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MODULE 14 - Patient Support > TOXICOLOGY - Clinical Approach to Poisoning > Flashcards

TOXICOLOGY - Clinical Approach to Poisoning Flashcards

1
Q

How do you manage a poisoning case?

A
  1. Stabilise the clinical signs
  2. Take a detailed history
  3. Prevent continual absorption of the toxin (decontamination)
  4. Give an antidote if available
  5. Removal of the toxin
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2
Q

Which six paramaters should be included when establishing a database for investigating poison cases?

A

PCV/TS
Urea/creatinine (to investigate renal function)
ALT (to investigate hepatic function)
Glucose
Electrolytes
Urinalysis

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3
Q

Which five decontamination techniques can you use to prevent further absorption of a toxin into the gastrointestinal tract?

A

Induce emesis
Gastric lavage
Absorbants
Enemas
Surgical removal

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4
Q

List six contraindications to inducing emesis

A

Patients with neurological dysfunction
Corrosive ingestion
Patients predisposed to aspiration
If toxin was ingested over 4 hours ago (emesis won’t be helpful at this point)
If patients have already vomited the toxin
Ingestion of button batteries

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5
Q

Why is inducing emesis contraindicated in patients with neurological dysfunction?

A

Patients with neurological dysfunction are at an increased risk of aspirating the vomit

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6
Q

What can you use as a decontamination technique instead of emesis in patients with neurological dysfunction?

A

Gastric lavage

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7
Q

Why is inducing emesis contraindicated in patients that have ingested button batteries?

A

If you induce emesis and the batteries get stuck in the oesophagus, they can establish an electrical current and cause oesophageal necrosis

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8
Q

Give two examples of toxins that prevent emesis

A

Cannibus
Codeine

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9
Q

Which emetic drug is most commonly used in dogs?

A

Apomorphine

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10
Q

What classification of drug is apomorphine?

A

Opioid

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11
Q

What is the mechanism of action of apomorphine?

A

Apomorphine acts on the dopamine receptors in the chemoreceptor trigger zone to trigger emesis

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12
Q

How should apomorphine be administered?

A

Subcutaneously

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13
Q

How can the sedative effects of apomorphine be reversed?

A

You can reverse the sedative effect of apomorphine with naloxone

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14
Q

Which emetic drug is most commonly used in cats?

A

Dexmedetomidine

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15
Q

What classification of drug is dexmedetomidine?

A

α2-adrenoreceptor agonist

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16
Q

What method is recommended to improve the effectiveness of dexmedetomidine?

A

Administer the dexmedetomidine followed by slowly spinning the cat on a chair

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17
Q

How can the sedative effects of dexmedetomidine be reversed?

A

The effects of dexmedetomidine can be reversed with atipamezole

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18
Q

How do you carry out a gastric lavage?

A
  1. Place your patient under general anaesthetic (making sure to intubate with a cuffed endotracheal tube to reduce the risk of aspiration)
  2. Advance a stomach tube and infuse with 5 - 10ml/kg of warm water
  3. Repeat until the water runs out clear
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19
Q

List three contraindications to carrying out a gastric lavage

A

Corrosive ingestion
Patient is a high anaesthetic risk
If toxin was ingested over 4 hours ago (gastric lavage won’t be helpful at this point)

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20
Q

Which three methods can you use to administer activated charcoal?

A

In small volumes of food
Syringe
Stomach tube

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21
Q

How often should you administer activated charcoal if your patient has ingested a toxin that undergoes enterohepatic recycling?

A

Administer activated charcoal every 4 hours for 24 - 48 hours

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22
Q

Give three examples of toxins which undergo enterohepatic recycling and thus require repeated doses of activated charcoal?

A

Paracetamol
Theobromine
Ibuprofen

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23
Q

Why should you leave two hours between giving activated charcoal and oral medication?

A

The activated charcoal with absorb the oral medication

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24
Q

What should you warn the owners of after administering activted charcoal?

A

Warn the owners activated charcoal will stain the faeces black

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25
Q

You can get formulations of activated charcoal with cathartics. What is the function of cathartics?

A

Cathartics speed up gut movement by pulling water into the gut - diluting the toxin as well as increasing gut motility

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26
Q

Which two common toxins are not absorbed by activated charcoal?

A

Xylitol
Ethylene glycol

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27
Q

Which two decontamination techniques can you use to prevent further topical absorption of a toxin?

A

Washing
Ocular irrigation

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28
Q

What can you use to prevent the animal from grooming themselves when you’re carrying out topical decontamination?

A

Buster collar
Shaving the fur

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29
Q

Why is it important to never wash an animal in an active seizure?

A

Animals in an active seizure are at risk of aspirating the water

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30
Q

How long should you carry out ocular irrigation to decontaminate the eye?

A

Irrigate the eye for at least 15 minutes with water or saline

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31
Q

What can you use to check the eye for corneal ulcers?

A

Fluoroscein

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32
Q

Which two methods can be used to help remove a toxin from the body?

A

Intravenous fluids
Intravenous lipid emulsion

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33
Q

How can intravenous fluids be used to help remove toxins from the body?

A

Intravenous fluids can be administered to increase renal elimination of toxins (e.g. theobromine)

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34
Q

How can intravenous fluids also be used as supportive care in poisoning cases?

A

Intravenous fluids can be used to support the kidneys, rehydrate patients exhibiting vomiting and diarrhoea and stabilise blood pressure in hypotensive patients

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35
Q

How can intravenous lipid emulsions be used to help remove toxins from the body?

A

Intravenous lipid emulsions can be used to eliminate lipophilic toxins and toxins with a short half life

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36
Q

Give three examples of toxins that can be removed from the body with intravenous lipid emulsions

A

Permethrin
Cannibis
Ibuprofen

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37
Q

What is important to note when using intravenous lipid emulsions?

A

Intravenous lipid emulsions are off-liscence drugs and thus should only be used for severe toxicosis when recognised treatments have been unsuccessful

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38
Q

What are three of the possible adverse effects of intravenous lipid emulsions?

A

Pancreatitis
Fluid overload as they act as colloid solutions
Coagulopathies

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39
Q

Why are cats so susceptibe to paracetomal toxicity?

A

Cats lack the enzyme glucoronyl transferase which makes them particularly susceptible to paracetamol toxicity as this enzyme usually metabolises the toxic by-product of paracetomal metabolism - N-acetyl-p-benzoquinone which causes hepatocellular necrosis, oxidative damage to red blood cells resulting in methaemaglobinaemia and heinz body anaemia

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40
Q

Which organ metabolises paracetamol?

A

Liver metabolises paracetamol

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41
Q

What are the seven clinical signs of paracetamol toxicity in the first 24 hours of ingestion?

A

Anaemia
Cyanosis or muddy brown mucous membranes
Tachycardia
Tachypneoa
Lethargy
Facial and paw oedema
Vomiting

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42
Q

What are the four clinical signs of paracetamol toxicity 24 hours after ingestion?

A

Signs of liver failure
Icterus
Seizures
Haematuria/haemoglobinuria

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43
Q

What is a rare clinical sign of paracetamol toxicity?

A

Kerratoconjunctivitis sicca

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44
Q

At what dose of paracetamol ingestion should you begin treatment for paracetamol toxicity in cats?

A

If the cat has ingested more than 10mg/kg of paracetamol you should begin treatment for paracetamol toxicity in cats

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45
Q

At what dose of paracetamol ingestion should you begin treatment for paracetamol toxicity in dogs?

A

If the dog has ingested more than 50 - 100mg/kg of paracetamol you should begin treatment for paracetamol toxicity in dogs

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46
Q

Which decontamination techniques can you use for paracetamol toxcicity?

A

Emesis
Activated charcoal (remember to repeat doses due to enterohepatic recycling)

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47
Q

Within how many hours after paracetamol ingestion would it still be effective to induce emesis?

A

Within 2 hours following paracetamol ingestion

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48
Q

What supportive care should you provide patients with paracetamol toxicity?

A

Goal directed fluid therapy
Oxygen supplementation
Whole blood or packed pRBC transfusion

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49
Q

What can you use to reverse methaemaglobinaemia due to paracetamol toxicity?

A

Ascorbic acid

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50
Q

What can be used as a liver protectant in animals with paracetomal toxicity?

A

S-adenosylmethionine (S-AME)

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51
Q

What is the antidote for paracetamol toxicity?

A

N-acetylcysteine

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52
Q

What is the toxic component found in slug bait?

A

Metaldehyde

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53
Q

(T/F) Metaldehyde poisoning has a slow onset

A

FALSE. Metaldehyde poisoning has a rapid onset of between 30 minutes and 3 hours

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54
Q

What are the four main clinical signs of metaldehyde poisoning?

A

Tremors
Seizures
Hyperthermia
Hyperaesthesia

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55
Q

What is hyperaesthesia?

A

Hyperaesthesia is excessive physical sensation

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56
Q

How can metaldehyde poisoning progress and cause death?

A

Metaldehyde poisoning can progress to severe seizures, respiratory arrest and disseminated intravascular coagulation (DIC) - which can all result in death

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57
Q

Which decontamination techniques can you use for metaldehyde poisoning?

A

Emesis if they have not started with tremors or seizures
Activated charcoal
Gastric lavage

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58
Q

What supportive care should you provide patients with metaldehyde poisoning?

A

Intravenous fluid therapy
Antiepileptic drugs to control the seizures
Muscle relaxant to help alleviate tremors and muscle rigidity

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59
Q

Which muscle relaxant drug can you give to patients with metaldehyde poisoning?

A

Methocarbamol

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60
Q

How can you administer methocarbamol if you are unable to administer them orally (i.e. if they are in active seizures) in patients with metaldehyde poisoning?

A

You can crush methocarbamol tablets and give them via an enema

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61
Q

What is the mechanism of action for anticoagulant rodenticides?

A

Anticoagulant rodenticides are slowly absorbed by the gastrointestinal tract and mechanically inhibit an enzyme which is crucial for the production of vitamin K1, a necessary component for clotting factors II, VII, IX and X. When the production of these clotting factors in the liver is inhibited, prothrombin cannot be adequately converted to thrombin, and coagulopathy results

62
Q

How long after ingestion does it usually take to see clinical signs of anticoagulant rodenticide poisoning?

A

1 to 5 days

63
Q

What are the six main clinical signs of anticoagulant rodenticide poisoning?

A

Epistaxis
Body cavity haemorrhage (haemothorax, haemoabdomen)
Gastrointestinal bleeding (meleana, haematemesis)
Haemoarthrosis
Haematomas
Anaemia

Signs of a coagulopathy

64
Q

Which diagnostic tools can you use to help identify anticoagulant rodenticide poisoning?

A

Coagulation profile
Platelet count
Haematology

65
Q

Which specific coagulation parameters should you look for when investigating anticoagulant rodenticide poisoning?

A

Prothrombin time (PT)
Activated partial prothrombin time (aPTT)

66
Q

When will a patient typically present with a prolonged prothrombin time (Pt) after ingesting anticoagulant rodenticides?

A

A prolonged prothrombin (PT) time typically occurs within the first 36 hours of ingestion

67
Q

When will a patient typically present with a prolonged activated partial thromboplastin time (aPTT) after ingesting anticoagulant rodenticides?

A

A prolonged activated patial prothrombin time (aPTT) typically occurs within the first 72 hours of ingestion

68
Q

How will the platelet count be affected by anticoagulant rodenticide poisoning?

A

The platelet will be normal or decreased due to increased platelet consumption

69
Q

Which decontamination techniques can you use for anticoagulant rodenticide poisoning?

A

Emesis
Activated charcoal

Will only be effective within 4 hours of ingestion

70
Q

What do you use to treat anticoagulant rodenticide poisoning?

A

Vitamin K1

71
Q

How long should you treat patients with vitamin K1 for anticoagulant rodenticide poisoning?

A

Up to six weeks

72
Q

Why is the treatment regime for anticoagulant rodenticide poisoning so lengthy?

A

Anticoagulant rodenticides have a very long plasma half-life and thus remain in the circulation for a long time

73
Q

How do you administer vitamin K1?

A

Administer the first dose of vitamin K1 subcutaneously and then the rest can be given as an oral tablet

74
Q

What can you advise owners to do to increase the bioavailability of oral vitamin K1 tablets?

A

Give oral vitamin K1 tablets with a fatty meal to increase their bioavailability

75
Q

Why is it important NOT to blanket treat all patients with vitamin K1 for anticoagulant rodenticide poisoning?

A

Not all cases require vitamin K1 treatment and since the treatment regimen with vitamin K1 can be lengthy, it is important to determine if it is necessary to avoid any unnecessary inconvenience for the owner

76
Q

How do you determine if a patient suspected of ingesting antigoagulant rodenticides requires vitamin K1 treatment?

A
  1. If they are clinically affected begin immediate treatment
  2. If they are not clinically affacted , determine if the patient ingested a toxic dose, if yes then begin treatment
  3. If they are not clinically affected and haven’t ingested a toxic dose, test their prothrombin time (Pt) 48 and 72 hours after ingestion. If their prothrombin time (Pt) is prolonged, begin treatment
77
Q

When should vitamin K1 administration begin to work?

A

Coagulation factors are produced within 6–12 hours of implementing treatment, prothrombin time (Pt) and activated partial prothrombin time (aPPT) improve within 12–24 hours

78
Q

What supportive care can you provide patients with symptomatic anticoagulant rodenticide poisoning?

A

Oxygen supplementation
Blood transfusion
Plasma transfusion

79
Q

What are the clinical signs of ethylene glycol poisoning within the first 12 hours of ingestion?

A

Neurological signs
Gastrointestinal signs
Metabolic acidosis

80
Q

What are the clinical signs of ethylene glycol poisoning 12 to 24 hours after ingestion?

A

Tachycardia
Tachypneoa
Pulmonary oedema
Shock
Metabolic acidosis

i.e. cardiorespiratory signs

81
Q

What are the six clinical signs of ethylene glycol poisoning 24 to 72 hours after ingestion?

A

Swollen and painful kidneys on palpation
Azotaemia
Anuria/oligouria
Uraemia
Hyperkalaemia
Metabolic acidosis

i.e. renal signs

82
Q

What are the four main clinical signs of uraemia?

A

Vomiting
Uraemic ulcers
Uraemic breath
Anorexia

83
Q

What treatment option should you consider if you see a cat exhibiting renal signs following ethylene glycol ingestion?

A

Euthanasia

84
Q

Which diagnostic tools can you use to diagnose ethylene glycol poisoning?

A

Haematology
Biochemistry
Urinalysis
Ultrasound

85
Q

What are the six characteristic changes in a blood sample that can indicate ethylene glycol poisoning?

A

Metabolic acidosis
Azotaemia
Hyperkalaemia
Hypocalcaemia
Hyperglycaemia
Hyperphosphataemia

86
Q

What are the six characteristic changes in urinalysis that can indicate ethylene glycol poisoning?

A

Calcium oxalate crystals in the urine
Urine casts
Low urine specific gravity (USG)
Glycosuria
Proteinuria
Urine pH of less than 6.5

87
Q

What is the medullary rim sign?

A

The medullary rim sign is a distinct hyperechoic zone in the outer renal medulla seen on ultrasound indicative of ethylene glycol poisoning

88
Q

What supportive care can you provide patients with ethylene glycol poisoning?

A

Intravenous fluid therapy
Correct the metabolic acidosis
Antiepileptic drugs
Oxygen supplementation

89
Q

What is the antidote for ethylene glycol poisoning?

A

20% ethanol

90
Q

Which two methods can you use to administer 20% ethanol?

A

Intravenous (IV)
Stomach tube

91
Q

What is the toxic component of chocolate?

A

Theobromine

92
Q

What dose of theobromine causes low dose theobromine toxicity?

A

20mg/kg theobromine

93
Q

What are the five clinical signs of low dose theobromine toxicity?

A

Vomiting
Diarrhoea
Hyperactivity
Panting
Shaking

94
Q

What dose of theobromine causes moderate dose theobromine toxicity?

A

40mg/kg theobromine

95
Q

What is the main clinical sign of moderate dose theobromine toxicity?

A

Signs of cardiotoxicity such as arrthythmias

96
Q

What dose of theobromine causes high dose theobromine toxicity?

A

60mg/kg theobromine

97
Q

What is the main clinical sign of high dose theobromine toxicity?

A

Seizures

98
Q

At what dose of milk chocolate should you treat for theobromine toxicity?

A

Over 14g/kg of milk chocolate

99
Q

At what dose of dark chocolate should you treat for theobromine toxicity?

A

Over 3.5g/kg of dark chocolate

100
Q

What calculation can you use to determine the accurate theobromine content in dark chocolate?

A

Theobromine content (mg/kg) = % Cocoa x 0.16

101
Q

Which decontamination techniques can you use for theobromine toxicity?

A

Emesis
Activated charcoal (remember to repeat doses due to enterohepatic recycling)
Gastric lavage (for patients presenting with neurological dysfunction)

102
Q

What supportive care should be provided for theobromine toxicity?

A
  • Goal directed fluid therapy promotes diuresis to excrete the theobromine, rehydrates the patient following the vomiting and diarrhoea and can stabilise blood pressure
  • Provide constant ECG and seizure monitoring and treat any arrhythmias if they are clinically relevant
  • Anti-emetics
  • Anti-epileptics if seizuring
  • Urinary catheterisation
103
Q

Which two arrhythmias can be seen with theobromine toxicity?

A

Supraventricular arrhythmias
Ventricular tachycardia

104
Q

What can you use to treat supraventricular arrhythmias?

A

β-blocker

105
Q

What can you use to treat ventricular tachycardia?

A

Lidocaine

106
Q

Give an example of an anti-emetic you can provide animals with theobromine toxicity

A

Maropitant

107
Q

Why may you consider placing a urinary catheter in a patient with theobromine toxicity?

A

Theobromine is renally excreted and thus will sit in the urine in the bladder where is can be absorbed into the bladder wall and re-enter the circulation

108
Q

What is the mechanism of action of xylitol?

A

Xylitol stimulates insulin release which moves glucose from the circulation into the cells, resulting in hypoglycaemia. When glucose moved into the cells, potassium and phosphate move with it resulting in hypokalaemia and hypophosphataemia

109
Q

At what dose of xylitol ingestion will animals develop hypoglycaemia?

A

Over 100mg/kg of xylitol

110
Q

How long after xylitol ingestion will an animal develop hypoglycaemia?

A

Animals will develop hypoglycaemia 30 minutes after xylitol ingestion

111
Q

At what dose can xylitol ingestion cause hepatic necrosis?

A

Over 500mg/kg of xylitol can cause hepatic necrosis which also results in coagulopathies

Remember the liver produces the coagulation factors

112
Q

Which three parameters should you monitor in animals with xylitol poisoning?

A

Blood glucose levels
Liver parameters
Clotting time

113
Q

What supportive care can you provide patients with xylitol poisoning?

A

IV dextrose with isotonic crystalloids
Whole blood or plasma transfusion
Vitamin K1

114
Q

What can be used as a liver protectant in animals with xylitol toxicity?

A

S-adenosylmethionine (S-AME)

115
Q

(T/F) Raisins/grapes are toxic to all dogs

A

FALSE. Raisins/grapes have an idiosyncratic reaction with only 10% of dogs experiencing raisin/grape toxicity

116
Q

What is the toxic component of raisins/grapes?

A

Tartaric acid

117
Q

What are the clinical signs of raisin/grape toxicity?

A

Vomiting
Diarrhoea
Abdominal pain
Acute renal failure

118
Q

(T/F) It is recommended to only treat a dog for raisin/grape toxicity if they have ingested more than one raisin/grape

A

TRUE. There have been no reported cases of dogs experiencing clinical signs after eating only one raisin/grape

119
Q

Which decontamination techniques can you use for raisin/grape toxicity?

A

Emesis
Activated charcoal

120
Q

Which blood parameters should you monitor in a patient that has ingested raisins/grapes?

A

Blood urea and creatinine levels

121
Q

Which urine parameters should you monitor in a patient that has ingested raisins/grapes?

A

Proteinuria
Glycosuria
Microscopic haematuria

122
Q

What supportive care can you provide patients with raisin/grape toxicity?

A

Intravenous fluid therapy

123
Q

What is the mechanism of action for lily toxicity?

A

The toxic principles of lily toxicity are unknown, however the renal failure caused by lily toxicity is due to necrosis of the renal tubular epithelial cells. However, the basement membrane remains intact which means that prompt treatment can result in regeneration of tubular epithelial cells

124
Q

Which lillies are nephrotoxic to cats?

A

True lillies
Day lillies

125
Q

Which components of the lily plants are toxic to cats?

A

All components of the lily plant are toxic

126
Q

What are the five main clinical signs of lily toxicity within the first 6 hours of ingestion?

A

Hypersalivation
Vomiting
Anorexia
Lethargy
Depression

Initial signs of lily ingestion are due to gastrointestinal irritation

127
Q

When should vomiting associated with lily toxicity resolve?

A

Vomiting associated with lily toxicity should resolve within 12 hours of ingestion

128
Q

What are the four main clinical signs of lily toxicity within the first 12 - 30 hours of ingestion?

A

Polyuria
Dehydration
Uraemia
Enlarged, painful kidneys on palpation

129
Q

What are the four main clinical signs of uraemia?

A

Vomiting
Uraemic ulcers
Uraemic breath
Anorexia

130
Q

Which decontamination techniques can you use for lily toxicity?

A

Emesis
Activated charcoal
Bathe to remove pollen

131
Q

(T/F) Gastrointestinal decontamination is required for all animals that have ingested lilies

A

FALSE. Gastrointestinal decontamination is only required in cats

132
Q

What supportive care can you provide patients with lily toxicity?

A

Intravenous fluid therapy
Antiemetics if indicated
Gastroprotectants if indicated
Analgesia if develop acute renal injury

133
Q

Which two diagnostic tools can you use to diagnose lily toxicity?

A

Bloods
Urinalysis

134
Q

What is the key laboratory finding in the blood that can indicate lily toxicity?

A

Azotaemia

135
Q

What are the key urinalysis findings that can indicate lily toxicity?

A

Haematuria
Proteinuria
Glycosuria
Isosthenuria
Urine casts

136
Q

What is the prognosis for lily toxicity?

A

There is a good prognosis if there has been rapid decontamination and fluid diuresis. However the prognosis will be poor if the animal is presented 18 hours after ingestion or develops anuria

137
Q

What is the mechanism of action for ibuprofen toxicity?

A

Ibuprofen is an NSAID. NSAIDs inhibit the cyclooxygenase (COX) enzymes and the subsequent production of prostaglandins. This inhibiton accounts for the majority of the clinical signs seen as a result of ibuprofen toxicity

138
Q

Which species is more susceptible to ibuprofen toxicity?

A

Dogs

139
Q

What are seven of the clinical signs of gastrointestinal ulceration due to ibuprofen toxicity?

A

Vomiting
Haematemesis
Diarrhoea
Meleana
Abdominal pain
Anorexia
Pale mucous membranes

140
Q

How do you determine the dose of ibuprofen that has been ingested?

A

Dose of ibuprofen = (mg per tablet x number of tablets ingested) / Body weight (kg)

141
Q

At what dose of ibuprofen will you sees signs of gastrointestinal ulceration?

A

Over 10 - 25mg/kg of ibuprofen

142
Q

What are three of the clinical signs of acute renal failure due to ibuprofen toxicity?

A

Polyuria
Polydipsia
Oliguria

143
Q

At what dose of ibuprofen will you sees signs of acute kidney injury?

A

Over 100 - 150mg/kg of ibuprofen

144
Q

At what dose of ibuprofen will you sees signs of neurological dysfunction?

A

Over 400mg/kg of ibuprofen

145
Q

Which decontamination techniques can you use for ibuprofen toxicity?

A

Emesis
Activated charcoal (remember to repeat doses due to enterohepatic recycling)
Gastric lavage (for patients presenting with neurological signs)

146
Q

How to you manage and treat ibuprofen toxicity?

A

Administer gastroprotectants
Administer antiemetics if the patient is still vomiting and anorexic
Intravenous fluid therapy to support the kidneys and rehydrate the patient due to vomiting and diarrhoea

147
Q

Give three examples of gastroprotenctants you can administer to patients with ibuprofen toxicity

A

Omeprazole
Misoprostol
Surfactants

148
Q

What is the contraindication to administering misoprostol?

A

Misoprostol is an abortion drug so shouldn’t be administered to pregnant animals, of be handled by pregnant owners

149
Q

When should surfactants be administered?

A

Surfactants should only be administered if there is evidence of gastrointestinal ulcers or they will be ineffective

150
Q

Give an example of an antiemetic you can administer to patients with ibuprofen toxicity

A

Maropitant

151
Q

Which parameters should you monitor when treating ibuprofen toxicity?

A

Renal parameters
Liver parameters (however hepatic toxicity is rare follwoing ibuprofen ingestion)

152
Q

What is the prognosis for ibuprofen toxicity?

A
  • Prognosis is goood in animals that present soon after acute ingestion and have treatment started promptly
  • Late-presenting animals are at greater risk of toxic effects
  • Animals with a large acute overdose with rapid onset of neurological signs, gastrointestinal perforation or chronic exposure to ibuprofen have a more guarded prognosis

MODULE 14 - Patient Support (24 decks)

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