Emergency and Poisons Flashcards

1
Q

What is triage?

A

Identify which patients need the urgent care and which problems need to be prioritised.

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2
Q

What is telephone triage?

A

Used to determine does the patients need to be seen at the clinic and to provide first aid advice.

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3
Q

If a patient needs to be brought in based off telephone triage, what 3 things could be done next?

A

Triage assessment
Primary survey
Secondary survey

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4
Q

What is triage assessment?

A

Major body system assessment is a less than 1 minute history to determine the main complaint and what has the progression been, generally performed with the owner.

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5
Q

What aspects of the cardiovascular system assessed in triage assessment?

A

Evidence of hypoperfusion:

  • Mucus membrane colour
  • CRT
  • HR
  • Auscultation of the heart
  • Peripheral pulse strength and mismatch
  • Sgns of external bleeding
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6
Q

What aspects of the respiratory system are assessed in triage assessment?

A

Evidence of dyspnoea:

  • RR
  • Auscultating
  • Respiratory effort and pattern
  • Percussion of chest to see if hollow sounding and resident or dull sounding over the lungs
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7
Q

What aspects of the neurological system are assessed in triage assessment?

A

Evidence of raised intracranial pressure and/or seizures:
- Patient’s mentation
- Response to the environment
- Pupils for symmetry
- PLR

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8
Q

What aspects of the renal system are assessed in triage assessment?

A

Evidence of urethral obstruction or bladder rupture (not always included):

  • Bladder size, pain and integrity
  • Ability to urinate
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9
Q

What is indicated if you cannot feel the bladder?

A

Patient has recently urinated or the bladder has ruptured

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10
Q

What other parameter is assessed during triage assessment?

A

Pain

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11
Q

What is primary survey?

A

Expands upon the major body system assessment/triage findings, the institution of quick monitoring, the identification and treatment problems that are immediately life-threatening.

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12
Q

What is assessed in primary survery?

A
  • ECG
  • Pulse oximetry
  • Blood pressure measurement
  • End tidal carbon dioxide
  • Minimum or emergency database
  • Point Of Care Ultrasound (POCUS)
  • Blood gas analysis
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13
Q

What is the minimum database generally considered to be?

A
  • Packed Cell Volume (PCV) and Total Solids (TS)
  • Blood Urea Nitrogen (BUN)
  • Lactate
  • Electrolytes (sodium, chloride and potassium)
  • Blood smear examination
  • Glucose
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14
Q

What is the advantage of primary survery?

A

Quick
Cheap
Requires little blood
Aids decision making

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15
Q

Based on clinical findings in primary survey, how is cardiogenic shock managed?

A

Fluid boluses contra-indicated

Clinically significant arrhythmia = anti-arrhythmic agents

Poor systolic function = inotropes
Pericardial effusion = pericardiocentesis

Presence of hyperkalaemia causing bradycardia = correct blood potassium

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16
Q

How is a patient’s respiratory system stabilised in primary survey?

A

Oxygen
Minimise stress
Body positioning
Pleural effusions = thoracocentesis
Cardiogenic pulmonary oedema = frusemide
Bronchoconstriction = terbutaline

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17
Q

How is stress minimised in a respiratory unstable pateint?

A

May need to postpone IV access and limit handling (risk of decompensating them and causing death), may sedate patient to keep them calm

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18
Q

Why is body positioning important for respiratory stabilisation?

A

Do not force into lateral recumbency, which is why radiography of dyspnoeic patients is dangerous, ultrasound is better

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19
Q

How is a patient stabilised if evidence of raised intracranial pressure?

A
  • Keep head elevated about 15˚
  • Avoid pressure on jugular veins
  • Maintain normal blood pressure but care with fluids if no evidence of hypovolaemia
  • Consider mannitol (an osmotic diuretic)
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20
Q

How are seizsures managed in a respiratory insecure patient?

A

Antiepileptic therapy

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21
Q

How are patients renally stabilised?

A

Urinary tract obstruction – obtain urine output, place urinary catheter, decompressive cystocentesis

Hypovolaemic shock - stabilise the CVS system first – poor perfusion to the kidneys will mean they are not producing any more urine anyway

Hyperkalaemia – correct blood potassium levels

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22
Q

What is secondary survey?

A

A full clinical examination, the collection of a detailed clinical history, monitoring the patient’s response to therapy and the creation of a more comprehensive diagnostic and therapeutic plan.

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23
Q

What are the management factors of farm animal poisoning cases?

A
  • Pasture management – activity there recently?
  • Weed control
  • Hedging and drainage
  • Housing
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24
Q

What are the human factors (negligence) of farm animal poisonings?

A
  • Garden refuse disposal
  • Fly tipping (can be a red herring)
  • Ration formulation errors
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25
Q

What are the nutritional factors of farm animal poisoning?

A
  • Feed shortage
  • Conserved forages (goes undetected by animal)
  • Inappropriate feeding
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26
Q

What are the animal factors of farm animal poisonings?

A
  • Age
  • Boredom
  • Unfamiliar surrounding
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27
Q

What are 4 possible principles of poisoning treatment?

A
  • Reduce toxin absorption
  • Speed toxin elimination
  • Symptomatic treatment
  • Antagonists
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28
Q

How can toxin absorption be reduced?

A
  • Absorbents such as activated charcoal
  • Purgatives – laxatives, paraffin
  • Oral fluid therapy – wash things through system
  • Rumenotomy and rumen lavage – open up and wash out rumen
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29
Q

How can toxin elimination be sped up?

A

Forced diuresis – intravenous fluid therapy and diuretics

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30
Q

What is an example of an antagonist used for poisoning treatment?

A

Rarely available, such as calcium disodium EDTA for lead poisoning

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31
Q

What should you do if a farm patient is siezing or hyperaesthetic?

A

Sedate with xylazine

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32
Q

How is post mortem done on farm?

A
  1. Full external examination of the carcass
  2. Evidence of seizuring – churned up soil or bedding
  3. Check pharynx, oesophagus and rumen for presence of yew
  4. Check rumen for presence of poisonous plants or chemicals
  5. Identify the predominant body system
  6. Does the PME suggest a non-toxic cause
  7. Collect blood, liver and kidney samples
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33
Q

List 7 poisons that could cause sudden death in farm animals.

A

Yew
Lead
Copper
Hemlock
Water dropwort/dead man’s fingers
Laburnum
Cyanogenic glycosides

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34
Q

List 12 poisons that could cause neurological signs in farm animals.

A

Lead
Oxalate containing plants
Hemlock
Water dropwort
Rhododendron
Laburnum
Ergot
Organophosphates
Urea
Black night shade
Blue green algae

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35
Q

List the poisons that could cause gastrointestinal signs in farm animals.

A

Vomiting = rhododendron

Diarrhoea = oak young leaves, ragwort, hemlock, rhododendron

Frothy bloat = legumes, lush pasture

Constipation = acorns

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36
Q

Name a poison that causes respiratory signs in farm animals.

A

L-tryptophan/fog fever

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37
Q

List the poisons that cause cardiovascular signs in farm animals.

A

Anaemia = bracken, brassica, copper, warfarin/coumarin

Altered mucous membrane colour = nitrate poisoning

Arrhythmias = foxgloves

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38
Q

Name 2 poisons that cause dermatological signs in farm animals.

A

Photosensitisation
Molybdenum

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39
Q

List 4 poisons that cause urine disolouration in farm animals.

A

Bracken
Brassicas
Oak
Copper

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40
Q

List 3 poisons that cause abortion and stillbirths in farm animals.

A

Brassicas
Some clovers
Fungal alphatoxins

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41
Q

Describe the effects of yew on cattle.

A

A few mouthfuls of leaves will kill a cow in minutes. Present in the mouth and fore-stomachs

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42
Q

How may farm animals ingest ragwort?

A

May graze if grazing is sparse. Dead plant is also toxic and may be present in conserved forage

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43
Q

What is the aetiology of ragwort in farm animals?

A
  • Pyrrolizidine alkaloids - dose dependent severity
  • Hepatotoxic
  • Acute/high exposure leads to acute liver failure
  • Chronic exposure leads to slow progressive liver damage and chronic liver failure
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44
Q

What are the neurological clinical signs of ragwort in farm animals?

A

Bilateral central blindness
Head-pressing
Weakness
Terminal coma

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45
Q

What are the gastrointestinal clinical signs of ragwort in farm animals?

A

Severe indigestion
Occasionally diarrhoea but more often constipation
With/without tenesmus

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46
Q

What are the dermatological signs of ragwort in farm animals?

A

Photosensitisation
Jaundice

47
Q

How is ragwort poisoning in farm animals diagnosed?

A

Nutritional history
Clinical signs
Liver enzymes/biopsy
Post-mortem

48
Q

How is ragwort controlled on farms?

A

Control of plant difficult due to hand pulling and burning

49
Q

What are the sources of lead poisoning on farms?

A
  • Buildings
  • Waste from old car batteries and roofing felt
  • Geostatic from localised geographical areas with heavy deposits in ground
50
Q

What are the acute clinical signs of lead poisoning in farm animals?

A

With/without sudden death
Convulsions
Blindness
Head-pressing
Excitability
Bellowing with odd timbe due to laryngeal swelling
Collapse and death in a few days

51
Q

What are the chronic clinical signs of lead poisoning in farm animals?

A

Unthriftiness
Weight loss
Scour
Fertility issues

52
Q

How is lead poisoning in farm animals diagnosed?

A
  • Clinical signs
  • Stomach may contain flakes of lead upon PM
  • High levels of lead found in blood, kidney, liver or faeces
53
Q

How is lead poisoning in farm animals treated?

A

Symptomatic and mildly affected animals may respond to calcium EDTA

54
Q

What must be done when lead poisoning occurs on a farm?

A

APHA must be informed due to human health risk from affected meat and milk

55
Q

Why do acorns cause disease in farm animals?

A

Due to the tannins they contain

56
Q

What are the gastrointestinal clinical signs of acorn poisoning in farm animals?

A

Severe indigestion
Cessation of rumination
Inappetence
Marked constipation with blood tinged faeces
Tenesmus
Depression
Excessive thirst

57
Q

What are the renal clinical signs of acorn poisoning in farm animals?

A

Chronic renal failure common from tannin damage in animals recovered from the acute stages – marked proteinuria with renal azotaemia

58
Q

How is acorn poisoning treated in farm animals?

A

IV fluids/laxatives

59
Q

What is fog fever and its aetiology?

A
  • L-tryptothan is converted to toTri-methyl indole in the rumen
  • Cytotoxic to lung tissue
  • Atypical interstitial pneumonia with pulmonary oedema
60
Q

What are the clinical signs of fog fever?

A

Dyspnoea/mouth breathing
Pale mucous membranes
Crackles on auscultation
Non-pyrexic

61
Q

How is fog fever treated?

A

Diuretics
Anti-inflammatories
Antibiotics to control secondary infection
Remove cattle from pasture

62
Q

What is photosensitisation?

A

Circulating chemicals absorb harmful rays from sunlight and damage skin and other tissues

63
Q

What are the primary causes of photosensitisation?

A

Direct action if ingested toxin

64
Q

What are the secondary causes of photosensitisation?

A

A damaged liver failing to break down toxic metabolites of chlorophyll

65
Q

What can photosensitisation cause in certain breeds?

A

Congenital porphyria

66
Q

What are the clinical signs of photosensitisation?

A

Pruritis
Cutaneous oedema
Blistering
Ulceration (white areas of skin)

67
Q

What should be done to manage photosensitisation?

A

Moved indoors immediately
Treat with NSAIDs
Prevent secondary infections

68
Q

What are the properties of bracken poisoning in farm animals?

A
  • Cattle are more sensitive than sheep
  • Effects usually cumulative over several weeks then clinical signs develop
69
Q

What does bracken poisoning in farm animals cause?

A

Haemorrhagic syndrome
Cancer of the oesophagus, stomach or bladder
Some act in conjunction with viruses that cause warts

70
Q

What are the clinical signs of haemorrhagic syndrome caused by bracken poisoning in farm animals?

A

Associated with bone marrow suppression:

  • Pass blood in faeces or milk
  • Petechial haemorrhages
  • Depression
  • Weakness
  • High fever
  • Profuse haemorrhage when wounded/injected
  • Often develop secondary infections
  • Can die in 1-5 days
71
Q

What are the clinical signs of the laryngitic form of bracken poisoning in calves?

A

Dullness
Dyspnoea with roaring respiration due to oedema of pharynx and larynx
External bleeding
Petechiation

72
Q

What are the clinical signs of upper alimentary tract neoplasia caused by bracken poisoning in farm animals?

A

Chronic bloat
Indigestion
Weight loss
Halitosis
Dropped cuds
Regurgitation

73
Q

How is bracken poisoning in farm animals symptomatically treated?

A
  • Remove from the source
  • Blood transfusions
  • Antibiotics for secondary infections
  • Clotting agents can be tried
  • Treat all animals with petechial haemorrhages/fever as if they are acute cases to prevent deterioration
74
Q

How is bracken poisoning in farm animals controlled and prevented?

A

Remove all other animals from pasture

Provide adequate access to supplementary forages in areas of marginal grazing

75
Q

What is the difference between small and large animal emergencies

A

There are safety risk with large animal emergencies to also consider.

76
Q

What are some examples of common equine emergencies?

A

Colic
Dystocia
Wound/trauma
Haemorrhage
Respiratory distress
Non-weight bearing lameness
Acute diarrhoea
Choke – oesophageal obstruction
Recumbent
Eyes – painful, traumatic injuries
Laminitis

77
Q

What is included in an equine colic kit?

A
  • Sedation
  • Injectable NSAIDs
  • Buscopan/buscopan compositum
  • Consumables – needles, syringes
  • Nasogastric tube
  • Rectal gloves/lubricant
  • Clippers
  • Somulose or pentobarbital – euthanasia drugs as your don’t know what you’ll get with emergencies
  • Ultrasound
  • Stethoscope
  • Thermometer
  • IV catheter
  • Fluids
78
Q

What is involved in an equine primary survey?

A
  • Clinical exam
  • Rectal exam
  • Nasogastric intubation
  • Medication – NSAIDs, sedation if required for examination or safety, buscopan/buscopan compositum
  • Bloods – lactate
79
Q

What is involved in an equine secondary survey

A
  • Response to treatment?
  • Referral required
  • Further diagnostics?
  • Any samples you need to run – results
80
Q

What is involved in a wound telephone triage primary survey?

A
  • Clinical examination – general of the horse
  • Specific examination of the wound
  • Lameness at walk or trot
  • Establish if any haemorrhage, location if synovial involvement, best treatment options if heal by first or second intention
81
Q

What is involved in a wound telephone triage secondary survey?

A
  • Further diagnostic tests necessary – inject with sterile saline, synoviocentesis, ultrasound, x-ray
  • Referral – may be before or after further diagnostics
  • Treatment is dependent on wound – suture, bandage, antimicrobials, analgesia, tetanus
82
Q

What is a true farm animal emergency?

A
  • Urgent – rapid deterioration/fatality without immediate intervention
  • Severe – potentially fatal/significant welfare implications
  • Client perception
83
Q

What are some specific examples of farm emergencies?

A
  • Haemorrhage
  • Hypomagnesaemia
  • Rumen tympany (bloat)
  • Airway obstruction
  • Toxin ingestion
84
Q

What are some examples of farm patient urgent visits?

A
  • Calving/prolapse
  • Toxaemia – down cow
  • Hypocalcaemia – down cow
  • Toxin ingestion
85
Q

How is rapid assessment for farm animal patients done?

A
  • Distant observation, such as is she in lateral recumbency
  • First aid, such as is there haemorrhage to be stopped, airway to be cleared, bloat to be corrected
  • Then TPR
86
Q

How is primary survey done in farm animal patients?

A
  • Blood sample for biochemistry and haematology
  • Cow side tests, such as for ketones may direct supportive treatment
  • Milk sample?
87
Q

What supportive therapies can be used for farm animal patients?

A

Fluids IV
Anti-endotoxic (flunixin)
Nursing care

88
Q

What are the clinical signs of endotoxaemia in farm animal patients?

A

Cold extremities
Congested mmbs
Sunken eyes
Tachycardia
Weakness/collapse

89
Q

When is emergency slaughter used in farm animal emergencies?

A

Only for acute presentations

90
Q

Where else could serious haemorrhage occur?

A

Respiratory and reproductive tracts

Uterine, middle uterine artery, torn milk vein

91
Q

How should you manage a uterine artery haemorrhage?

A

Apply pressure: leave clamps in place, pack towels, oxytocin

92
Q

What is the average duration of 2nd stage labour in the cow?

A

30-60 mins

93
Q

What marks the transition from 1st to 2nd stage labour?

A

Rupture of the water bag and abdominal contractions begin

94
Q

When should you intervene in 2nd stage labour for farm animal patients?

A
  • Straining vigorously for 30 minutes without the appearance of a calf
  • Failure of the calf to be delivered within 2 hours of the amnion appearing at the vulva
  • Obvious malpresentation, malposture or malposition
  • Detached chorioallantois, foetal meconium or blood stained amniotic fluid
95
Q

What are the infectious causes of sudden death in cattle?

A

Anthrax
Clostridial disease (blackleg/malignant oedema, black disease, bacillary haemoglobinuria, tetanus, botulism)
Pasturellosis
Salmonellosis
Septicaemia

96
Q

What are the metabolic causes of sudden death in cattle?

A

Hypomagnesaemia
Hypocalcaemia

97
Q

What are the neurological causes of sudden death in cattle?

A

Meningitis
CCN in calves

98
Q

What are the shock related causes of sudden death of cattle?

A

Hypovolaemia (internal haemorrhage, external haemorrhage)
Endotoxic
Mixed

99
Q

What are the intoxication causes of sudden death in cattle?

A

Plant - yew, laburnum, water dropwort, fog fever
Chemical - lead, copper, organophosphate

100
Q

For cases of sudden death, who decides if an anthrax test is needed?

101
Q

What does ergot fungus cause in cattle poisoning?

A

Vascular damage

102
Q

Where is the fungus ergot found?

A

Hay/haylage and on grain so store/grain-fed animals are most at risk. Less risk on pasture.

103
Q

What treatment is indicated for ergot poisoning in farm animals?

A

Euthanasia

104
Q

What treatment is indicated for St John’s wort poisoning?

A

Clean and debride raw areas, protect against infection and fly strike, NSAIDs

105
Q

What could be the source of excess copper for cattle?

A

Inappropriate feed – dairy cow concentrated are usually supplemented. Unnecessary supplementation

105
Q

What signs might you expect to see with copper poisoning in cattle?

A

Malaise
Dark scour
Enlarged liver
Haemaolysis
Anaemia
Haemoglobinuria
Jaundice
Black kidneys
Rapid death

106
Q

You diagnose lead toxicity as the cause of scour and ill thrift in some suckler cows. The farmer has some fattened animals fit for slaughter, and asks you if it’s ok to send these on?

A

No not fit for human consumption

107
Q

If there is toxic acute onset azotaemia, what substance exposure should you enquire about?

A

Paracetamol
NSAIDs
Anti-freeze
Vitamin D analogues leading to renal calcification
Lilies
In dogs, grapes

108
Q

What is the mechanism of toxicity of lilies in cats?

A
  • Renal tubular epithelial necrosis – mechanism unknown
  • Lethargy, anorexia and vomiting in 2-6h
  • Acute kidney injury azotaemia 2-3 days
109
Q

What is the optimal management of lily poisoning in cats?

A
  • Dermal decontamination
  • Induce emesis depending on time frame
  • Activated charcoal
  • Check bloods at onset and 2-4 days post injury – the significance of baseline creatinine
  • Monitor acute kidney injury
110
Q

How does ethylene glycol present?

A

Ethylene glycol (anti-freeze) – calcium oxalate monohydrate crystals in urinalysis

111
Q

How many grapes/raisins doe s a 20kg dog have to eat to result in kidney injury?

A

Could be any amount – dose is not well-defined

112
Q

What drug can be used as an antidote in cases of NSAID overdose?

A

Misoprostol – a PGE2 analogue which are removed by COX enzymes, which reduces renal perfusion among other things.