Blackwell's Five-Minute Veterinary Consult Clinical Companion: Small Animal Emergency and Critical Care, Second Edition provides essential information about treating medical emergencies using a quick-reference format ideal for the fast-paced emergency setting.
Offers fast access to important information during a small animal emergency
Presents topics alphabetically with identically formatted topics for ease of use
Adds information on 25 new diseases and updates throughout, plus updated references and more information on drugs available outside the US
Features color photographs to depict the diseases and conditions discussed
Includes access to a companion website with client education handouts to download and use in practice
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Yes, you can access Blackwell's Five-Minute Veterinary Consult Clinical Companion by Elisa M. Mazzaferro in PDF and/or ePUB format, as well as other popular books in Medicine & Veterinary Medicine. We have over one million books available in our catalogue for you to explore.
Acetaminophen (N-acetyl-p-aminophenol) is a common OTC or prescription medication with antipyretic and analgesic properties. It is commonly known as “Tylenol,” APAP, or paracetamol.
Acetaminophen does not have antiinflammatory properties and is not considered an NSAID.
Acetaminophen can result in accidental toxicosis in dogs, cats, and ferrets. Ingestion may be accidental or by well-intentioned pet owners who are unaware of the toxic dose or safety profile of this common medication.
In dogs, clinical signs of toxicosis are seen at >100–150 mg/kg, while in cats and ferrets, toxic doses can be seen at 10–50 mg/kg.
Acetaminophen toxicosis results in methemoglobinemia (cats, less commonly dogs) or hepatotoxicity (dogs, less commonly cats).
Clinical signs of toxicosis typically include malaise, anorexia, paw or facial swelling, vomiting, respiratory distress, brown mucous membranes, and icterus.
Unlike the majority of toxicants, acetaminophen toxicosis does have an antidote N-acetylcysteine (NAC), making the prognosis fair to excellent with supportive care.
ETIOLOGY/PATHOPHYSIOLOGY
Acetaminophen is a COX-3 inhibitor.
Acetaminophen is metabolized through two pathways: the major pathway creates inactive metabolites through conjugation to inactive glucuronide and sulfate metabolites. The other pathway metabolizes acetaminophen by the cytochrome p450 enzyme pathway to the toxic metabolite, N-acetyl-para-benzoquinoneimine (NAPQI). Toxicosis occurs when the metabolic pathways for glucuronidation and sulfation are depleted; this results in toxic metabolites building up and secondary oxidative injury to RBCs and hepatic proteins.
Acetaminophen is rapidly absorbed from the stomach and GIT; peak blood levels are reached within 30–60 minutes.
Systems Affected
Gastrointestinal: vague GI signs may be seen early in acetaminophen toxicosis; more severe signs may be seen with advanced hepatic failure.
Skin/exocrine: facial or paw swelling may be seen in both cats and dogs via an unknown mechanism; icterus with hepatotoxicity.
Hemic/lymphatic/immune: oxidative injury to RBC and Hb molecules following glutathione depletion, resulting in MetHb and Heinz body anemia.
Respiratory: respiratory distress secondary to the presence of MetHb and the inability to carry oxygen.
Cardiovascular: shock secondary to anemic hypoxia.
Hepatobiliary: hepatocellular injury and hepatic necrosis due to NAPQI.
Nervous: hepatic encephalopathy secondary to hepatotoxicity.
Ophthalmic: KCS has been reported with acetaminophen in dogs, even at subtoxic doses.
Renal/urologic: rarely, large doses can result in renal tubular necrosis; this has only been reported in humans.
SIGNALMENT/HISTORY
Risk Factors
Puppies and younger dogs appear to be overrepresented with poisoning due to their curious nature.
Neonates, geriatric patients, or those with underlying hepatic disease may be more at risk for acetaminophen toxicosis due to abnormal or delayed metabolism.
Cats are more susceptible to acetaminophen toxicosis, as they lack sufficient glucuronyl transferase to metabolize acetaminophen and have limited sulfate-binding capacity. Cats are also more susceptible as their hemoglobin contains eight sulfhydryl groups compared to four in other species; this makes feline RBC more prone to oxidative injury and results in MetHb developing earlier into toxicosis.
Chronic administration.
Historical Findings
Evidence of a tampered or chewed container or prescription bottle.
Owner administration.
Clinical signs consistent with acetaminophen toxicosis.
CLINICAL FEATURES
Gastrointestinal.
Anorexia
Hypersalivation
Vomiting
Diarrhea
Melena
Abdominal pain
Miscellaneous.
Facial or paw swelling
Generalized malaise
Hypothermia
Hemic/lymphatic/immune.
Brown or cyanotic mucous membranes
Hemoglobinemia
Hemoglobinuria
Respiratory.
Tachypnea progressing to dyspnea
Brown-colored mucous membranes
Increased respiratory rate and effort
Cardiovascular.
Tachycardia
Hypotension
Cardiovascular collapse
Hepatobiliary.
Malaise
Icterus
Bruising
Melena
Nervous.
Dull mentation
Generalized malaise
Ataxia
Head pressing, star gazing, or abnormal mentation
Tremors
Seizures
Coma
Op...
Table of contents
Cover
Title page
Copyright
Contributor List
Preface
About the Companion Website
Chapter 1 Acetaminophen Toxicity
Chapter 2 Acute Respiratory Distress Syndrome
Chapter 3 Anterior Uveitis
Chapter 4 Anticoagulant Rodenticide Toxicity
Chapter 5 Arterial Thromboembolism
Chapter 6 Atrial Fibrillation and Atrial Flutter
Chapter 7 Atrial Standstill
Chapter 8 Atrioventricular Block
Chapter 9 Blood Transfusion Reaction
Chapter 10 Brachial Plexus Injury
Chapter 11 Bromethalin Rodenticide Toxicity
Chapter 12 Bundle Branch Block – Left
Chapter 13 Bundle Branch Block – Right
Chapter 14 Canine Distemper
Chapter 15 Cardiopulmonary Arrest and Cardiopulmonary Resuscitation
