ACP2 CPGs Flashcards
Clinical features of aortic dissection
- Sudden chest pain often described as sharp/ripping/tearing
- Pain linked to dissection location (anterior, neck/jaw, scapula, lumbar/abdominal)
- Pulse differences between heart beats and radial
- Visceral symptoms (pallor, vomiting, diaphoresis)
- Paraplegia
- Altered sensation in extremities
- Chest pain with associated neurological deficit
- Syncope
- Clinical features associated with cardiac tamponade
Risk factors for development of acute aortic dissection
- Males
- > 50 years
- Increased aortic wall stress (HTN, stimulant use, stress, blunt trauma)
- Medical conditions affecting connective tissues (Ehlers-Danlos syndrome, Marfans syndrome)
- Iatrogenic wall injury
- Pregnancy
Rx points to consider for suspected aortic dissection
- Oxygen
- IV access
- Analgesia
- Antiemetic
- IV fluids
- Blood products (request support)
Clinical features of acute coronary syndrome (ACS)
- Chest pain/discomfort
- Referred pain (arms/jaw/teeth)
- Dyspnoea
- Diaphoresis
- N+V
- Feeling of impending doom
Typical presentation of RVMI
- Hypotension
- Jugular vein distension
- Clear lung fields
Rx points to consider for ACS
- Oxygen
- IV access
- Aspirin
- GTN
- Antiemetic
- Fentanyl
Conditions associated with cardiac classified bradycardia
- Diseased SA node/AV node/His-Purkinje system
Types of conditions associated with non-cardiac classified bradycardia
- Environmental
- Metabolic
- Endocrine
- Toxicology
Clinical features of bradycardia
- Hypotension
- Syncope
- ALOC
- Chest pain/discomfort
- Congestive heart failure (CHF)
- Dyspnoea
- Diaphoresis
- N + V
- Dizziness
Common cause and initial mx focus for bradycardia
Hypoxia - mx should focus on improving oxygenation and ventilation
Definition of cardiac arrest
Cessation of blood circulation due to the inability of the heart to maintain adequate tissue perfusion
Two shockable cardiac rhythms
- Pulseless ventricular tachycardia (VT)
- Ventricular fibrillation (VF)
Two non-shockable cardiac rhythms
- Pulseless electrical activity (PEA)
- Asystole
Definition of cardiogenic shock
Prolonged hypotension with inadequate tissue perfusion perfusion in spite of adequate left ventricular filling pressure
Possible causes of cardiogenic shock
- AMI
- Drugs (beta blockers, calcium channel blockers, some chemo rx)
- Hypocalcaemia
- Ventricular hypertrophy
- Cardiomyopathy
- Aortic stenosis
- Aortic or mitral regurgitation
- Malignant HTN
- Catecholamine excess
Clinical features of cardiogenic shock
- AMI
- Chest pain/discomfort
- Diaphoresis
- Cold mottled/cyanotic peripheries
- ALOC
- Tachycardia/bradycardia
- Hypotension
- Respiratory distress secondary to pulmonary oedema (tachypnoea, hypoxia, wheeze)
Rx points to consider for cardiogenic shock
- Oxygen
- IPPV/CPAP
- IV access
- Aspirin
- Adrenaline
- IV fluids
Clinical features of broad complex tachycardia
- Palpitations
- Chest pain/discomfort
- Dyspnoea
- ALOC
- Syncope
- Haemodynamic compromise
Mx considerations for broad complex tachycardia without haemodynamic compromise
- Amiodarone
- Magnesium sulphate
Mx considerations for broad complex tachycardia with haemodynamic compromise
Synchronised cardioversion
Aetiology associated with cardiac classified narrow complex tachycardia
- SVT (due to stimulants, increased sympathetic tone, electrolyte/acid-base disorders, hyperventilation, emotional stress, pre-excitation syndromes [WPW])
- Atrial (AF, multiple atrial ectopics, atrial flutter)
Aetiology associated with non-cardiac classified narrow complex tachycardia
- Pain/anxiety
- Hyperthermia/fever
- Drug induced
- Anaemia
- Shock
Clinical features of narrow complex tachycardia
- Palpitations
- Chest pain/discomfort
- Dyspnoea
- ALOC
- Haemodynamic instability
Mx considerations for narrow complex tachycardia
- Oxygen
- Aspirin (if MI suspected)
- Modified Valsalva (if not compromised and regular)
- IV fluid (if compromised)
Major incident mx handover mnemonic
METHANE
- Major incident confirmation
- Exact location
- Type of incident
- Hazards identified
- Access via
- Number of pts, nature, and priority of injured
- Emergency services/resources required
Cause of diving emergencies
Changes in ambient pressure
Three types of diving emergencies
- Decompression illness (decompression sickness and arterial gas embolism; DCS and AGE)
- Barotrauma
- Hypoxic blackouts
Pathophysiology of DCS
If a diver is unable to perform a slow controlled ascent, inhaled nitrogen is unable to leave the body naturally which causes bubbles to form in blood and tissues. These reduce blood flow and cause end tissue/organ cellular ischaemia.
Pathophysiology of AGE
Results from pulmonary barotrauma when expanding gas in the alveoli rupture the alveoli/capillary membrane, allowing bubbles to enter arterial circulation via the lungs.
Pathophysiology of barotrauma
Occurs when trapped air expands during ascent due to decreasing pressure, causing trauma.
Where in the body barotrauma can occur
Any gas filled space including the pulmonary system, ears, eyes, sinuses, dental structures, GIT, as well as dive mask and suit.
Description and explanation of hypoxic/shallow water blackout
Hypoxic/shallow water blackout is a loss of consciousness that may occur during free diving near the surface or just after surfacing. It is commonly due to hypoxia secondary to relative hypocapnia from hyperventilating prior to the dive.
Neurological clinical features of diving emergencies
- Headache
- Visual changes
- Motor/sensory deficit
- Cranial nerve palsies
- Seizures
- Paralysis
- ALOC
Respiratory clinical features of diving emergencies
- Dyspnoea
- Haemoptysis
- Chest pain
- APO
- Pulmonary barotrauma (pneumothorax/pneumomediastinum/subcutaneous emphysema)
Localised clinical features of diving emergencies
- Skin itch/rash
- Pain in the joints and/or muscles
- Tremors
Cardiac clinical features of diving emergencies
- Chest pain
- Cardiac arrest
Rx points to consider for diving emergency pts who are unconscious/respiratory distress
- Position pt supine
- High flow oxygen
- IPPV
- IV fluid
- LMA/ETT
- Maintain normothermia
Pathophysiology of hyperthermia
Hyperthermia results from thermoregulation failure and occurs when the body produces or absorbs more heat than it can dissipate, exceeding the normal limits required to maintain homeostasis.
Mechanisms of heat transference to and from the body
- Radiation
- Conduction
- Convection
- Evaporation
Definition of environmental exposure hyperthermia
Environmental exposure hyperthermia occurs when the body’s thermoregulatory mechanisms are overwhelmed through exposure to high environmental temperaturs, lack of acclimatisation to hot environments, poor physical fitness, or the wearing of excessive amounts of clothing in high temperatures.
Explanation of intrinsic hyperthermia
Heat is produced internally through chemical reactions of metabolism, skeletal muscle contraction, and chemical thermogenesis, and can be exacerbated by illnesses and medications with or without the pt’s internal thermostat.
Conditions that may exacerbate intrinsic hyperthermia
- Infection (may also present hypothermic)
- Malignant hyperthermia
- Serotonin syndrome
- Neuroleptic malignant syndrome
- Anticholinergic syndrome
- Status epilepticus
- CVA
- CNS infection
- Endocrine disorders (thyroid storm, phaeochromocytoma)
- Drug toxicity (sympathomimetics) or withdrawal (alcohol)
Definition and temp range of heat exhaustion
37’ - 40’C, heat exhaustion is a systemic reaction to heat stress where the depletion of fluids and electrolytes occurs without adequate replacement. May progress to heat stroke quickly if not managed.
Definition and temp range of heat stroke
> 40’C, heat stroke is potentially life-threatening and can result in multi-organ failure and death.
Clinical features of heat exhaustion
- Severe headache/dizziness
- Diaphoresis/N+V
- Tachypnoea
- Tachycardia
- Hypotension
- Muscle pain/fatigue/cramps
Clinical features of heat stroke
- CNS dysfunction (abnormal behaviour, seizures, ALOC)
- Fatigue, headache, syncope
- Facial flushing, N+V, diarrhoea
- Hot skin, possibly dry/nil diaphoresis
- Dysrhythmias, hypotension
- Tachypnoea, ARDS
- Hypoglycaemia, hyperkalaemia
Rx to consider for heat exhaustion/heat stroke
- Remove pt from heat source
- Remove clothes
- Rapid cooling if >40’ with cold packs to groin/axilla/neck
- Gentle cooling if <40’
- Cooled IV fluid
- Analgesia
- Antiemetic
- Paracetamol (if suspected infective cause)
- Oxygen
- IPPV/LMA/ETT if indicated
Definition and pathophysiology of hypothermia
Hypothermia is a core body temp <35’C and is caused by excessive cold stress and/or inadequate body heat production.
Early compensatory mechanisms for hypothermia
- Shivering
- Increased muscle tone
- Peripheral vasoconstriction
- Tachypnoea
- Increased cardiac output
Three classifications of causes of hypothermia
- Increased heat loss
- Decreased heat production
- CNS dysfunction
Causes of hypothermia classified under increased heat loss
- Vasodilation
- Environmental
- Trauma
- Loss of skin integrity (e.g. burns)
- Neuropathy
Causes of hypothermia classified under decreased heat production
- Age
- Endocrine disorders
- Nutritional deficits
- Immobility
Causes of hypothermia classified under CNS dysfunction
- Trauma
- CVA
- Hypoxaemia
- Malignancy
- Encephalopathy
Clinical features of mild hypothermia (35-32’C)
- Vasoconstriction
- Apathy/lethargy
- Ataxia
- Tachycardia
- Tachypnoea
- Normotension
Clinical features of moderate hypothermia (32-28’C)
- Confusion
- Delirium
- ALOC
- Hypotension
- Bradycardia
- Muscle rigidity
Clinical features of severe hypothermia (<28’C)
- Stupor
- Coma
- Diminished/absent signs of life
- Dilated pupils
- Reduced/absent reflexes
- Apnoea
- Dysrhythmias
Additional clinical features of hypothermia that may develop
- Blunted catecholamine release
- Hypo/hyperglycaemia
- Hypo/hyperkalaemia
- Coagulopathy/DIC/thromboembolitic disorders
- Rhabdomyolysis
Rx considerations for hypothermia
- Minimise pt movement (increased risk of VF)
- Prevent further heat loss (remove wet clothes, ensure pt is dry)
- Commence rewarming (warming blanket, heated environment)
- Oxygen
- LMA/ETT
- 12-lead ECG
- IV fluid
- BGL
- Serial temp monitoring
- Rx concurrent conditions
Examples of time critical (non-traumatic) abdominal emergencies
- Ectopic pregnancy
- Ruptured abdominal aortic aneurysm (AAA)
- Peritonitis and sepsis (usually caused by perforation of a visceral organ)
- Testicular/ovarian torsion
- Uncontrolled GIT haemorrhage (upper - oesophagus, stomach, duodenum; lower - small bowel, colon)
- Acute bowel obstruction
- Acute pancreatitis
High risk features of nont-traumatic abdominal emergencies
- Elderly/paediatric pts
- Severe abdominal pain/tenderness
- Altered VSS
- N+V
- Hx haematemesis and/or melaena
- Female of child bearing age
Rx considerations for abdominal emergencies
- Oxygen
- IV access
- Analgesia
- Antiemetic
- IV fluids
- Blood products
Pathophysiology of acute dystonic reactions
Acute dystonic reactions are extrapyramidal side effects resulting from an imbalance between dopaminergic deficiency and cholinergic excess neurotransmission in the basal ganglia.
Explanation of dystonia
Dystonia refers to involuntary, sustained, repetitive muscle contractions that may be painful. It is different to akathisia (wherein the pt feels the need to constantly move), though this may also occur with these medications.
Examples of medications that can cause acute dystonic reactions
- Antipsychotics (haloperidol, droperidol, fluphenazine, clozapine, olanzapine, quetiapine, risperidone)
- Antiemetics (metoclopramide, prochlorperazine)
- Antidepressants (SSRIs, e.g. fluoxetine)
- Antibiotics (erythromycin)
- Anticonvulsants (carbamazepine)
- Antihistamines (ranitidine)
- Illicit stimulants (cocaine)
Clinical features of acute dystonic reaction
- Normal mentation
- Oculogyric crisis (deviated gaze/eye spasm)
- Laryngospasm (stridor, dysphonia, throat pain, dyspnoea)
- Torticollis
- Opisthotonus (arms flexed, legs extended, back arched)
- Macroglossia (tongue feels enlarged and protrudes)
- Buccolingual crisis (trismus, dysarthria, grimacing)
- Tortipelvic crisis (hips, pelvis, abdominal wall muscles)
- Spasticity of trunk or limbs
Additional clinical features that may be present in acute dystonic reactions
- Anxiety
- Agitation
- Diaphoresis
- Tachycardia
- Tachypnoea
Rx considerations for acute dystonic reactions
- Oxygen/assisted ventilation as indicated
- IV fluids
- Benzatropine
Pathophysiology of adrenal insufficiency
Adrenal insufficiency is an endocrine disorder involving reduced hormone secretion from the adrenal glands, resulting in deficiency of adrenal hormones including cortisol and aldosterone.
Function of cortisol
Cortisol regulates glucose and protein metabolism as well as affecting blood pressure and immune function, and is critically important as a stress response hormone.
Function of aldosterone
Aldosterone assists in regulating blood volume and pressure by effecting the renal reabsorption of sodium and secretion of potassium.
Term for acute form of adrenocortical insufficiency
Adrenal crisis
Cause of primary adrenal insufficiency
Primal adrenal insufficiency results from an intrinsic adrenal gland problem that affects hormone production, often due to an autoimmune disease (e.g. Addison’s disease and congenital hyperplasia)
Cause of secondary adrenal insufficiency
Secondary adrenal insufficiency occurs when the pituitary gland fails to produce enough adrenocorticotropin (ACTH), a hormone that stimulates the adrenal glands to produce cortisol (e.g. exogenous steroid consumption, panhypopituitarism)
Cause of tertiary adrenal insufficiency
Tertiary adrenal insufficiency is due to hypothalamic dysfunction resulting in a decrease in corticotropin releasing hormone (CRH), the hormone which stimulates the pituitary to produce ACTH
Clinical features of symptomatic adrenal insufficiency/adrenal crisis
- Postural symptoms
- Hypotension and/or shock
- ALOC
- Non-specific abdo pain
- Anorexia
- N+V
- Diarrhoea
- Hyperthermia
- Hypoglycaemia
- Hyperkalaemia
Rx considerations for symptomatic adrenal insufficiency/adrenal crisis
- IV fluids
- Hydrocortisone
Definition of anaphylaxis
Any acute onset illness with typical skin features plus involvement of respiratory and/or cardiovascular and/or persistent severe GIT symptoms
- OR -
Any acute onset of hypotension or bronchospasm or upper airway obstruction where anaphylaxis is considered possible, even if skin features are not present.
Clinical features of anaphylaxis
- Cutaneous: urticaria, angioedema, pruitus, flush
- Respiratory: difficulty breathing, wheeze, upper airway swelling, rhinitis
- Cardiovascular: hypotension, dizziness, brady/tachycardia, collapse
- Abdominal: N+V+D, abdo pain
Positioning of pt with anaphylaxis
Supine
Rx considerations for anaphylaxis
- IM adrenaline
- Oxygen
- IV fluid bolus
- Salbutamol
- Ipatropium bromide
- Nebulised adrenaline
- Hydrocortisone
Definition of hyperglycaemia
Hyperglycaemia is a fasting BGL >7mmol/L
Presentations of hyperglycaemia
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycaemic syndrome (HHS)
- Asymptomatic
Common causes of DKA/HHS
- Acute illess
- Non-compliance with rx
Components of DKA
- Type 1 diabetes mellitus
- Hyperglycaemia
- Ketosis
- Metabolic acidosis
Pathophysiology of DKA
- Absolute insulin deficiency or resistance
- High BGL increases blood osmolarity and draws water out of cells, causing cellular dehydration
- High BGL in kidneys cause osmotic diuresis and polyuria, leading to severe dehydration and hypovolaemia
- Alternative fuel sources (including fatty acids) are used, producing organic acids called ketones which accumulate and cause metabolic acidosis
- Dehydration leads to polydipsia
- Loss of potassium from the body
Components of HHS
- Type 2 diabetes mellitus
- Hyperglycaemia
- Hyperosmolarity
- Severe dehydration
Pathophysiology of HHS
- Relative insulin deficiency (where there is sufficient insulin to limit ketone production and preventing metabolic acidosis)
- Hyperglycaemia causes polyuria, polydipsia, and polyphagia
- Fluid deficits often exceed those of DKA
Mortality in DKA vs HHS
HHS has a greater mortality rate due to the severity of underlying illnesses, typically sepsis.
Neurological symptoms of DKA/HHS
- ALOC
- Lethargy
- Seizure
- Coma
Cardiovascular symptoms of DKA/HHS
- Hypovolaemia (hypotension, tachycardia)
- Pale/cool/clammy OR flushed/hot
BGL in DKA vs HHS
DKA > 10mmol/L
HHS > 40mmol/L
Kussmaul respiration in DKA vs HHS
Kussmaul respiration is usually due to severe metabolic acidosis and so is not usually seen in HHS
Rx considerations for hyperglycaemia with severe dehydration/altered perfusion status
- IV access
- IV fluids
- Oxygen
- 12-lead ECG
Reason for caution with quick correction of dehydration with IV fluids
Correcting fluid deficits too quickly can cause cerebral oedema, particularly in paeds
Definition of hypoglycaemia
Hypoglycaemia is defined as a BGL < 4.0mmol/L regardless of diabetes hx
First line mx for pts unable to swallow oral glucose
IV glucose
Aim of rx for hypoglycaemic pts unable to swallow oral glucose
BGL between 4 and 8 mmol/L
Consideration if there is a no improvement in conscious state after bringing a hypoglycaemic BGL up between 4 and 8 mmol/L
Other causes of ALOC
Automatic features (warning signs) of hypoglycaemia
- Diaphoresis
- Hunger
- Tingling around the mouth
- Tremor
- Tachycardia
- Pallor
- Palpitations
- Anxiety
Neurological features of hypoglycaemia
- ALOC
- Lethargy
- Behavioural changes
- Headache
- Visual disturbance
- Slurred speech
- Dizziness
- Seizures
- Coma
- Stroke-like symptoms
Medication that may mask signs of hypoglycaemia
Beta blockers
Meaning of ‘relative’ hypoglycaemia
Chronic, poorly controlled diabetics may be relatively hypoglycaemic despite a BGL > 4 mmol/L
Rx for pts able to take oral glucose vs pts unable to take oral glucose
Safely capable - oral glucose
Unable - IV access, glucose 10%
Definition of hyperkalaemia
Hyperkalaemia is a serum potassium of > 5.5mEq/L
Danger of severe hyperkalaemia
Fatal cardiac dysrhythmias
ECG rhythm that indicates pre-terminal hyperkalaemia
Sine wave
Common medical causes of hyperkalaemia
- Renal impairment
- DKA
- Addisons disease
- Metabolic acidosis
Medications that can cause hyperkalaemia
- Potassium-sparing diuretics
- ACE inhibitors
- NSAIDS
Types of cellular injuries that can cause hyperkalaemia
- Rhabdomyolysis
- Crush injury
- Burns
Clinical features of hyperkalaemia
- Weakness, paraesthesia
- Signs of underlying cause
- N+V+D
- ECG progression: peaked T waves, flat/lost P waves, wide QRS, T wave fusion (sine wave)
Function of calcium gluconate 10% in rx of hyperkalaemia
Calcium gluconate 10% stabilises the myocardium, but does not reduce serum potassium.
Function of sodium bicarbonate 8.4% in rx of hyperkalaemia
Sodium bicarbonate 8.4% reduces serum potassium and provides temporary effect to allow rx of underlying cause.
Rx considerations for hyperkalaemia
- IV access
- Calcium gluconate 10%
- Sodium bicarbonate 8.4%
- Sodium chloride 0.9%
- Nebulised salbutamol
Description of meningococcal septicaemia
Meningococcal septicaemia is a life-threatening infection which can cause rapid and irreversible deterioration, and for which rx becomes less effective with progression.
Aim of prehospital mx of meningococcal septicaemia
- Early recognition
- AB ceftriaxone
- IV fluids for haemodynamic compromise
Clinical features of meningococcal septicaemia
- Non-blanching petechial (pin-point) or purpuric (bruises) rash
- Myalgia
- Meningism: photophobia, neck stiffness, headache, N+V
- Severe lethargy
- Fever
- Shock
Definition of sepsis
Sepsis is a syndrome of infection complicated by systemic inflammation that can progress along a continuum and result in organ dysfunction, shock, and death.
Most common causes of sepsis
- Respiratory infections (~50%)
- Genitourinary infections
- Abdominal infections
Key components of prehospital sepsis mx
- Early identification
- Early oxygenation
- Early haemodynamic resus
- Hospital notification
Clinical features of systematic inflammatory response syndrome (SIRS)
- Presumed/known site of infection, and two or more of the following:
- Temp >38.3’ pr >36.0’
- Heart rate >90bpm
- Resp rate >20/min
- BGL >6.6mmol/L
- Acutely altered mental status
Two components of severe sepsis
- Sepsis
- Evidence of organ hypoperfusion or dysfunction
Clinical characteristics of severe sepsis
- Systolic BP < 90 or MAP < 65
- SpO2 <90%
- Nil urine output for > 8 hours
- Prolonged bleeding from minor injury/gums
Most common presenting symptom in sepsis
Tachypnoea
Rx considerations for sepsis (not severe/shock)
- Antipyretic
- IV fluid
Rx considerations for severe sepsis/septic shock
- Oxygen
- IV fluid
- Adrenaline
Causes of cauda equina and conus medullaris syndromes
- Lumbar or thoracic disc protrusion/extrusion
- Trauma
- Tumours
- Infections
- Spinal stenosis
- Epidural haematomas
Pathophysiology of epidural abscess
Infection of the epidural space that can lead to spinal cord damage by direct infection, compression, or vascular compromise.
Pathophysiology of vertebral osteomyelitis or discitis
Infection of the bones of the spine or inflammation of the vertebral disc space respectively that can lead to significant neurological compromise if misdiagnosed or left untreated.
Clinical features of spinal emergencies
- Diaphoresis/hunger/tingling
- Temp < 36’C or > 38’C
- Age <20 or >50
- Recent onset of pain without trauma or lifting
- Severe pain at rest or progressively worsening
- Bilateral sciatic nerve pain
- Obvious structural deformity
- Urinary retention and/or incontinence
- Bowel incontinence
- Lower extremity neurological deficit
- Hx cancer
- Fever/chills/night sweats/recent weight loss
- Recent infection or immunosuppression
- Perineal/perianal/saddle sensory loss
- IV drug use or recent steroid therapy
Rx considerations for spinal emergencies
- IV access
- Antiemetic
- Analgesia
Main categories of ALOC
- Intracranial pathology (structural)
- Extra-cranial pathology (non-structural)
Clinical features of ALOC
- Unable to arouse and respond appropriately to environmental stimuli
- Confused (disorientated, impaired thinking and response)
- Delirious (disorientated, restless, hallucinations, delusions)
- Somnolent (sleepy)
- Obtunded (decreased alertness, slowed psychomotor response)
- Stuporous (sleep-like state with little/no spontaneous activity)
- Comatose (unable to rouse, no response to stimuli)
Rx considerations for ALOC
- Oxygen
- IPPV
- Mx reversible causes (AEIOUTIPS)
Pathophysiology of autonomic dysreflexia
Autonomic dysreflexia is a syndrome of massive imbalanced reflex sympathetic discharge occuring in pts with an existing non-acute spinal cord injury about T6.
Causes of autonomic dysreflexia
- Distended bladder due to blocked/kined catheter
- UTI
- Bowel irritation (constipation/faecal impaction)
- Skin irritations (pressure sores, ingrown toenails, burns, sunburn)
- Contracting uterus, fractures, or any other event that would normally be deemed painful
Cause of complications of autonomic dysreflexia
Sustained severe peripheral HTN
Examples of complications of autonomic dysreflexia
- Cerebral haemorrhage
- Myocardial infarction
- Seizures
Preferred mx of autonomic dysreflexia and why this may not always be possible
Preferred mx is removal of the noxious stimuli, but this may not be possible in the prehospital environment so symptomatic mx to prevent cerebrovascular catastrophe may be the primary goal
Clinical features of autonomic dysreflexia
- Relative hypertension (BP for SCI pts is typically low)
- Flushing of skin above injury or paleness below injury
- Bradycardia
- Profuse sweating and piloerection above injury
- Pounding headache
- Blurred vision/CVA-like symptoms
- ACS
Rx considerations for autonomic disreflexia
- Sit pt upright with legs dependent where possible
- Loosen clothing
- Ensure IDC or SPC is not kinked
- Remove noxious stimuli if possible
- GTN
- Morphine OR fentanyl
Categories of headache
- Primary (no underlying cause and the problem is due to an abnormality at the molecular level. These account for 90% presentations including migraines, tension, and cluster headaches)
- Secondary (clearly identifiable underlying cause, many with significant consequences if not treated. These include intracranial haemorrhage, tumours, and infections)
Evaluation and differential dx of headache
Detailed history should be followed by a general and neurological examination, including psychological factors, life events, and stressful incidences.
Red flags for headaches
- Thunderclap headache
- Headaches associated with fever/rash/ALOC
- Meningeal signs (stiff neck, photophobia, N+V)
- New onset headache in pts >50 or <10
- Persistent morning headache with nausea
- New onset headache in pts with cancer or HIV
- Progressive headache, worsening over weeks
- Headaches associated with postural changes
- Aura lasting longer than an hour/different than previous auras/occurs for first time using oral contraceptive
Yellow flags for headaches
- Worsening headache following recent head trauma
- Taking an anticoagulant or antiplatelet drug
- HTN during pregnancy
- Previous hx of intracranial bleeding
- Onset during sexual activity
- Family hx of cerebral vascular abnormalities
Green flags for headaches
- Symptoms associated with influenza
- Known headache with ‘usual’ symptoms and triggers
- Normal vital signs, normal FAST assessment, able to walk normally
Rx considerations for headache
- Analgesia
- Antiemetic
- IV fluids
Definition of seizure
A seizure is a transient disturbance of cerebral function caused by abnormal neuronal activity in the brain.
Definition of epilepsy
Epilepsy is a disorder of brain function with recurring seizures and is due to many diverse aetiologies.
Two categories of seizures
Focal and generalised
Description of focal seizures
Abnormal neuronal activity originates and is limited to one hemisphere of the cerebral cortex. Seizure symptoms are representative of the area of the cerebral cortex where the abnormal neuronal discharge exists. Focal seizures can evolve to become bilateral convulsive seizures.
Difference between and focal and a focal dyscognitive seizure
Focal - seizure activity that does not impair awareness or responsiveness
Focal dyscognitive - seizure activity where level of awareness or responsiveness is reduced but full consciousness is not lost
Description of generalised seizures
Abnormal neuronal activity rapidly engages both hemispheres of the cerebral cortex.
Types of generalised seizures
- Absence
- Atonic
- Tonic
- Myoclonic
- Tonic clonic
Description of an absence seizure
Brief loss of awareness and responsiveness with no post-ictal phase
Description of an atonic seizure
Sudden loss of muscle tone that results in a sudden fall
Description of a tonic seizure
Sudden increased muscle tone that most often occurs in clusters during sleep
Description of a myoclonic seizure
A brief, sudden jerking action of a muscle or muscle group that may occur in a series leading into a tonic clonic seizure
Description of a tonic clonic seizure
An abrupt loss of consciousness that is concurrent with involuntary muscular contractions (tonic phase) followed by symmetrical jerking movements (clonic phase). Typically lasts 1 - 3 minutes and is followed by a post-ictal period.
Definition of status epilepticus
A medical emergency in which seizure activity > 5 minutes duration or recurrent seizure activity where the pt does not recover to GCS 15 prior to another seizure.
Seizure triggers in epilepsy
- Lack of sleep/stress
- Sudden stopping/changing medications
- Fever/infection
- Dehydration/V+D
- Alcohol/illict drug use
- Menstruation
- Photosensitivity
- Extreme temperatures, particularly heat
- Electrolyte disturbances
Definition of psychogenic non-epileptic seizures (PNES, previously known as pseudoseizures)
Episodic behavioural events that mimic seizure activity but are not epileptic seizures, and arise due to different factors in different individuals. Midazolam is appropriate if doubt exists as to seizure causation.
Examples of provoked seizures
- Hypoxia and hypercarbia
- Hypotension
- Metabolic (hypoglycaemia, hyponatraemia, hypocalcaemia, hyperthyroidism, uraemia)
- Eclampsia
- Meningitis/encephalitis
- Hyperthermia/febrile convulsions
- Drugs/toxins (intoxication/withdrawal)
- Cerebral pathology (tumour, stroke, trauma)
Typical seizure presentations
- Visual hallucinations
- Localised twitching of muscles without impaired consciousness
- Localised tingling and numbness
- Nonsensical speech
- Disorientated movements
- Sudden pause in acitvity or fixed gaze
- Nystagmus
- Automatism
- Increase or loss of tone
- Alternating tonic/clonic posturing
- Incontinence
- Post-ictal: confusion, fatigue, headache, nausea
Associated clinical features of prolonged seizures or status epilepticus
- Hypoxia, hypercarbia
- Progressive lactic and respiratory acidosis
- Hyperthermia, HTN, tachycardia
- Hypo/hyperglycaemia
- Hyperkalaemia
Rx considerations for seizure
- Reversible causes
- Midazolam
- Oxygen
Definition of transient ischaemic attack (TIA)
A TIA is a brief episode of neurological dysfunction (typically < 24 hours) resulting from focal temporary cerebral ischaemia.
Clinical features of TIA
- Hemiparesis/hemiplegia
- Dysphasia/aphasia
- Dysphagia
- Visual disturbances
- Sudden onset headache associated with neurological symptoms/ALOC
Conditions that may mimic TIA/stroke
- Hypoglycaemia
- Cerebral lesions
- Seizures/post-ictal states
- Hemiplegic migraine
- Electrolyte abnormalities
- Conversion disorder
Rx considerations for TIA
- Oxygen
- Antiemetic
- Analgesia
- IV fluids
- Acute stroke referral
Definition of breech birth
Breech birth occurs when the foetus enters the birth cancal with the buttocks or feet first, with common variations being frank, complete, footling, and kneeling.
Description of frank breech
The foetus’s buttocks present first, with legs flexed at the hip and extended at the knees, placnig the feet near the ears. Most breech babies are in the frank position.
Description of complete breech
The foetus’s hips and knees are flexed so the foetus is sitting cross-legged with feet beside the buttocks.
Description of footling breech
One or both feet present first, with buttocks at a higher position. Rare at term but common with premature births, footling breech carries increased risk of prolapsed cord.
Description of kneeling breech
The foetus is in a kneeling position with or both legs extended at the hips and flexed at the knees. Rare and often grouping with footling breech to form ‘incomplete breech’, this carries increased risk of prolapsed cord.
Management process for breech birth
- Once recognised, prepare for neonatal resuscitation
- Position mother so neonate can hang freely, and encourage pushing (hands off)
- If arms do not release spontaneously, perform Lovesets manoeuvre
- When occiput is visible, perform adapted Mauriceau-Smelli-Viet manoeuvre
- Commence post-delivery assessments immediately
Description of cord prolapse
Cord prolapse is an obstetric emergency occuring after membranes have ruptured when the umbilical cord slips down in front of the presenting part of the foetus and protrudes into the vagina. As labour progresses and the presenting part descends, the cord is compressed which cuts off foetal blood supply, leading to foetal hypoxia.
Clinical features of cord prolapse
- Umbilical cord visible at or external to the vaginal opening
- Evidence of membranes having ruptured
- Change in foetal movement pattern
- Meconium in the amniotic fluid
Risk factors for cord prolapse
- Multiparity
- Low birth weight
- Pre-term labour
- Foetal congenital abnormalities
- Breech presentation
- Transverse, oblique, and unstable lie (repeatedly changing foetal position after 37w)
- Second twin
- Polyhydramnios
- Unengaged presenting part
- Low-lying placenta
Management for cord prolapse if pulsative cord is evident at vaginal opening/loop is hanging down
- Assist the mother into exaggerated Sims position
- Ask mother to gently push cord back using a dry pad
Management for cord prolapse if pulsative cord is not evident at vaginal opening/loop is not hanging down
- Assist mother to assume knees-to-chest position
- Carefully attempt to push the presenting part off the cord
- Tx in exaggerated Sims position
Definition of an ectopic pregnancy
Pregnancy in which the developing embryo implants outside the uterine cavity.
Clinical features of unruptured ectopic pregnancy
- Hx of amenorrhoea (at least one missed period)
- Abnormal vaginal bleeding
- Pelvic and/or abdominal pain
- Nausea
- Presyncopal symptoms
Clinical features of ruptured ectopic pregnancy
- Syncope
- Shock
- Acute severe pelvic and/or abdominal pain
- Shoulder tip pain (Kehr’s sign) caused by free blood irritating the diaphragm when supine
- Abdominal distention
- Rebound tenderness and/or guarding
Rx for pts with suspected ectopic pregnancy
- Analgesia
- Antiemetic
- IV fluids
Definition of miscarriage
Miscarriage is the spontaneous loss of pregnancy before 20 weeks gestation, the aetiology of most cases unknown.
Clinical presentation of miscarriage
- Lower abdominal discomfort
- Vaginal bleeding
- Hypotension
- Tachycardia
- Postural symptoms
Clinical features suggesting intrauterine infection
- Severe pelvic pain and/or rigidity and/or guarding
- Purulent discharge
- Fever
Management of miscarriage if a foetus is delivered (often placenta remains attached)
- Cut and clamp the cord
- Wrap the foetus (mother may or may not wish to hold the foetus)
- Acknowledge the foetus as the mother’s baby, provide psychological cares
Signs of imminent birth
- Loss of operculum plug
- Increasing frequency and severity of contractions with an urge to push, or open bowels
- Membrane rupture
- Bulging perineum
- Appearance of the presenting part
Management of physiological cephalic birth
- Allow mother to assume a comfortable position
- Prepare equipment
- Consider analgesia
- Ensure controlled birth of the head
- Dry baby, place prone and skin-to-skin on mother’s chest
- Clamp and cut the cord when it stop pulsating
- Assess APGAR (1 and 5 minutes)
- Encourage breastfeeding
- Consider third stage management (oxytocin)
Definition of placental abruption
Placental abruption occurs when a normally situated placenta partially or completely separates from the uterine wall, causing haemorrhage prior to foetal delivery.
Maternal complications associated with placental abruption
- Disseminated intravasular coagulopathy (DIC)
- Shock
- Uterine rupture
- Acute renal failure
Clinical features of placental abruption
- Constant pain in the abdo-pelvic region
- Bleeding may range from absent to profuce, occurring in waves as the uterus contracts
- Tetanic uterine contractions
- Uterine hypertonicity (feels rigid on palpation)
- Fundal height may increase (due to expanding intrauterine haemorrhage)
- Signs of maternal shock
Three categories of placental abruption
- Marginal, where an edge has separated away
- Central, where the centre has detached
- Complete, where the whole placenta has comes away from the uterine wall
Rx considerations for placetal abruption
- IV access
- IV fluid
- Analgesia
- Antiemetics
Definition of placenta praevia
Placenta praevia occurs when the placenta is situated either partially or wholly in the lower uterine segment.
Reason placenta praevia becomes an issue in the third trimester.
The downward and outward thrust of the developing foetus is accommodated by the thinning and stretching of the lower uterine wall. This causes some degree of placental separation and subsequent bleeding. This can worsen during cervical effacement if the placenta is near or over the cervical os. The placenta may also physically prevent normal vaginal delivery.
When placenta praevia becomes an obstetric emergency
Placenta praevia becomes an obstetric emergency in the presence of antepartum haemorrhage, as initial small bleeds have potential to develop into profuse blood loss that can threaten both mother and foetus.
Focus of pre-hospital management of placenta praevia
Preventing maternal hypotension
Clinical features of placenta praevia
- Several small warning bleeds
- Bright red blood
- No pain (other than those
