P
Pain
BASIC INFORMATION 
DEFINITION
An unpleasant sensory or emotional experience associated with actual or potential tissue damage
CLINICAL PRESENTATION
ETIOLOGY AND PATHOPHYSIOLOGY
• Nociceptors transduce noxious chemical, mechanical, or thermal stimuli into electrochemical potentials that are transmitted via sensory nerves from affected tissue to spinal cord.
• In the spinal cord dorsal horn, incoming first-order peripheral neurons synapse with ascending spinal neurons that extend to the brainstem.
• Incoming noxious input is modulated at the level of the dorsal horn by other incoming sensory information, descending inhibitory nerve impulses, or pharmacologic interventions.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
• Since animals cannot self-report pain, the veterinarian must accurately identify it when it is present.
• Pain must be differentiated from:
○ Distress associated with other factors (restraint, restrictive bandaging, confinement, separation from owners)
• Once a presumptive diagnosis of pain is made, veterinarians should investigate the underlying cause.
TREATMENT 
CHRONIC TREATMENT
• Dietary changes and nonpharmacologic treatment (e.g., physiotherapy, acupuncture) may be beneficial.
Gaynor JS, Muir WIII, editors. Handbook of veterinary pain management, ed 2, St Louis: Mosby, 2009.
Lamont LA. Adjunctive analgesic therapy in veterinary medicine. Vet Clin North Am Small An Pract. 2008;38:1187-1203.
Lamont LA. Multimodal pain management in veterinary medicine: the physiologic basis of pharmacologic therapies. In Vet Clin Small Anim. 2008;38:1173-1186.
Pallor
BASIC INFORMATION 
CLINICAL PRESENTATION
PHYSICAL EXAM FINDINGS
• Tachypnea, cool mucous membranes, tachycardia, and weakness may be seen with either anemia or shock.
• Capillary refill time (CRT):
○ Unless there is severe anemia, CRT should be normal (<2 sec) in an anemic animal that is not in shock.
• Visualization of stool via rectal examination may identify fresh blood or melena in cases with gastrointestinal (GI) hemorrhage.
ETIOLOGY AND PATHOPHYSIOLOGY
• Severe blood loss or severe anemia can lead to shock, so both conditions may exist in the same animal.
• Anemia causes pallor due to blood with diminished hemoglobin (i.e., decreased red blood cells) traversing through easily seen capillary beds, creating a pale red color in the mucous membranes.
DIAGNOSIS 
DIFFERENTIAL DIAGNOSIS
There are two major forms of anemia: regenerative and nonregenerative.
• Regenerative anemia:
There are four major types of shock:
INITIAL DATABASE
• PCV will help differentiate anemia from shock in most cases. Unless the animal was anemic beforehand, cases of acute shock should have a normal PCV, including those with acute blood loss. Anemic animals, by definition, have a diminished PCV.
• BP is usually diminished in cases of shock. Unless the anemia is severe or acute, BP is typically normal in anemic animals.
ADVANCED OR CONFIRMATORY TESTING
• Evidence of saline-diluted RBC agglutination on a slide suggests an immune-mediated hemolytic anemia, as would a positive Coombs’ test result.
• Thoracic radiographs to look for evidence of primary heart disease, trauma (e.g., rib fractures, lung contusions), or an infectious focus causing sepsis (e.g., pneumonia)
• Abdominal radiographs and/or ultrasound to visualize fluid (e.g., blood loss, congestive heart failure), neoplasia, and metallic (zinc) objects in the GI tract
TREATMENT 
ACUTE GENERAL TREATMENT
• Patients with severe anemia or acute blood loss may require transfusion of RBC ± plasma (see p. 1347).
• Hypovolemic, traumatic, and septic shock cases are usually treated with vigorous intravenous crystalloids, + colloids (see pp. 1591 and 1592).
PEARLS & CONSIDERATIONS 
COMMENTS
• Because there are many causes of pallor, the clinician especially needs to be aware of the differential diagnoses and methods to distinguish anemia from shock.
Palm (Cycad/Sago) Toxicosis
BASIC INFORMATION 
EPIDEMIOLOGY
RISK FACTORS: Presence of palm in the pet’s environment.
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Within 24 hours, onset of vomiting, diarrhea, lethargy, and anorexia; chewed leaves, seeds, plant material may be in vomitus.
ETIOLOGY AND PATHOPHYSIOLOGY
• Sago palms (cycad plants) are palmlike plants in the family Cycadaceae. These are woody, coarse plants with leaves originating from a thickened stem and are found in dry sandy soils of tropical and subtropical regions throughout the world.
• Toxins: cycasin and methylazoxymethanol, a neurotoxic amino acid, and an unidentified high molecular-weight compound.
• The glucose molecule on cycasin is hydrolyzed by the gut bacterial enzyme alpha-glycosidase, yielding sugars and methylazoxymethanol, which then alkylates DNA and RNA. This process causes hepatotoxic, teratogenic, carcinogenic, and gastrointestinal (GI) effects.
DIAGNOSIS 
TREATMENT 
ACUTE GENERAL TREATMENT
• Decontaminating the animal:
○ Emesis (see p. 1364): only in animals not showing clinical signs; may remain effective within a couple of hours of ingestion
○ Gastric lavage (see p. 1281) only if a very large dose has been ingested and emesis cannot be induced (e.g., comatose animal)
• Controlling CNS and GI signs:
• Treating signs of liver damage (see p. 503):
○ Clinicians should monitor and treat secondary effects of acute hepatic failure, such as hepatic encephalopathy (see p. 501), coagulopathy/bleeding tendencies (see p. 493), and hypoproteinemia (see p. 1347).
○ If serum levels of liver enzymes are elevated or signs of liver dysfunction are present, oral antibiotics (e.g., neomycin, 10-20 mg/kg PO q 6-8 h) and lactulose (15-30 mL PO q 6-8 h [dogs]; 0.25-1 mL PO q 8-12 h [cats]) may help reduce the risk of hepatic encephalopathy (see p. 501).
PEARLS & CONSIDERATIONS 
COMMENTS
• All sago palm exposures should be taken seriously because the overall mortality rate in dogs can be 33%.
• All parts are considered toxic, and seeds concentrate more toxins; one to two ingested seeds potentially can be lethal in a medium-sized dog.
Pancreatic Adenocarcinoma
BASIC INFORMATION 
EPIDEMIOLOGY
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Typically vague and nonspecific: anorexia, weight loss, lethargy, vomiting, constipation, diarrhea, abdominal distension (mass, ascites), and paraneoplastic alopecia (cats)
DIAGNOSIS 
INITIAL DATABASE
• CBC, serum biochemical profile, and urinalysis:
○ Variable neutrophilia, anemia, hyper-bilirubinemia, azotemia, hyperglycemia, and elevations in hepatic enzymes
• Abdominal radiographs: nonspecific; may reveal cranial abdominal mass effect and/or loss of abdominal organ detail due to ascites
• Abdominal ultrasound (high yield):
○ In most cases, a soft-tissue mass can be identified in the region of the pancreas. It may not be possible to conclusively identify the mass as pancreatic in origin on the ultrasound exam.
○ Benign pancreatic nodular hyperplasia, a common incidental finding in cats, must be considered when pancreatic nodules are identified. There is a tendency for neoplastic lesions to manifest as a single larger lesion and for nodular hyperplasia to manifest as multiple smaller lesions, although there can be overlap of the imaging findings for both entities.
○ Allows identification of metastatic lesions (liver “target lesions,” peritoneal masses, lymphadenopathy) and ascites, but not specific for pancreatic adenocarcinoma
○ Metastases are already present in a majority of cases of pancreatic adenocarcinoma and may be visible ultrasonographically.
ADVANCED OR CONFIRMATORY TESTING
• Cytologie or histologic diagnosis is essential, owing to the inability to differentiate grossly between pancreatic adenocarcinoma, chronic pancreatitis, and pancreatic nodular hyperplasia.
• Cytologie evaluation of ascites may reveal neoplastic cells in some cases (neoplastic cells may not exfoliate).
• Ultrasound-guided percutaneous fine-needle aspirate for Cytologie examination (variable yield; neoplastic cells may not exfoliate; differentiation between neoplastic lesions and nodular hyperplasia may be difficult).
• Ultrasound-guided percutaneous core biopsy, laparoscopic biopsy, or surgical biopsy for histopathologic evaluation of tissue.
• Pancreatic lipase immunoreactivity (PLI): has not been evaluated with pancreatic neoplasia; increased levels would be expected if there is secondary pancreatitis.
TREATMENT 
TREATMENT OVERVIEW
• Surgical excision of the tumor may be palliative but is not indicated if metastasis is present (majority of cases).
ACUTE GENERAL TREATMENT
• Surgery is indicated for solitary masses without evidence of metastasis, although a high metastatic rate makes this situation uncommon.
CHRONIC TREATMENT
• Chemotherapy or radiation therapy: no effective chemotherapy or radiation therapy protocols have been described.
• Gemcitabine (Gemzar) is approved for the treatment of pancreatic adenocarcinoma in people, and although cures are rare, gemcitabine has improved survival times in human patients. A recent case series of cats with pancreatic adenocarcinoma that underwent surgery and/or chemotherapy reported a median survival time of 3.8 months, with a range of 1 day to 17 months.
PEARLS & CONSIDERATIONS 
COMMENTS
• Pancreatic adenocarcinoma is an aggressive malignancy with high potential for metastasis and generally no effective treatment.
• Must be differentiated from non-neoplastic pancreatic lesions. It is important to have a Cytologie or histologic diagnosis, because chronic pancreatitis may closely resemble pancreatic adenocarcinoma.
