Module 4 - Trauma/metabolic/OD Flashcards
(20 cards)
Discuss the physiological effects and management implications of immersion injuries
“respiratory impairment due to submersion of the airway, or immersion of the body including the airway”
fatal
- breath holding until respiratory drive overcomes -> gasp in water
- Aspirated water -> washes away surfactant in alveoli -> alveolar collapse -> O2 exchange cannot occur -> shunting & V/Q mismatch => hypoxia -> cardiovascular collapse and eventually death
non-fatal
- hypothermia & infection
- surfactant dysfunction
- pulmonary oedema
- v lung compliance, bronchospasm
Worsening factors
- age
- water temperature
- duration
- effectiveness of rescue
Management
- DRABCS
- dry and warm
- c-spine considerations
- NGT consideration
- Midazolam for seizures
- Maintain MAP of 80mmHg
- hypovolaemia from hypothermia -> fluids
- BGL - correct
- Maintain c-spine precautions in trauma setting
Discuss the physiological effects and management implications of hypothermia
Vulnerable populations: elderly & neonates
Causes: cold environment, water
Hypothermia -> decreased metabolic rate -> heat reduction = positive feedback
Mild 32-35C
- Shivering
- Shivering uses up glucose stores
- Ataxia, slurred speech, minor cognitive impairment
- ^SNS -> vasoconstriction, ^HR, ^BP
- Vasoconstriction -> ^urination
- ^RR - cilia fcn decrease -> accumulation of mucous in bronchi
Moderate 28-32C
- Loss of shivering due to lack of glucose stores
- Progressive decrease in consciousness -> CNS depression
- Progressive loss of reflexes
- Sluggish responses
- v cardiac conductivity due to slowed channel opening -> bradycardia -> vCO -> vBP
- Predisposed to arrhythmia
- vRR, hypoventilation due to v neuron fcn
Severe 20-28C
- Decreased CO2 production -> decreased cerebral blood flow -> decreased O2 supply -> loss of reflexes, pupillary, ocular -> areflexia
- Decrease in catecholamine response -> vCO, vHR, vasodilation, more and more heat loss
- Arrhythmia -> cardiac arrest
- Symptoms of renal failure
- hypoxia
Management
- Warming, remove wet clothing and dry - space blankets
- Move carefully -> arrhythmia
Hypothermic arrest
<30C
- Max 3 shocks
- Withhold cardiac arrest drugs
30-35C
- double drug intervals
- otherwise normal resus
- consider transport under CPR to receiving facility
Discuss the physiological effects and management implications of chest trauma
Pneumothorax = accumulation of air in the pleural space – between visceral and parietal plural
Occurs due to
- Rupture of visceral pleura – spontaneous/traumatic/iatrogenic -> closed
- Penetrating trauma to chest wall – rupturing parietal (outer) pleura (and possibly visceral pleura too) -> open
- Traumatic -> Open = penetrating trauma, air from outside, Closed = results from blunt trauma/fracture/rob displacement, air from the lung
- Can progress to tension pneumothorax
o When pressure of air in pleural space > atmospheric pressure -> formation of a valve - air in but air can’t get out
o Lung cannot expand/collapses -> decreased ventilation
o ^intrathoracic pressure -> reduce venous return -> vCO -> decreased perfusion => obstructive shock
o Chest asymmetry, tracheal deviation, severe dyspnoea, absent breaths sounds on affected side
o Obstructive shock = tachypnoea, tachycardia, JVD, hypotension
Tension Pneumo management
- Improve gas exchange -> O2, chest needle decompression (2nd intercostal space, midclavicular line, just above 3rd rib)
Penetrating chest trauma
- Cardiac tamponade - ^intrapericardial pressure -> compression of heart -> obstructive shock
- Haemothorax -> haemorrhagic shock
- Pneumothorax -> tension pneumothorax -> obstructive shock
- Tracheobronchial injury – damage to large airway structures
- Diaphragmatic injury
- SCI
- Fractures – ribs/flail chest
Discuss the various classifications of burns and physiological effects and management implications of such injuries
Discuss the physiological effects and management implications of penetrating trauma
Penetrating chest trauma
- Cardiac tamponade - ^intrapericardial pressure -> compression of heart -> obstructive shock
- Haemothorax -> haemorrhagic shock
- Pneumothorax -> tension pneumothorax -> obstructive shock
- Tracheobronchial injury – damage to large airway structures
- Diaphragmatic injury
- SCI
- Fractures – ribs/flail chest
Penetrating abdominal trauma
- Hollow viscus perforation => peritonitis => shock
o Potential large volume haemorrhage into abdominal, retroperitoneal, pelvic cavities
- Vascular injury – abdominal aorta
- Solid organ injuries
o Liver laceration
o Splenic laceration
- Diaphragmatic injury -> diaphragmatic hernia
- Genitourinary trauma
General management - DRCABCs - Supplemental O2 (94-98%) and posturing – upright for ventilation, supine for haemodynamics - Do not remove impaled objects – minimise pt movement, stabilise objects unless pulsating - Decompress tension when signs of decompensation e.g., radial pulse loss OR altered GCS - Analgesia - Chest Trauma Assessment o Look – open/penetrating wounds, bubbling/sucking wounds, asymmetry, paradoxical chest wall movement o Listen – abnormal breath sounds, decreased air entry o Feel – tenderness, crepitus, flail segment, deformity, subcutaneous emphysema
Discuss the physiological effects and management implications of crush injuries
Crush injuries
- larger, less defined, high energy to a limb
- e.g., getting run over, heavy object fallen on you
- widespread, hard to determine damage
- skeletal, vascular, soft tissue, nervous tissue damage
- Not all crush injuries will result in crush syndrome -> quite rare
- Compartment syndrome can occur
Crush syndrome
- significant area of body and delayed release of object
- hypoxic tissue below area being crushed
- influx of inflammatory mediators -> vasodilation -> profound hypotension -> no CO
- Rhabdomyolysis - muscle breakdown -> large proteins -> kidney failure
- 2x large bore IVs, preloading with fluid
Crush injury
- Support ABCs - especially in crush injuries of the chest
- Fluids in proportion to the crush - to alleviate kidney injury
- Tourniquet?
- Clinical monitoring
Discuss the principles and practices relating to intravenous fluid therapy for the traumatic injured hypotensive patient
Permissive hypotension = maintaining a lower than normal MAP to maintain perfusion to major organs - GCS responding to commands
Aim = maintain vital organ perfusion while limiting adverse effects from aggressive fluid administration
- 10ml/kg 0.9% saline 250ml bolus up to 20ml/kg aiming for response to verbal commands
Lethal triad
= coagulopathy, hypothermia, acidosis
- Fluid is cold -> decrease effective clot formation -> further bleeding
- Saline 0.9% is acidic -> large volumes of fluid can result in hyperchloremic metabolic acidosis -> further vasodilation, oedema, worsening poor perfusion, worsening of clotting
- Aggressive fluid resus can disrupt clots
- Haemodilution -> worsening clotting
Discuss the classifications and features of shock
Discuss the pathophysiology and classifications of non-insulin dependent diabetes
Diabetes mellitus
“Abnormal carbohydrate metabolism that is characterized by
hyperglycaemia. There is a relative or absolute impairment of insulin secretion, along with
varying degree of peripheral resistance to action of insulin”
T2DM -> makes insulin but tissues do not respond to it
- Not fully understood why
- Risk factors = obesity, HTN, lack of exercise, genetics
Non insulin dependent (type 2)
- Tissues not responding to normal insulin levels -> body produces more insulin
- Beta cell hyperplasia (^beta cells) and hypertrophy -> pump out more insulin
- Allows for normoglycaemia
- Beta cell compensation not sustainable
- Weight loss, exercise, healthy diet, antidiabetic meds can be enough to reverse insulin resistance
Discuss the pathophysiology and classifications of insulin dependent diabetes
Insulin dependent
Type 1
Type 4 hypersensitivity
- T cells attack beta cells of the pancreas which produce insulin
- No insulin production
- Thus no glucose can get into the cells, leaving high glucose in blood and no glucose in cells for energy production
- Cells use lipolysis to produce energy creating ketones and acid as byproduct
- Requires exogenous insulin to survive
Type 2
- Body becomes resistant to insulin
- Tissues not responding to normal insulin levels -> body produces more insulin
- Beta cell hyperplasia (^beta cells) and hypertrophy -> pump out more insulin
- Allows for normoglycaemia
- Beta cell compensation not sustainable
- Beta cells become hypotrophic and cannot produce sufficient insulin
- Requires insulin!
Discuss the features, diagnosis, and out-of-hospital management of hypoglycaemia
- Low BGL (<2.8-3.3mmol/L)
- Decreased GCS
Causes
Diabetics
- too much insulin,
- decreased endogenous glucose production (alcohol consumption)
- Increased glucose utilisation (exercise)
No history of diabetes - rare
- Beta blocker OD,
- Pituitary insufficiency
- Liver disease
- Addison’s disease
- Starvation, malnutrition
Prehospital treatment
- Try oral carbohydrates or oral glucose 15mg first if GCS allows
- IV glucose 10% titrated to effect - follow with 100ml IV saline
- IM glucagon 1mg (least ideal for diabetics, decreases glucose stores)
- Supportive care
If return of normal neuro function and considering non-transport, adult pts must have:
- Consumed complex carbs
- BGL stable range
- be a previously stable diabetic
- have an identified cause for the episode
- reside in a suitable environment
Paediatric
- oral carbs/glucose paste
- glucagon <25kg = 0.5mg, >25kg = 1mg
- Consult for glucose IV
- Transport
Discuss the features, diagnosis, and out-of-hospital management of hyperglycaemia
Causes: DKA, AKA
DKA
- insulin deficiency - glucose cannot enter the cell to be used as energy -> ^BGL
- Liver thinks it is hypoglycaemic - attempts to use glucose stores, releases glucagon to turn glycogen into glucose raised BGL even more
- metabolism of triglycerides and amino acids instead of glucose for energy -> ketones produced as a by-product
- Ketones decrease pH -> metabolic acidosis
- Kidneys cannot reabsorb glucose - osmosis of water -> polyuria -> excretion of sodium, potassium, chloride -> electrolyte imbalances
- In the cells, Hydrogen ion-potassium pump makes potassium leave cell, and insulin-dependent sodium-potassium pump cannot move potassium into the cell -> hyperkalaemia
- Abdominal pain
- Decreased GCS
- Kussmal breathing
DKA can occur with stress
stress -> adrenaline release -> glucagon release -> ^BGL
Prehospital management
- Oxygen and SGA if required
- IV saline
- antiemetics
- analgesia
- Transport
Discuss the features of the renal system
Kidneys -> Ureters -> bladder -> urethra
- Retroperitoneal, under the 12th ribs
- Cortex, medulla, renal pelvis, ureter
- Adrenal glands
Nephrons (functional units)
- Glomerulus -> proximal tubule -> loop of Henle (descending limb, ascending limb) -> distal convoluted tubule ->collecting ducts
Blood flow
- Renal artery -> afferent arteriole -> glomerulus -> efferent arteriole -> peritubular capillaries -> renal vein
- Filtration, 2. reabsorption, 3. secretion, 4. excretion
Discuss the consequences of chronic renal failure
CKD = “subtle decrease in kidney function that occurs over greater than 3 months”
Kidneys function is to regulate water balance, electrolytes, remove wastes and make hormones
GFR - glomerular filtration rate = 100-120ml/min/1.73m2
CAUSES
HTN
- walls of arteries thicken to withstand pressure
- Narrows lumen => less blood and o2 supply => ischaemic injury => hardening and scarring => decreased ability to filter blood => CKD
Diabetes
- Excess glucose sticks to proteins => efferent arteriole becomes stick and narrows => obstructs blood from leaving glomerulus => ^pressure and hyperfiltration => decreases ability to filter blood => CKD
Other causes
- Systemic disease = rheumatoid arthritis
- HIV
- Medications (NSAIDS)
- Toxins
CONSEQUENCES
Overview
- Increased urea, potassium, calcium in blood
- Thus: CNS problems, arrhythmia, renal osteodystrophy, HTN, anaemia
PATHOPHYSIOLOGY
Urea
- Decreased GFR = more urea in blood
- mild = nausea, loss of appetite
- More severe function of CNS - encephalopathy => tremor
- Coma and death
- less platelet aggregation => bleeding
- Uraemic frost - urea deposits on skin
Potassium
- Potassium build up in blood - hyperkalaemia
- Arrhythmia
Calcium
- Less activated vitamin D
- Hypocalcaemia => Parathyroid hormone release => calcium reabsorption from bones => renal osteodystrophy
Hormones
- Renin release to increase BP
- Falling GFR => ^renin secretion => hypertension => vicious cycle
- Erythropoietin Production of RBCS => v RBC production => anaemia
TREATMENT
- Looking at underlying cause
- Dialysis and transplant may be required
Discuss the physiological effects and management implications snake envenomation injuries relevant to Australasian environment
Australian venomous snakes
- Brown snakes
- Tiger snakes
- Black snakes
- Taipans
- Death adders
Adelaide
- Brown snakes
- Red bellied black
- Copperhead
- Tiger snake
Effects
Local
- Variable swelling/bruising/bleeding
General systemic
- N&V
- Headache
- Abdominal pain
- Collapse
- Convulsions
Specific systemic
- Neurotoxic paralysis
- Systemic myolysis
- Coagulopathy
- Renal damage
- Microangiopathic hemolytic anaemia (RBC destruction due to platelet activation and consumption)
Management
- Pressure bandage immobilisation
- Supportive care
Discuss the pathophysiology, features, and out-of-hospital management of paracetamol overdose
- Analgesic anti-pyretic
- Overdose causes hepatic necrosis
- single ingestion of 200mg/kg ~10g
- Pts initially asymptomatic - well for 12-24 hrs
- “silent killer”
Clinical features
Stage 1 (1-24hrs)
- N&V
- Diaphoresis
- Pallor
- Lethargy
Stage 2 (24-72hrs)
- Evidence of hepatoxicity
- RUQ pain
Stage 3 (72-96hrs)
- Stage 1 symptoms +
- Jaundice
- Altered mentation (hepatic encepalopathy)
Management
- NAC (N-acetylcysteine) antidote in hospital
- Dose and time of ingestion Hx
Discuss the pathophysiology, features, and out-of-hospital management of beta blocker overdose
- Beta blockers are B1 and B2 adrenergic receptor antagonists used for HTN, CHF, arrhythmia, CAD etc.
- They block inotropic, chronotropic (^HR), and dromotropic (conduction) effects reducing the FOC, HR, and cardiac conduction
- Onset of effects 1-2 hrs
- Worse toxicity expected in elderly, cardio-respiratory co-morbidities, co-ingestion
General clinical features:
- CVS: hypotension, negative dromotropy (progress AV block – PR prolongation may be the first sign of beta blocker toxicity) and negative chronotropy (bradycardia), heart failure (including pulmonary oedema), cardiovascular collapse
- RESP: bronchospasm
- METABOLIC: hypoglycaemia, hyperkalaemia
- NEURO: stupor or coma
**Propranolol is especially dangerous due to sodium channel blocking effects – CVS: QRS prolongation, ventricular arrhythmia, cardiac arrest NEURO: delirium, coma, seizures
Pre-hospital management
- Resuscitation - DRABCS
- Bradycardia – atropine 0.01-0.03mg/kg IV, consider adrenaline infusion, transcutaneous pacing
- Hypotension – 20mL/kg bolus, adrenaline
- QRS widening – suspect impending ventricular dysrhythmia, defib, amiodarone contraindicated
- CNS – usually corrected with correction to hypotension, with propranolol – prepare for seizures, may require SGA/intubation if GCS<12
- Supportive care/monitoring ECG, glucose
- Transport
- Lack of evidence for glucagon as antidote
Discuss the pathophysiology, features, and out-of-hospital management of quetiapine overdose
- Quetiapine is a 2nd generation antipsychotic medication that antagonises the D2 dopaminergic receptors and serotonin 2A receptors - full MOA not fully understood
- Used for schizophrenia, acute mania
- In toxicity, D2, serotonin, histamine, muscarinic M1, alpha 1 adrenergic receptor antagonism occurs
- Anticholinergic effects (M1) and drowsiness (H1)
- Rapidly absorbed
- Sedation
- Tachycardia
- Hypotension
- Seizures
- Anticholinergic effects (mild-moderate)
Prehospital management
- May require SGA and IPPV
- Hypotension - 10-20mL/kg saline, consider vasopressors
- Seizures - prepare midazolam
- Supportive care and monitoring
- Transport
- Delirium may require chemical/physical restraint - use least restrictive practices
Discuss the pathophysiology, features, and out-of-hospital management of tricyclic overdose
- TCAs used in the treatment of severe depression
- Inhibit reuptake of serotonin and noradrenaline in synaptic cleft to improve mood, concentration etc.
- Narrow therapeutic index
- TCAs are non-selective and in high doses antagonise serotonin and noradrenaline transport proteins, histamine receptors, muscarinic ACh, adrenergic, voltage gated sodium and calcium channels, GABA-A receptors
- Main effects are anticholinergic and cardiovascular
Anticholinergic
- Tachycardia
- Vomiting
- Blurred vision
- Delirium
- Ataxia
- Urinary retention
- Ileus
Antiadrenergic
- Vasodilation
- Hypotension
Sodium channel
- widened QRS
- Risk of VT/VF
Other
- Seizures
- Drowsiness
- Hyperthermia
Discuss the pathophysiology, features, and out-of-hospital management of gamma hydroxybutyrate overdose
- GHB is a CNS depressant drug often used in the clubbing scene
- Stimulates dopamine release at low doses
- GABA-B sedative effect
- GHB receptors - release glutamate - excitatory
- At high doses acts on both GABA-B and GHB receptors to have a paradoxical effect of both stimulatory and sedative
Signs
- Vomiting
- Respiratory depression, CNS depression
- Seizures
- Confusion, irritation, agitation
- Hallucinations
- Memory loss
Prehospital care
- Supportive care
- IPPV if required
- Prepare midazolam in case of seizures
- Transport
