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QAS > ACP2 CPGs > Flashcards

ACP2 CPGs Flashcards

1
Q

Clinical features of aortic dissection

A
  • 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
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2
Q

Risk factors for development of acute aortic dissection

A
  • 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
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3
Q

Rx points to consider for suspected aortic dissection

A
  • Oxygen
  • IV access
  • Analgesia
  • Antiemetic
  • IV fluids
  • Blood products (request support)
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4
Q

Clinical features of acute coronary syndrome (ACS)

A
  • Chest pain/discomfort
  • Referred pain (arms/jaw/teeth)
  • Dyspnoea
  • Diaphoresis
  • N+V
  • Feeling of impending doom
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5
Q

Typical presentation of RVMI

A
  • Hypotension
  • Jugular vein distension
  • Clear lung fields
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6
Q

Rx points to consider for ACS

A
  • Oxygen
  • IV access
  • Aspirin
  • GTN
  • Antiemetic
  • Fentanyl
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7
Q

Conditions associated with cardiac classified bradycardia

A
  • Diseased SA node/AV node/His-Purkinje system
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8
Q

Types of conditions associated with non-cardiac classified bradycardia

A
  • Environmental
  • Metabolic
  • Endocrine
  • Toxicology
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9
Q

Clinical features of bradycardia

A
  • Hypotension
  • Syncope
  • ALOC
  • Chest pain/discomfort
  • Congestive heart failure (CHF)
  • Dyspnoea
  • Diaphoresis
  • N + V
  • Dizziness
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10
Q

Common cause and initial mx focus for bradycardia

A

Hypoxia - mx should focus on improving oxygenation and ventilation

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11
Q

Definition of cardiac arrest

A

Cessation of blood circulation due to the inability of the heart to maintain adequate tissue perfusion

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12
Q

Two shockable cardiac rhythms

A
  • Pulseless ventricular tachycardia (VT)

- Ventricular fibrillation (VF)

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13
Q

Two non-shockable cardiac rhythms

A
  • Pulseless electrical activity (PEA)

- Asystole

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14
Q

Definition of cardiogenic shock

A

Prolonged hypotension with inadequate tissue perfusion perfusion in spite of adequate left ventricular filling pressure

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15
Q

Possible causes of cardiogenic shock

A
  • AMI
  • Drugs (beta blockers, calcium channel blockers, some chemo rx)
  • Hypocalcaemia
  • Ventricular hypertrophy
  • Cardiomyopathy
  • Aortic stenosis
  • Aortic or mitral regurgitation
  • Malignant HTN
  • Catecholamine excess
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16
Q

Clinical features of cardiogenic shock

A
  • AMI
  • Chest pain/discomfort
  • Diaphoresis
  • Cold mottled/cyanotic peripheries
  • ALOC
  • Tachycardia/bradycardia
  • Hypotension
  • Respiratory distress secondary to pulmonary oedema (tachypnoea, hypoxia, wheeze)
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17
Q

Rx points to consider for cardiogenic shock

A
  • Oxygen
  • IPPV/CPAP
  • IV access
  • Aspirin
  • Adrenaline
  • IV fluids
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18
Q

Clinical features of broad complex tachycardia

A
  • Palpitations
  • Chest pain/discomfort
  • Dyspnoea
  • ALOC
  • Syncope
  • Haemodynamic compromise
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19
Q

Mx considerations for broad complex tachycardia without haemodynamic compromise

A
  • Amiodarone

- Magnesium sulphate

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20
Q

Mx considerations for broad complex tachycardia with haemodynamic compromise

A

Synchronised cardioversion

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21
Q

Aetiology associated with cardiac classified narrow complex tachycardia

A
  • 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)
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22
Q

Aetiology associated with non-cardiac classified narrow complex tachycardia

A
  • Pain/anxiety
  • Hyperthermia/fever
  • Drug induced
  • Anaemia
  • Shock
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23
Q

Clinical features of narrow complex tachycardia

A
  • Palpitations
  • Chest pain/discomfort
  • Dyspnoea
  • ALOC
  • Haemodynamic instability
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24
Q

Mx considerations for narrow complex tachycardia

A
  • Oxygen
  • Aspirin (if MI suspected)
  • Modified Valsalva (if not compromised and regular)
  • IV fluid (if compromised)
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25
Q

Major incident mx handover mnemonic

A

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
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26
Q

Cause of diving emergencies

A

Changes in ambient pressure

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27
Q

Three types of diving emergencies

A
  • Decompression illness (decompression sickness and arterial gas embolism; DCS and AGE)
  • Barotrauma
  • Hypoxic blackouts
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28
Q

Pathophysiology of DCS

A

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.

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29
Q

Pathophysiology of AGE

A

Results from pulmonary barotrauma when expanding gas in the alveoli rupture the alveoli/capillary membrane, allowing bubbles to enter arterial circulation via the lungs.

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30
Q

Pathophysiology of barotrauma

A

Occurs when trapped air expands during ascent due to decreasing pressure, causing trauma.

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31
Q

Where in the body barotrauma can occur

A

Any gas filled space including the pulmonary system, ears, eyes, sinuses, dental structures, GIT, as well as dive mask and suit.

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32
Q

Description and explanation of hypoxic/shallow water blackout

A

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.

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33
Q

Neurological clinical features of diving emergencies

A
  • Headache
  • Visual changes
  • Motor/sensory deficit
  • Cranial nerve palsies
  • Seizures
  • Paralysis
  • ALOC
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34
Q

Respiratory clinical features of diving emergencies

A
  • Dyspnoea
  • Haemoptysis
  • Chest pain
  • APO
  • Pulmonary barotrauma (pneumothorax/pneumomediastinum/subcutaneous emphysema)
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35
Q

Localised clinical features of diving emergencies

A
  • Skin itch/rash
  • Pain in the joints and/or muscles
  • Tremors
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36
Q

Cardiac clinical features of diving emergencies

A
  • Chest pain

- Cardiac arrest

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37
Q

Rx points to consider for diving emergency pts who are unconscious/respiratory distress

A
  • Position pt supine
  • High flow oxygen
  • IPPV
  • IV fluid
  • LMA/ETT
  • Maintain normothermia
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38
Q

Pathophysiology of hyperthermia

A

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.

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39
Q

Mechanisms of heat transference to and from the body

A
  • Radiation
  • Conduction
  • Convection
  • Evaporation
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40
Q

Definition of environmental exposure hyperthermia

A

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.

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41
Q

Explanation of intrinsic hyperthermia

A

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.

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42
Q

Conditions that may exacerbate intrinsic hyperthermia

A
  • 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)
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43
Q

Definition and temp range of heat exhaustion

A

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.

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44
Q

Definition and temp range of heat stroke

A

> 40’C, heat stroke is potentially life-threatening and can result in multi-organ failure and death.

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45
Q

Clinical features of heat exhaustion

A
  • Severe headache/dizziness
  • Diaphoresis/N+V
  • Tachypnoea
  • Tachycardia
  • Hypotension
  • Muscle pain/fatigue/cramps
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46
Q

Clinical features of heat stroke

A
  • 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
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47
Q

Rx to consider for heat exhaustion/heat stroke

A
  • 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
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48
Q

Definition and pathophysiology of hypothermia

A

Hypothermia is a core body temp <35’C and is caused by excessive cold stress and/or inadequate body heat production.

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49
Q

Early compensatory mechanisms for hypothermia

A
  • Shivering
  • Increased muscle tone
  • Peripheral vasoconstriction
  • Tachypnoea
  • Increased cardiac output
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50
Q

Three classifications of causes of hypothermia

A
  • Increased heat loss
  • Decreased heat production
  • CNS dysfunction
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51
Q

Causes of hypothermia classified under increased heat loss

A
  • Vasodilation
  • Environmental
  • Trauma
  • Loss of skin integrity (e.g. burns)
  • Neuropathy
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52
Q

Causes of hypothermia classified under decreased heat production

A
  • Age
  • Endocrine disorders
  • Nutritional deficits
  • Immobility
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53
Q

Causes of hypothermia classified under CNS dysfunction

A
  • Trauma
  • CVA
  • Hypoxaemia
  • Malignancy
  • Encephalopathy
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54
Q

Clinical features of mild hypothermia (35-32’C)

A
  • Vasoconstriction
  • Apathy/lethargy
  • Ataxia
  • Tachycardia
  • Tachypnoea
  • Normotension
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55
Q

Clinical features of moderate hypothermia (32-28’C)

A
  • Confusion
  • Delirium
  • ALOC
  • Hypotension
  • Bradycardia
  • Muscle rigidity
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56
Q

Clinical features of severe hypothermia (<28’C)

A
  • Stupor
  • Coma
  • Diminished/absent signs of life
  • Dilated pupils
  • Reduced/absent reflexes
  • Apnoea
  • Dysrhythmias
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57
Q

Additional clinical features of hypothermia that may develop

A
  • Blunted catecholamine release
  • Hypo/hyperglycaemia
  • Hypo/hyperkalaemia
  • Coagulopathy/DIC/thromboembolitic disorders
  • Rhabdomyolysis
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58
Q

Rx considerations for hypothermia

A
  • 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
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59
Q

Examples of time critical (non-traumatic) abdominal emergencies

A
  • 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
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60
Q

High risk features of nont-traumatic abdominal emergencies

A
  • Elderly/paediatric pts
  • Severe abdominal pain/tenderness
  • Altered VSS
  • N+V
  • Hx haematemesis and/or melaena
  • Female of child bearing age
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61
Q

Rx considerations for abdominal emergencies

A
  • Oxygen
  • IV access
  • Analgesia
  • Antiemetic
  • IV fluids
  • Blood products
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62
Q

Pathophysiology of acute dystonic reactions

A

Acute dystonic reactions are extrapyramidal side effects resulting from an imbalance between dopaminergic deficiency and cholinergic excess neurotransmission in the basal ganglia.

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63
Q

Explanation of dystonia

A

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.

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64
Q

Examples of medications that can cause acute dystonic reactions

A
  • 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)
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65
Q

Clinical features of acute dystonic reaction

A
  • 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
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66
Q

Additional clinical features that may be present in acute dystonic reactions

A
  • Anxiety
  • Agitation
  • Diaphoresis
  • Tachycardia
  • Tachypnoea
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67
Q

Rx considerations for acute dystonic reactions

A
  • Oxygen/assisted ventilation as indicated
  • IV fluids
  • Benzatropine
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68
Q

Pathophysiology of adrenal insufficiency

A

Adrenal insufficiency is an endocrine disorder involving reduced hormone secretion from the adrenal glands, resulting in deficiency of adrenal hormones including cortisol and aldosterone.

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69
Q

Function of cortisol

A

Cortisol regulates glucose and protein metabolism as well as affecting blood pressure and immune function, and is critically important as a stress response hormone.

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70
Q

Function of aldosterone

A

Aldosterone assists in regulating blood volume and pressure by effecting the renal reabsorption of sodium and secretion of potassium.

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71
Q

Term for acute form of adrenocortical insufficiency

A

Adrenal crisis

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72
Q

Cause of primary adrenal insufficiency

A

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)

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73
Q

Cause of secondary adrenal insufficiency

A

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)

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74
Q

Cause of tertiary adrenal insufficiency

A

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

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75
Q

Clinical features of symptomatic adrenal insufficiency/adrenal crisis

A
  • Postural symptoms
  • Hypotension and/or shock
  • ALOC
  • Non-specific abdo pain
  • Anorexia
  • N+V
  • Diarrhoea
  • Hyperthermia
  • Hypoglycaemia
  • Hyperkalaemia
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76
Q

Rx considerations for symptomatic adrenal insufficiency/adrenal crisis

A
  • IV fluids

- Hydrocortisone

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77
Q

Definition of anaphylaxis

A

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.

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78
Q

Clinical features of anaphylaxis

A
  • 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
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79
Q

Positioning of pt with anaphylaxis

A

Supine

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80
Q

Rx considerations for anaphylaxis

A
  • IM adrenaline
  • Oxygen
  • IV fluid bolus
  • Salbutamol
  • Ipatropium bromide
  • Nebulised adrenaline
  • Hydrocortisone
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81
Q

Definition of hyperglycaemia

A

Hyperglycaemia is a fasting BGL >7mmol/L

82
Q

Presentations of hyperglycaemia

A
  • Diabetic ketoacidosis (DKA)
  • Hyperosmolar hyperglycaemic syndrome (HHS)
  • Asymptomatic
83
Q

Common causes of DKA/HHS

A
  • Acute illess

- Non-compliance with rx

84
Q

Components of DKA

A
  • Type 1 diabetes mellitus
  • Hyperglycaemia
  • Ketosis
  • Metabolic acidosis
85
Q

Pathophysiology of DKA

A
  • 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
86
Q

Components of HHS

A
  • Type 2 diabetes mellitus
  • Hyperglycaemia
  • Hyperosmolarity
  • Severe dehydration
87
Q

Pathophysiology of HHS

A
  • 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
88
Q

Mortality in DKA vs HHS

A

HHS has a greater mortality rate due to the severity of underlying illnesses, typically sepsis.

89
Q

Neurological symptoms of DKA/HHS

A
  • ALOC
  • Lethargy
  • Seizure
  • Coma
90
Q

Cardiovascular symptoms of DKA/HHS

A
  • Hypovolaemia (hypotension, tachycardia)

- Pale/cool/clammy OR flushed/hot

91
Q

BGL in DKA vs HHS

A

DKA > 10mmol/L

HHS > 40mmol/L

92
Q

Kussmaul respiration in DKA vs HHS

A

Kussmaul respiration is usually due to severe metabolic acidosis and so is not usually seen in HHS

93
Q

Rx considerations for hyperglycaemia with severe dehydration/altered perfusion status

A
  • IV access
  • IV fluids
  • Oxygen
  • 12-lead ECG
94
Q

Reason for caution with quick correction of dehydration with IV fluids

A

Correcting fluid deficits too quickly can cause cerebral oedema, particularly in paeds

95
Q

Definition of hypoglycaemia

A

Hypoglycaemia is defined as a BGL < 4.0mmol/L regardless of diabetes hx

96
Q

First line mx for pts unable to swallow oral glucose

A

IV glucose

97
Q

Aim of rx for hypoglycaemic pts unable to swallow oral glucose

A

BGL between 4 and 8 mmol/L

98
Q

Consideration if there is a no improvement in conscious state after bringing a hypoglycaemic BGL up between 4 and 8 mmol/L

A

Other causes of ALOC

99
Q

Automatic features (warning signs) of hypoglycaemia

A
  • Diaphoresis
  • Hunger
  • Tingling around the mouth
  • Tremor
  • Tachycardia
  • Pallor
  • Palpitations
  • Anxiety
100
Q

Neurological features of hypoglycaemia

A
  • ALOC
  • Lethargy
  • Behavioural changes
  • Headache
  • Visual disturbance
  • Slurred speech
  • Dizziness
  • Seizures
  • Coma
  • Stroke-like symptoms
101
Q

Medication that may mask signs of hypoglycaemia

A

Beta blockers

102
Q

Meaning of ‘relative’ hypoglycaemia

A

Chronic, poorly controlled diabetics may be relatively hypoglycaemic despite a BGL > 4 mmol/L

103
Q

Rx for pts able to take oral glucose vs pts unable to take oral glucose

A

Safely capable - oral glucose

Unable - IV access, glucose 10%

104
Q

Definition of hyperkalaemia

A

Hyperkalaemia is a serum potassium of > 5.5mEq/L

105
Q

Danger of severe hyperkalaemia

A

Fatal cardiac dysrhythmias

106
Q

ECG rhythm that indicates pre-terminal hyperkalaemia

A

Sine wave

107
Q

Common medical causes of hyperkalaemia

A
  • Renal impairment
  • DKA
  • Addisons disease
  • Metabolic acidosis
108
Q

Medications that can cause hyperkalaemia

A
  • Potassium-sparing diuretics
  • ACE inhibitors
  • NSAIDS
109
Q

Types of cellular injuries that can cause hyperkalaemia

A
  • Rhabdomyolysis
  • Crush injury
  • Burns
110
Q

Clinical features of hyperkalaemia

A
  • 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)
111
Q

Function of calcium gluconate 10% in rx of hyperkalaemia

A

Calcium gluconate 10% stabilises the myocardium, but does not reduce serum potassium.

112
Q

Function of sodium bicarbonate 8.4% in rx of hyperkalaemia

A

Sodium bicarbonate 8.4% reduces serum potassium and provides temporary effect to allow rx of underlying cause.

113
Q

Rx considerations for hyperkalaemia

A
  • IV access
  • Calcium gluconate 10%
  • Sodium bicarbonate 8.4%
  • Sodium chloride 0.9%
  • Nebulised salbutamol
114
Q

Description of meningococcal septicaemia

A

Meningococcal septicaemia is a life-threatening infection which can cause rapid and irreversible deterioration, and for which rx becomes less effective with progression.

115
Q

Aim of prehospital mx of meningococcal septicaemia

A
  • Early recognition
  • AB ceftriaxone
  • IV fluids for haemodynamic compromise
116
Q

Clinical features of meningococcal septicaemia

A
  • Non-blanching petechial (pin-point) or purpuric (bruises) rash
  • Myalgia
  • Meningism: photophobia, neck stiffness, headache, N+V
  • Severe lethargy
  • Fever
  • Shock
117
Q

Definition of sepsis

A

Sepsis is a syndrome of infection complicated by systemic inflammation that can progress along a continuum and result in organ dysfunction, shock, and death.

118
Q

Most common causes of sepsis

A
  • Respiratory infections (~50%)
  • Genitourinary infections
  • Abdominal infections
119
Q

Key components of prehospital sepsis mx

A
  • Early identification
  • Early oxygenation
  • Early haemodynamic resus
  • Hospital notification
120
Q

Clinical features of systematic inflammatory response syndrome (SIRS)

A
  • 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
121
Q

Two components of severe sepsis

A
  • Sepsis

- Evidence of organ hypoperfusion or dysfunction

122
Q

Clinical characteristics of severe sepsis

A
  • Systolic BP < 90 or MAP < 65
  • SpO2 <90%
  • Nil urine output for > 8 hours
  • Prolonged bleeding from minor injury/gums
123
Q

Most common presenting symptom in sepsis

A

Tachypnoea

124
Q

Rx considerations for sepsis (not severe/shock)

A
  • Antipyretic

- IV fluid

125
Q

Rx considerations for severe sepsis/septic shock

A
  • Oxygen
  • IV fluid
  • Adrenaline
126
Q

Causes of cauda equina and conus medullaris syndromes

A
  • Lumbar or thoracic disc protrusion/extrusion
  • Trauma
  • Tumours
  • Infections
  • Spinal stenosis
  • Epidural haematomas
127
Q

Pathophysiology of epidural abscess

A

Infection of the epidural space that can lead to spinal cord damage by direct infection, compression, or vascular compromise.

128
Q

Pathophysiology of vertebral osteomyelitis or discitis

A

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.

129
Q

Clinical features of spinal emergencies

A
  • 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
130
Q

Rx considerations for spinal emergencies

A
  • IV access
  • Antiemetic
  • Analgesia
131
Q

Main categories of ALOC

A
  • Intracranial pathology (structural)

- Extra-cranial pathology (non-structural)

132
Q

Clinical features of ALOC

A
  • 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)
133
Q

Rx considerations for ALOC

A
  • Oxygen
  • IPPV
  • Mx reversible causes (AEIOUTIPS)
134
Q

Pathophysiology of autonomic dysreflexia

A

Autonomic dysreflexia is a syndrome of massive imbalanced reflex sympathetic discharge occuring in pts with an existing non-acute spinal cord injury about T6.

135
Q

Causes of autonomic dysreflexia

A
  • 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
136
Q

Cause of complications of autonomic dysreflexia

A

Sustained severe peripheral HTN

137
Q

Examples of complications of autonomic dysreflexia

A
  • Cerebral haemorrhage
  • Myocardial infarction
  • Seizures
138
Q

Preferred mx of autonomic dysreflexia and why this may not always be possible

A

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

139
Q

Clinical features of autonomic dysreflexia

A
  • 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
140
Q

Rx considerations for autonomic disreflexia

A
  • 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
141
Q

Categories of headache

A
  • 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)
142
Q

Evaluation and differential dx of headache

A

Detailed history should be followed by a general and neurological examination, including psychological factors, life events, and stressful incidences.

143
Q

Red flags for headaches

A
  • 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
144
Q

Yellow flags for headaches

A
  • 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
145
Q

Green flags for headaches

A
  • Symptoms associated with influenza
  • Known headache with ‘usual’ symptoms and triggers
  • Normal vital signs, normal FAST assessment, able to walk normally
146
Q

Rx considerations for headache

A
  • Analgesia
  • Antiemetic
  • IV fluids
147
Q

Definition of seizure

A

A seizure is a transient disturbance of cerebral function caused by abnormal neuronal activity in the brain.

148
Q

Definition of epilepsy

A

Epilepsy is a disorder of brain function with recurring seizures and is due to many diverse aetiologies.

149
Q

Two categories of seizures

A

Focal and generalised

150
Q

Description of focal seizures

A

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.

151
Q

Difference between and focal and a focal dyscognitive seizure

A

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

152
Q

Description of generalised seizures

A

Abnormal neuronal activity rapidly engages both hemispheres of the cerebral cortex.

153
Q

Types of generalised seizures

A
  • Absence
  • Atonic
  • Tonic
  • Myoclonic
  • Tonic clonic
154
Q

Description of an absence seizure

A

Brief loss of awareness and responsiveness with no post-ictal phase

155
Q

Description of an atonic seizure

A

Sudden loss of muscle tone that results in a sudden fall

156
Q

Description of a tonic seizure

A

Sudden increased muscle tone that most often occurs in clusters during sleep

157
Q

Description of a myoclonic seizure

A

A brief, sudden jerking action of a muscle or muscle group that may occur in a series leading into a tonic clonic seizure

158
Q

Description of a tonic clonic seizure

A

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.

159
Q

Definition of status epilepticus

A

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.

160
Q

Seizure triggers in epilepsy

A
  • 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
161
Q

Definition of psychogenic non-epileptic seizures (PNES, previously known as pseudoseizures)

A

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.

162
Q

Examples of provoked seizures

A
  • 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)
163
Q

Typical seizure presentations

A
  • 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
164
Q

Associated clinical features of prolonged seizures or status epilepticus

A
  • Hypoxia, hypercarbia
  • Progressive lactic and respiratory acidosis
  • Hyperthermia, HTN, tachycardia
  • Hypo/hyperglycaemia
  • Hyperkalaemia
165
Q

Rx considerations for seizure

A
  • Reversible causes
  • Midazolam
  • Oxygen
166
Q

Definition of transient ischaemic attack (TIA)

A

A TIA is a brief episode of neurological dysfunction (typically < 24 hours) resulting from focal temporary cerebral ischaemia.

167
Q

Clinical features of TIA

A
  • Hemiparesis/hemiplegia
  • Dysphasia/aphasia
  • Dysphagia
  • Visual disturbances
  • Sudden onset headache associated with neurological symptoms/ALOC
168
Q

Conditions that may mimic TIA/stroke

A
  • Hypoglycaemia
  • Cerebral lesions
  • Seizures/post-ictal states
  • Hemiplegic migraine
  • Electrolyte abnormalities
  • Conversion disorder
169
Q

Rx considerations for TIA

A
  • Oxygen
  • Antiemetic
  • Analgesia
  • IV fluids
  • Acute stroke referral
170
Q

Definition of breech birth

A

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.

171
Q

Description of frank breech

A

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.

172
Q

Description of complete breech

A

The foetus’s hips and knees are flexed so the foetus is sitting cross-legged with feet beside the buttocks.

173
Q

Description of footling breech

A

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.

174
Q

Description of kneeling breech

A

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.

175
Q

Management process for breech birth

A
  • 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
176
Q

Description of cord prolapse

A

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.

177
Q

Clinical features of cord prolapse

A
  • 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
178
Q

Risk factors for cord prolapse

A
  • 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
179
Q

Management for cord prolapse if pulsative cord is evident at vaginal opening/loop is hanging down

A
  • Assist the mother into exaggerated Sims position

- Ask mother to gently push cord back using a dry pad

180
Q

Management for cord prolapse if pulsative cord is not evident at vaginal opening/loop is not hanging down

A
  • Assist mother to assume knees-to-chest position
  • Carefully attempt to push the presenting part off the cord
  • Tx in exaggerated Sims position
181
Q

Definition of an ectopic pregnancy

A

Pregnancy in which the developing embryo implants outside the uterine cavity.

182
Q

Clinical features of unruptured ectopic pregnancy

A
  • Hx of amenorrhoea (at least one missed period)
  • Abnormal vaginal bleeding
  • Pelvic and/or abdominal pain
  • Nausea
  • Presyncopal symptoms
183
Q

Clinical features of ruptured ectopic pregnancy

A
  • 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
184
Q

Rx for pts with suspected ectopic pregnancy

A
  • Analgesia
  • Antiemetic
  • IV fluids
185
Q

Definition of miscarriage

A

Miscarriage is the spontaneous loss of pregnancy before 20 weeks gestation, the aetiology of most cases unknown.

186
Q

Clinical presentation of miscarriage

A
  • Lower abdominal discomfort
  • Vaginal bleeding
  • Hypotension
  • Tachycardia
  • Postural symptoms
187
Q

Clinical features suggesting intrauterine infection

A
  • Severe pelvic pain and/or rigidity and/or guarding
  • Purulent discharge
  • Fever
188
Q

Management of miscarriage if a foetus is delivered (often placenta remains attached)

A
  • 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
189
Q

Signs of imminent birth

A
  • 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
190
Q

Management of physiological cephalic birth

A
  • 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)
191
Q

Definition of placental abruption

A

Placental abruption occurs when a normally situated placenta partially or completely separates from the uterine wall, causing haemorrhage prior to foetal delivery.

192
Q

Maternal complications associated with placental abruption

A
  • Disseminated intravasular coagulopathy (DIC)
  • Shock
  • Uterine rupture
  • Acute renal failure
193
Q

Clinical features of placental abruption

A
  • 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
194
Q

Three categories of placental abruption

A
  • 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
195
Q

Rx considerations for placetal abruption

A
  • IV access
  • IV fluid
  • Analgesia
  • Antiemetics
196
Q

Definition of placenta praevia

A

Placenta praevia occurs when the placenta is situated either partially or wholly in the lower uterine segment.

197
Q

Reason placenta praevia becomes an issue in the third trimester.

A

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.

198
Q

When placenta praevia becomes an obstetric emergency

A

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.

199
Q

Focus of pre-hospital management of placenta praevia

A

Preventing maternal hypotension

200
Q

Clinical features of placenta praevia

A
  • Several small warning bleeds
  • Bright red blood
  • No pain (other than those

QAS (2 decks)

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