom

SVDK

• Not used to determine whether envenomation or not
• If any doubt 2 or monovalent better than polyvalent
• Perform using bite site swab via cutting a key hole in PIB
• Second line - urine
• Should not be perfomed on serum or blood
• First well to turn blue in 10 minutes

Indications for polyvalent venom

• Severe Established envenomation - collapse, unconscious, paralusis, DIC - delay for tests unacceptable
• Unable to identify appropriate monovalent
• Appropriate monovalent unavailable

• Resus area and monitoring
• SVDK - appropriate anti-venom
• 2 x large IV bore IVC
• 1:10 dilution
• Anticipate anaphylaxis -adrenaline IM/IV/Infusion
• Verbal consent
• Remove PIB
• Infuse over 15-30min
• Dose may need to be repeated in discussion with toxicologist and patient clinical course
• After administration patient clinical status is monitored and lab investigations repeated after 6 and 12 hours. Then every 12 hours until normalised.
• Need to be counseled about possibility of serum sickness 4-21 days after antivenom
• Prednisolone 1mg/Kg/day
• Use of blood products such as FFP or cryo in management of VICC is controversial

Mushroom Poisoning

General Overview

• Benign self limited GIT disturbance most common
• Consider cyclopeptide hepatotoxic poisoning when GIT symptoms >6 hours
• Investigations - Mycologist, electrolytes, LFTs 24-48 hours post if cyclopeptide hepatotoxin considered

Decontamination: Activated Charcoal 50g

Enhanced Elimination: MDAC

Antidotes - many but no evidence

• High dose penicillin G
• Cimetidine
• NAC
• Silibinin

Muscarin: Cholinergic effects - lacrimation, salivation, bronchorrhoea

Psilocybin: Hallucinogenic

Glutaminergic: CNS depression/seizures

Resuscitation

• If uncontrolled haemorrhage
• FFP 10-15ml/Kg
• Prothrombin X 25-50IU/Kg
• Vitamin K 10mg IV

Risk assessment

• Following acute single ingestions, coagulopathy may not be evidenced for 12 hours. Peak effect at 72-96 hours
• Single accidental ingestion does not cause signficant anticoagulation
• Brodifacoum - 0.1mg/Kg (approx 3 50g pellets) will cause coagulopathy
  
• Anticoagulation is associated with repeated ingestions, weeks to months

Investigations

• Screening - ECG, BSL, paracetamol
• INR - vitamin K must be withhedl until anticoagulation is documented. Normal INR at 48 hours excludes toxic ingestions
• Do serial INRs every 12 hours for 48 hours

Decontamination

• Charcoal 50g <12 hours
  

Enhanced Elimination - Nil

Antidotes

• Vitamin K to achieve INR <4
• Often large daily oral doses required for weeks to months
• Do not inititate vitamin K prophylactically to normal INR as delays onset of toxicity

• Inhibits vitamin K metabolism, leading to depletion of the active reduced form of cofactor for synthesis of II, VII, IX, X and protein C and S
• 8-12 hour delay is due ot half lives of pre-existing vitamin K dependent co factors
• Risk of bleeding increases with INR >5
• INR is normal for the first 6 hours, normal INR at 48 hours excludes warfarin overdose

Management of uncontrolled bleeding

• Prothrombin complex 25-50IU/Kg
• FFP 150-300ml
• VItamin K 10mg IV

Decontamination: 50 g activated charcoal if within 1 hour

Antidotes: Vitamin K - if therapeutic need for warfarin careful titration of vitamin K

Disposition

• Nontherapeutic requirement - 10-20mg PO vitamin K and repeat INR at 48 hours
• If therapeutic need - titrated vitamin K dose as inpatient

Beta Blockers

Mechanism

Clinical Features

Overdose other than with propranolol or sotalol results in little toxicity

Toxic Mechanism

• Excess beta blockade --> decreased icAMP and blunting of metabolic, chronotropic and inotropic effects of catecholamines
• Propranolol also has Na+ Blocking effects -> QRS widening and ventricular arrhythmias. Also lipid soluble and enters CNS - direct toxicity
• Sotalol - Blocks K+ channels - interfering with cardiac repolarisation and leading to QT prolongation

Clinical Features

• Occurs within 4 hours
• Cardiovascular: Hypotension, bradycardia, Bradyarrhythmias - sinus, 1st to 3rd degree HB, junctional or ventricular bradycardia, QRS widening (propranolol), QT prolongation (sotalol)
• CNS: Delirium, coma, seizures (propranolol)
• Bronchospasm, pulmonary oedema
• Hyperkalaemia
• Hypo/Hyperglycaemia

Risk Assessment

• Toxicity does not correlate well with ingested dose
• Factors increasing risk of severe toxicity
• Ingestions of propranolol/sotalol
• Underlying heart or lung disease
• Co-ingestions with CCB or digoxin
• Advanced age
• Threshold dose for severe toxicity from propranolol may be as little as 1g
• PR interval prolongation even in absence of bradycardia is an early sign of toxicity

Beta-Blockers

Management

Resuscitation

• Propranolol is measured the same as TCA overdose
• Ventricular arrhythmias - sodium bicarbonate
• Bradycardia and hypotension - Atropine 0.01-0.03mg/Kg, Isoprenaline 0.1mcg/kg/minute, adrenaline, high dose insulin
• Wide QRS - sodium bicarbonate 1-2mmol/Kg
• Torsades (Sotalol) - Isoprenaline, magnesium, overdrive pacing

Decontamination: Activated charcoal within 2 hours but caution in propranolol due to risk of coma and seizures

Enhanced Elimination - Nil

Antidote - No

• Glucagon has been previously used but offers no advantage over standard inotropes and chronotropes. Can be difficult to source sufficient stocks
• Role of IV lipid emulsion in propranolol is yet undefined (1-1.5ml/Kg and repeat every 5 min)

Dispostion

• Patients with normal ECG and asymptomatic at 6 hours - clear

CCB Overdose

Mechanism

Clinical Features

Non-dihydopyridines:Diltiazem, Verapamil

Dihydropyridines: Amlodipine, Felodipine, Lercandipine, Nifedipine, Nimodipine

Verapamil and diltiazem commonly cause cardiovascular collapse. May be delayed after XR ingestions.

Toxic Mechanisms

• Prevent opening of L-type calcium channels
• Non-dihydropyridines: Central cardiac effects and peripheral vasodilation
• Dihydropyridines: Peripheral vasodilation

Clinical Features

• Vascular smooth muscle relaxation, Hypotension, Bradycardia, Decreased contractility, Hyperglycaemia and lactic acidosis
• MI, stroke or non-occlusive mesenteric ischaemia may occur
• Seizures and coma are rare - indicates a co-ingested agent

Risk Assessment

• Ingestion of as little as 2-3 times the normal therapuetic dose of verapamil or diltiazem can cause severe toxicity
• Ingestion >10 tablets of verapamil or diltiazem - life threatening
• Onset is 2 hours in standard or 16 hours following XR
• Increased risk: Advanced age, co-morbidities like cardiac disease, co-ingestions of other cardiotoxic agents

Investigations

• ECG, paracetamol, BSL
• Serial ECGs
• eLFTs
• Calcium
• Serum lactate
• ABG
• CXR

CCB

Management

Resuscitation

• Once significant toxicity has occured (hypotension following 20mL/Kg fluid bolus) do not delay ETT
• Potential life threats - Hypotension, cardiac dysrhythmias, cardiac arrest
• Mentation adn airway reflexes are preserved until cardiac arrest is imminenet - early I&V

Graduated apporach to hypotension

• Fluid resuscitation
• Calcium - 60ml 10% calcium gluconate or 20ml 10% calcium chloride. Can produce a temporary increase in HR and BP and may be repeated 3 imes whilst other therapies are started. Commence infusion to maintain calicum levels >2
• Atropine - 0.6mg ever 2 minutes up to 3mg
• Catecholamine infusion - dopamine, adrenaline (0.1mcg/Kg/min), NA
• High dose insulin 50ml of 50% dextrose (25g) and then 1unit/Kg short acting insulin bolus. Followed by infusion of dextrose 25g/hr and insulin 0.5units/Kg/hr. May increase infusion up to 1unit/Kg/hr
• Sodium Bicarbonate - 50-100mmol for metabolic acidosis
• Cardiac pacing - to bypass AV block, rate no greater than 60
• Cardiopulmonary bypass and IABP

Decontamination

• Charcoal within 1 hour of ingestions and 4 hours for XR - administer to all intubated patients
• Whole bowel irrigation - after activated charcoal in cooperative patients without evidence of established toxicity and within 4 hours of overdose

Disposition

• Well and normal ECG at 4 hours (standard) and 16 hours (XR)

Amiodarone

Acute

Chronic

Acute: Uncommonly produces toxicity, atrial flutter, hypotension and T wave inversion. Monitoring for 24 hours

Chronic toxicity: Pulmonary toxicity, cardiovascular effects - bradycardia, AV blocks, torsades, hypotension and negative inotropy, thryoid dysfunction, hepatic toxicity, corneal micro-deposits

Intoxication manifests clinically with triad of - drowsiness, miosis, bradycardia

Mechanism

• Centrally acring alpha 2 agonist (HTN, migraine, withdrawal, menopause and pain control)
• Sympathoplegic agent - decrease central nervous sympathetic outflow
• Increases endothelial nitric oxide levels
• Decreases renin activity

Clinical Features

• Transient early HTN
• Severe intoxication - coma, bradycardia, hypotension
• Hypothermia, respiratory depression and apnoea
• Symptoms resolve within 24 hours

Investigations

• Serial ECGs

Management - Supportive

Antidote

• Naloxone inconsistently transiently provides transient revesal of CNS and respiratory depression
• Give 0.1mg IV ever 30-60 seconds

Dispostion

• If well without symptoms at 4 hours - discharge home

Acute Digoxin Overdose

Mechanism

Clinical Features

Toxic Mechanisms

• Inhibits membrane Na+K+ATPase pump - increased intracellular calcium - enhances automaticity, positive inotropic, and increased K
• Enhances vagal tone - decreased SA and AV node conduction

Clinical Features

• Manifests with early onset of vomiting and hyperkalaemia and progress to life threatening cardiac dysrhythmias and cardiovascular collapse
• Cardiovascular complications are refractory to conventional resuscitation measures
• GIT: N&V
• Bradycardia - 1-3rd AV block, AF with VR <60
• Increased automaticity - ventricular ectopic beats, bigemny, SVT with AV block, VT
• Hypotension
• CNS: Lethargy, confusion

Risk Assessment

• Acute intoxication if >10times daily dose
• Potentially lethal dose - >10mg, serum digoxin level >15nmol/L, serum K+ >5.5mmol/L

Investigations

• Screening
• eLFTs - Hyperkalaemia, renal function
• Serum digoxin levels - confirm poisoning, indication for Ab treatment, level 4 hours post ingestion, then every 2 hours until definitive treatment or toxicity resolving

Acute Digoxin Overdose

Management

Potential early life threats

• Hypotension
• Cardiac Dysrythmias
• Cardiac arrest

Cardiac Arrest

• Standard resuscitation measures are futile
• 20 ampoules of digoxin immune Fab
• Attempts at resuscitatin should continue for at least 30 minutes after administration of antidote
• If immune Fab not avaialble - temporising measures - Hyperkalaemia (Sodium bicarbonate, Insulin, dextrose, calcium is CI), AV block (atropine 0.6mg IV), VT (Lignocaine 1mg/Kg)

Decontamination - Charcoal within 1st hour

Enhanced Elimination - No

Antidote - Digoxin immune Fab when

• Cardiac arrest
• Life threatening cardiac dysrhythmias
• Ingested dose >10mg
• Serum digoxin level >15mmol/mL
• Serum potassium >5mmol/L
• Dosing is empirical or based on the dose known to be ingested
• One ampoule of Fab binds 0.5mg digoxin
• Has greater affinity for digoxin than NaK+ ATPase receptor
  
• If uknown dose commence empiric dosing with 5 ampoules if stable
• 10 ampoules if unstable
• Give repeat doses of 5 amps until reversal of digoxin toxicity
• A single dose given over 30 minutes in 100ml normal saline is usually sufficient
• If known dose: Number of ampoules = ingested dose (mg) x 0.8 x 2
• End points - restoration of normal rhythm/conduction, resolution of GI symptoms
• Do not repeat digoxin levels following administration of antidote as most labs measure both bound and unbound
• Adverse effects: Hypokalaemia, allergy, exacerbation of underlying cardiac failure , loss of rate control of pre-existing AF

Tips

• Cardiac Failure - 20 ampoules
• Levels following treatment high as measure both bound and unbound
• Hyperkalaemia due to digoxin poisoning is treated with Fab not calcium

Disposition

• Falling serum digoxin levels, normal K+, no GIT symptoms, no cardiotoxicity at 6 hours - discharge
• Patients who receive antidote and are symptom free after 6 hours - discharge

• Narrow therapeutic index: Intoxication common in elderly and those with comorbidities (Normal digoxin level 0.5-0.1ng/ml)
• Usually develops in the context of intercurrent illness
• Symptoms are non specific but can mirror acute toxicity
• Same clinical features as acute with addition of visual sypmtoms - decreased VA, aberration of colour vision (chromatopsia), yelow halos (xanthopsia)

Investigations

• Digoxin level - based on a steady state level 6 or more hours after the last dose
• Levels correlate poorly with severity of intoxication
• eLFTs - hypokalaemia exacerbates toxicity
  

Management

• Same as acute if resuscitation required

Antidote

• Indicated whenever clinical features of digoxin intoxication are associated with an elevated level
• A dose of 1-2 amps is sufficient to reverse all features of toxicity within 12 hours

Tips

• Consider diagnosis in any patient on digoxin who presents with collapse, hypotension, bradycardia, dysrhythmias, GIT complaints, ALOC or general deterioration

Can use digoxin immune Fab - reduces LOS and mortality

Overdose results in predictable dose dependent CNS and anticholinergic effects. Management is primarily supportive with the selected use of enhanced elimination

Mechanism

• Structurally similar to TCA
• Inhibits inactivated sodium channels preventing further APs
• Block NA reuptake
• Antagonists at muscarinic, nicotinic and adenosine receptors
• NMDA antagonism
• Following large overdoses - ileus - ongoing absorption for several days

Clinical Features

• 20-50mg/Kg: Mild to moderate CNS and anticholinergic effects. Nystagmus, dysarthria, ataxia, sedation, delirium, mydriasis, opthalmoplegia and myoclonus. Urinary retention, tachycardia and dry mouth common in early stages
• >50mg/Kg: Fluctuating mental status with intermittent agitation and risk of progression to coma within the first 13 hours. Risk of hypotension and cardiotoxicity (wide QRS, VF, VT, asystole) with extreme doses.
• Symptoms evident within 4 hours
• Following massive ingestions  coma is anticipated to last several days secondary to ongoing absorption, slow elimination and presence of an active metabolite
• One 400mg tablet can cause harm in a toddler

Resuscitation

• Cardiotoxicity - Sodium Bicarbonate
• Seizures - Benzodiazepines

Investigations

• Carbamazepine level (8-12 therapeutic range)
• Serial 12 lead ECG - Na+ blockade, 1st degree HB, increased QRS duration

Decontamination

• Activated charcoal for ingestions <50mg/Kg or large ingestions of CR

Enhanced Elimination

• MDAC in intubated patients
• Haemodialysis

Disposition

• Children 20mg/Kg - observe 8 hours
• If undectable levels after first hour - excludes ingestion
• Patients who are well at 8 hours - discharge
• Nystagmus, ataxia, drowsiness, and anticholinergic effects - observe in ED for 8 hours

• Most overdoses result in CNS depression and are managed successfully with supportive care
• Large overdoses can cause MOF and death
• Death is preventable with early haemodialysis

Mechanism

• Increases levels of GABAa a central inhibitory neurotransmitter
• In large doses inhibits mitochondrial metabolism and leads to MOF
  

Clinical Features

• Frequently present asymptomatic
• Deterioration in conscious state is paralleled closely to rising serum levels
• Following large overdoses, coma is accompanied by - HAGMA, hypoglycaemia, hypernatraemia, hypocalcaemia, hyperammonaemia
• Hypotension, renal impairment, bone marrow depression
• Severe poisoning - cerebral oedema, prolonged coma, cardiovacular instability, death
• In severe poisoning coma may be present for several days after serum valproate levels return to normal

Investigations

• Serum valproate levels

Decontamination

• oral activated charocal not in patients <400mg/Kg
• Larger doses via ETT
• A repeated dose of activated charcoal at 3-4 hours may reduce absorption and peak serum levels

Enhanced Elmination - Haemodialysis

• Ingestions >1000mg/Kg with serum level >1000mgl/L
• Serum level >1500mg/L
• Severe valproic poisoning with lactic acidosis or cardiovascular instability

Consider overdose in any patient with unexplained coma, particularly where there is hypernatraemia, hypocalcaemia or lactic acidosis

Non Sedating Antihistamines

Loratadine, Cetirizine

• Rare association with QT prolongation
• Mild sedation or anticholinergic effects following overdose

Mechanism

• Less likely to cross BBB
• Selective competitive reversible inhibitors of peripheral H1 receptors
• In overdose selelctivity may be lost and some sedation, anticholinergic effects and hypotension

Features

• Minor sedation, nausea, ataxia
• Mild anticholinergic symptoms
• Symptoms develop within 4-6 hours of ingestion

Management of QT prolongation

• Correction of hypoxaemia and hypokalaemia
• Administration of Magnesium
• If HR <100 - isoprenaline infusion
• Overdrive pacing

Antihistamines Sedating

Brompheniramine, cyproheptadine, doxylamine, promethazine

• OVerdose is characterised by dose dependent sedation and anticholinergic effects
• Cardiovascular toxicity is associated with massive ingestions

Mechanism

• Competitive inhibition of histamine receptors
• Side effects and toxicity are due to antagonism at muscarinic, adrenergic and serotenergic receptors

Clinical Features

• CNS depression
• Anticholinergic syndrome including delirium
• Seizures, hyperthermia, rhabdomyolysis
• Hypotension requiring inotropic support and cardiac conduction abnormalities secondary to fast sodium channel blockage

Risk assessment

• Dose dependent sedation, anticholinergic effects and orthostatic hypotension
• Lowers seizure threshold
• Massive overdose - cardiac conduction abnormalities (increased QRS or QT)

Mechanism

• Synthetic derivative of GABA - at therapeutic doses it acts at GABAa receptors. It also mediates pre and post synaptic inhibition causing paradoxical seizures in overdose and withdrawal symptoms

Clinical Features

• Large overdoses are characterised by rapid onset of delirium, respiratory depression, coma and seizures and are potentially lethal
• Develop within 2 hours
• CNS: delirium, respiratory depression, profound and prolonged coma, seizures
• Cardiovascular: Sinus bradycardia, HTN, 1st degree heart block and QT prolongation
• Following large ingestions coma may be profound - may appear brain dead with fixed dilated pupils, absent brainstem reflexes and profound hypotonia
• Duration of coma is 24-48 hours
• >200mg associated with CNS effects

Baclofen withdrawal syndrome - occurs between 24 to 48 hours post cessation and is manifested by seizures, hallucinations, dyskinesia and visual disturbance

Risk Assessment

Phenobarbitone, thiopentone

Mechanism

• Enhance GABA mediated inhibitory neurotransmission
• Bind to GABAa and increase duration of chloride channel opening (vs benzo which increase the frequency of opening)
• Antagonise effect of excitatory neurotransmiter glutamate
• Inhibition of medullary cardiorespiratory centres and hypothalamic autonomic nuclei results in hypotension, hypothermia and respiratory arrest

Clinical Features

• Uncommon presentation but can cause profound and prolonged coma mimicking brain death
• Symptoms within minutes of IV administration of thiopentone or within 1-2 hours of PO
• Tachycardia
• Hypoerthermia
• Reduced bowel sounds
• Skin bullae over pressure areas

Risk Assessment

• Ingestion >8mg/Kg likely toxic

Management - Supportive

Investigation

• Phenobarbitone assays routinely avaialble - used to follow enhanced elimination

Decontamination - Activated charcoal via NGT in intubated patients

Enhanced Elimination

• MDAC increases the rate of elimination by interrupting enterohepatic and enteroenteric circulation (if patient has active bowel sounds)
• Haemodialysis, haemoperfusion, haemofiltration

Disposition

• If asymptomatic 6 hours post ingestion can discharge

Lithium

Acute Overdose

Acute gastro intestinal symptoms including N&V, abdominal pain adn diarrhoea. Provided adequate urinary lithium excretion is maintained significant neurotoxicity of chronic lithium overdose does not occur

Mechanism

• Acts as a direct irritant to the GIT
• Once absorbed substitute for Na+ and K+ ion and through to modulate intracellular second messengers

Clinical Features

• GIT
• Neurological symptoms are delayed - earliest and most frequent is tremor
• Minor ST and T wave changes due to interference of Na+ , prolonged QT, sinus bradycardia, AV block

Risk assessment

• <25g minor GI symptoms
• >25g more significant GI symptoms, provided good supportive care is instituted so as to avoid dehydration, sodium depletion or renail impariemnt
• Acute or chronic impairment of renal function, dehydration or sodium depeletion impairs urinary lithium excretion - lithium is redistributed to tissue compartment including CNS

Investigations

• ECG, paracetamol, BSL
• eLFT - renal impairment
• Serum lithium levels

Management

• Immediate life threats - hyoptension
• Fluid resuscitation - Maintaina adequate hydration and sodium repletion if necessary UO >1ml/Kg/hr
• Monitor fluid and electrolyte status, renal function, serum lithium and clinical features of neurotoxicity
• Cardiac monitoring is not required

Decontamination: Not adsorbed by charcoal

Enhanced Elimination: Haemodialysis, however, in patient with normal function whose hydration and Na levels are ensured, is not clinially useful. Useful for patients with established renal failure.

Dispostion

• Patients with no evidence of neurotoxicity and serum lithium level <2.5 and falling do not require further medical care.
• Coma in context of acute deliberate self poisoning is never secondary to lithium

Lithium

Chronic Overdose

Nephrogenic DI and hypothyroidism are associated with lithium therapy

Develops in patients on lithium therapy when renal lithium excretion is impaired for any reason. Drugs that impair clearance

• NSAID
• ACEI
• SSRI
• Thiazide diuretics
• Topiramate

Risk Assessment

• Consider in any patient on lithium therapy who presents with neurological signs or symptoms
• Significant obtundation or seizure activity is an indication of severe toxicity that carries a risk of permanent neurological sequelae
• Serum lithium concentration correlates poorly with clinical features of toxicity

Clinical features

• Neurological - Hansen & Amdisen,                           I - tremor, hyperreflexia, agitation, muscle weakness, ataxia.                                                 II - stupor, rigidity, hyertonia, hypotension           III - coma, convulsion and myoclonus
• GIT symptoms not prominent
• Most common causes of impaired lithium excretion - impaired renal function, diabetes insipidus, sodium depletion, dehydration and drug interactions

Investigations

• Serum lithium levels - does not correlate with CSF levels
• ELFTs
• TFTs

Management

• Acute resuscitation unlikely to be necessary
• Correct water and soidum deficits and restore renal function to maximise lithium excretion
• cease drugs that may impair clearance

Enhanced Elimination

• Haemodialysis considered in patients with neurological dysfunction and serum lithium >2.5mmol/L

• Use is restricted and closely supervised
• Most poisonings follow a benign course
• Consider in patients with features of anticholinergic poisoning but small pupils and hypersalivation
• QT prolongation uncommon

Mechanism of Atypical Antipsychotics

Clozapine, Olanzapine, Quetiapine, Risperidone

Dopamine, serotonin, histamine, muscarinic and peripheral alpha antagonist

Posioning is associated with sedation, delirium, coma, tachycardia and hypotension

• Quetiapine is a leading cause of toxic coma requiring ICU
• Associated with predictable dose-dependent CNS depression ranging from sedation to coma and a characteristic brisk tachycardia
• Onset: 2-4 hours, lasts 24-72 hours
• No decontamination, elimination, antidote
• If hypotension not responding to IVF - NA

Phenothiazone: Chlorpromazine, fluphenazine, prochloperazine

Butyrophenones: Droperidol, haloperidol

Mechanism

• Central dopamine antagonism
• Adverse effects are secondary to antagonist action at 5HT, histamine, GABA, muscarinic

Clinical Features

• CNS depression, orthostatic hypotension and anticholinergic effects
• Cardiac dysrhythmias are uncommon
• Seizures are uncommon
• In children, ingestions of even one tablet warrants observation.
• Urinary retention common

Management

• Supportive
• Hypotension is secondary to peripheral vasodilation and responds well to IVF

Decontamination: Activated charcoal after ETT

• Monocyclic antidepressant with similar toxicity profile to TCA but a high risk of seizures with any overdose
• >9g risk of cardiovascular complications - prolonged QRS and QT, tachycarrhythmias and collapse

Management

• As per TCA - I&V + hyperventilation + NaHCO3 for broad complex tachyarrhythmias
• Early RSI if Hx and clinical progress consistent with >9g ingestion
• Consider prophylactic benzodiazepine
• Treat seizures with titrated benzos
• Routine supportive cares

Investigations

• ECG (QT + QRS prolongation)
• BSL, paracetamol
• VBG

Decontamination - activated charcoal only after definitive airway

No enhanced elimination, antidotes

Disposition - Observe 24 hours, high risk of seizures, cardiotoxicity, warrants ICU

Overdose produces rapid onset of hypotension, CNS depression, cardiac conduction defects and hypokalaemia

Mechanism

• Direct toxic effects on the CNS via voltage dependent Na+ channels
• Toxic mechanism is similar to TCAs
  

Clinical Features

• Onset within 1-2 hours
• Non-specific symptoms
• CVS: hypotension, cardiac conduction defects (QRS widening, QT prolongation), cardiac arrest, direct myocardial depression
  
• CNS: Depressed conscious state, seizures
• Metabolic: Hypokalaemia (K+ uptake)

Risk assessment

• 10mg/Kg is potentially toxic
• 30mg/Kg usually severe
• Narrow therapeutic window

Management

• Supoprtive
• As per TCA, early intubation, hyperventilation, NaHCO3
  
• Broad complex tachycardia - serum alkalinasation, sodium bicarbonate for QRS prolongation
• Hypokalaemia - anticipated but avoid repalcement as total potassium is not depelted

Disposition

• All children even if one table observe overnight

Characterised by cinchonism consisting of nausea, vomiting, tinnitus, vertigo and deafness

Large overdoses may result in life threatening cardiotoxicity and severe, potentially permanent visual disturbance

Toxic Mechanism

• Class 1a antidysrhythmic with Na channel and K channel blocking function
• Prolongation of both QRS and QT intervals
• Directly toxic to retina
• Stimulated pancreatic insulin release

Clinical Features

• Cinchonism: Nausea, vomiting, alteration in hearing, tinnitus and vertigo. Occurs early adn resolves as blood concentration falls
• CVS: Hypotension, sinus tachy, QRS widening and prolongation of QT and PR
• CNS: Drowsiness and confusion
• Eyes: VIsusal disturbance is delayed - recovery over days to weeks

Risk Assessment

• All cases should be regarded as having potential to cause cardiotoxicity and visual disturbance
• Cardiotoxicity, CNS disturbance and blindness if >10g
• 2 tablets (600mg) in chidren potentially lethal

Investigations

• ECG, BSL, Paracetamol
• Serial ECGs - QRS duration, HR, QT
• Visual field mapping
• VA is visual symptoms

Management

• Resuscitation
• Coma - I&V
• Broad complex tachy - Intubate and hyperventilate, NaHCO3
• pH 7.55
• Consider isoprenaline, overdrive pacing
• Antiemetics and IVF for cinchonism

Decontamination: 50g activated charcoal to all overdoses who are awake

Enhanced Elimination: MDAC anyone with ingestion >5g or any visual disturbance

Dispostion

• ECG monitoring for at least 6 hours
• if ECG normal, asymptomatic at 6 hours can discharge
  

Severe poisoning presents with rapid onset of seizures, coma and severe metabolic acidosis

Mechanism

• Anti TB
• Structurally similar to pyridoxine and inhibits it's activation to P5p which is essential in the conversion of glutamate to GABA --> acute GABA deficiency
• seizures and lactic acidosis

Investigations

• ABG - severe HAGMA, high lactate

Management

• Seizures are controlled with high dose IV diazepam until pyridoxine can be secured

Decontamination: acitvated charcoal once airway secured

Enhanced Elimination: Haemodialysis but not useful as too late

Antidote: Pyridoxine

• If coma or seizures
• 1g for each gram of isoniazid

Disposition

• Asymptomatic patients observed for 6 hours
  
• All patients with seizures need I&V + pyridoxine + ICU
  

Always consider isoniazid overdose in the differential of status epileptics

Acute ingestions is followed by severe gastroenteritis with a characteristic sequential life threatening MOF

Toxic Mechanism

• Binds to numerous cellular enzymes - interferes with cellular respiration and inhibits DNA replication and repair. Binds to SH groups and substitutes for phosphate in ATP - produces reactive oxygen intermediates causing lipid peroxidations

Clinical Features

• Rapid onset severe, watery diarrhoea, vomiting and abdominal pain
• Gastrointestinal haemorrhage
• Encephalopathy, seizures, cardiovascular collapse within hours
• Hypersalivation and garlic odour
• Acute cardiomyopathy, ECG changes (prolonged QT) and cardiac dysryhtmias
• ARDS, renal failure and hepatic injury
• Bone marrow depression within 24-72 hours reaching a nadir in 2-3 weeks
• Alopecia
• Peripheral neuropathic - ascending motor neuropathy, may mimic guillian barre and progress to respiratory failure

Management

Risk Assessment

• Ingestion of >1mg/Kg is potentially lethal

Investigation

• ECG, BSL, Paracetamol
• Spot urinary arsenic
• 24 hour urinary arsenic excretion
• FBC, coags, eLFTs
• ABG
• CXR, AXR - inorganic arsenic compounds are radio-opaque

Decontamination

• Activated charcoal does not bind arsenic
• whole bowel irrigation with polyethylene glycol

Enhanced Elimination - Nil

Antidotes

• Chelation is indicated when there are objective clinical features --> Succimer PO or Dimercaprol IM

Disposition

• Clinically well 12 hours post ingestion without GI symptoms are not poisoned and can be discharged

Inorganic: ground water, semiconductors, glass, pesticides, wood preservatives, APML, herbal

Organic: Fish and shell fish

• Occurs from industrial accidents, food contamination and ingestions of arsenic containing herbal medicines

Clinical Features

• Gastrointestinal symptoms, leukopenia, deranged LFTs, haematuria
• Peripheral neuropathy

• Follows long term drinking of contaminated water

Clinial Features

• Constitutional symptoms
• Cutaneous lesions (hyperkeratosis of palms and soles, hyperpigmentation)
• Nail changes
• Peripheral neuropathy
• Malignancies of skin or bladder

Associated with encephalopathy, cerebral oedema and death

Pregnancy: Major malformation

Children: Neurotoxic

Toxic Mechanism

• Interference with intracellular functions including maintenance of cell wall integrity, haem synthesis, neurotransmitter systems and steroid production
• Major organs effects: CNS, kidneys, reproductive, hematopoietic

Clinical Features

• Abdominal pain, nausea, vomiting, haemolytic anaemia, hepatitis
• Cerebral oedema, encephalopathy, seizures and coma
• In children IQ reductions. <10mcg/dL - minor subclinical IQ reductions - increase with values towards 10. 10-30 subtle devolepmental abnormalities. Children 30-100 neuropathy, non specific constitutional symptoms, renal impairment, decreased fertility. >100 severe Gi symptoms, seizures, coma
  

Investigations

• Lead level
• FBC - normochromic, normocytic anaemia with basophilic stipple
• Free erythrocyte proroprophyrin
• AXR
• Nerve conduction

Management

• Mannitol 1g/Kg
• Dexamethasone 10mg if cerebral oedema present (0.15mg/Kg)
  

Decontamination

• Lead foreign body ingestion - endoscopic retrieaval if above GOJ, below GOJ - high residue diet plus oral polyethylene glycol then repeat AXR
• Shrapnel or bullets adjacent to synovial tissue - surgical excision

Enhanced Elimination - Nil

Antidotes

• Chelation therapy in symptomatic lead poisoning or long term neurological injury is anticipated
• Sodium calcium edetate (EDTA) - acute lead induced encephalopathy, symptomatic patient with blood level >100mcg/dL
• Succimer if less severe or lead >60 in adults, >45 in children
  

Vague multi system disorder with potential for permanent neurological and neuropsychological sequelae

• Risk of long term neurological sequelae loosely correlated to blood levels

Elemental mercury: minimal absorption from GIT but well absorbed from respiratory tract and broken skin. Inadvertant topical exposure or ingestion is benign. Inhalation of aerosolised elemental mercury can cause systemic toxicity and interstitial pneumonitis. 

Inorganic mercury: 10% absorbed from GIT

Organic mercury: absorbed from GIT

Clinical Features

• Headache, nausea, vomiting, chills, fevers, salivation, metallic taste, visual disturbances, dyspnoea and dry cough
• Ingestion of inorganic salts - haemorrhagic gastroenteritis with massive fluid loss
  
• Organic mercury: GIT, respiratory distress, tremor, dermatitis, delayed permanent neurotoxicity.
• Psychological: Poor concentration, short and long term memory loss, emotional lability, depression and coma
• Cerebellar: Ataxia, incoordination, dysdiadochokinesis
• Sensory: glove-stocking paraesthesia, deafness, tunnel vision, scanning speech
• Motor: Spasticity, tremor, weakness, paralysis
• Chronic exposure - neuropscyhological dysfunction - mad as a hatter
  

Investigations

• Whole blood mercury (normal <20)
• Urine mercury level
• X-rays: elemental mercury is radio-opaque
• IV injection produces multiple mercuric pulmonary emboli and milky way appearane on CXR

Resuscitation

• Inorganic salts may need very aggressive fluid resuscitation

Decontamination

• Environmental - avoid vacumming, discard contamination carpets or surfaces
• Personal - removing clothing, remove from skin
• Adminstration of oral polyethylene glycol enhances removal from GIT
• Surgical excision

Enhanced elimination

• Polythiol resin for organic mercury

Antidotes

• Chelation with dimercaprol (inorganic), penicillamine, succimer
• Chelation therapy is indicated when there are objective clinical featurs of mercury intoxication or markedly elevated urine or blood mercury levels
• Dimercaprol is contraindicated followign elemental mercury exposure, as concern that increases distirbution of mercury to the brain

Acute effects are secondary to tissue hypoxia

Delayed neurological sequelae are secondary to an incompletely understood cascade of endovascular oxidative injury and inflammation

Toxic Mechanism

• CO 250 x affinity for Hb - hypoxia
• Bind to intracellular cytochromes/mitochondria - interrupt cellular respiration
• Endothelial oxidative injury, lipid peroxidation, inflammatory cascade - delayed neurological sequelae

Clinical Features

• CNS: Headache, nausea, dizziness, confusion, poor concentration, MMSE errors, incoordination, ataxia, seizures, coma, persistent neurological sequelae are evident from time of poisoning and seen in 30% at 1 month
• CVS: Tachycardia, HTN, ischaemic changes, hypotension, dysrythmias, acute MI
• Respiratory: Non cardiogenic pulmonary oedema
• Metabolic: Lactic acidosis, rhabdomyolysis, hyperglycaemia
• DIC, bullae, alopecia, sweat gland necrosis

Risk Assessment

• CO deaths occur before hospital
• High risk features: signficant LOC or coma, persistent neurological dysfunction, abnormla cerebellar examination, metabolic acidosis, MI, age >55
• Outcome is poorly correlated with carboxyhaemoglobin level
• Pregnancy - fetal Hb binds CO more avidly, rendering the foetus more susceptible to injury

Investigations

• ECG, BSL, Paracetamol
• Carboxyhaemoglobin level
• Lactate
• ABG, FBC, Tn, eLFTS, CT or MRI brain (cerebral oedema, atrophy, basal ganglia injury, cortical demyelination