VMD-411-

1. Disease of Lymphatic System,

2. Emergency Medicine and Critical Care

1. DISEASES OF LYMPHATIC SYSTEM

Learning objectives
 Lymphoma and its management
CANINE LYMPHOMA
 Canine lymphoma : The following secrets or rules are to be known.
o Clinical Stage: IV+V worse than I-III; dogs with clinical signs worse than if asymptomatic.
o Hypercalcemia: worse when associated with an anterior mediastinal mass.
o Pretreatment corticosteroids: worse.
o High grade: higher response rate and longer duration of remission.
 Malignant lymphoma is a lymphoproliferative tumor of solid lymphoid tissues with possible
marrow metastasis and a leukemic phase.
 Etiology for the canine is unknown.
CLINICAL SIGNS
 Multicentric nature with peripheral lymphadenopathy
 Any organ may be affected.
 In the cat alimentary involvement is the most common presentation.
 Anterior mediastinal
 Cutaneous
 Unclassified (e.g., mucocutaneous, CNS, renal) forms.
 Ocular involvement (anterior uveitis, hypopyon, hemorrhage, infiltrate)
 Involvement of the spleen, liver, and bone marrow

ENLARGED LYMPH NODES

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 Enlargement of popliteal and mandibular lymph nodes in a Great Dane dog

DIAGNOSIS

 Malignant lymphoma --replacement of normal lymph nodes by a uniform population of

pleomorphic and bizarre lymphocytes.
 A tissue core biopsy -- a node --excised for final confirmation.
 Clinical staging is mandatory.
 Clinical staging determines the extent of disease in the living animal.

Clinical staging done with

 Radiography of the thorax and abdomen

 Complete blood count and platelet count
 Bone marrow aspirate and core
 An ophthalmic exam,
 Measurement of representative enlarged lymph nodes and
 A biochemistry panel
 Hypercalcemia associated with a parathyroid-hormone-like substance is observed in some dogs
with malignant lymphoma. This is most often encountered in dogs with anterior mediastinal
lymphoma and bone marrow involvement.

TREATMENT

 Treatment for malignant lymphoma must be systemic in nature since it is a multi-system disease.
Chemotherapy is most frequently utilized; however, some immunotherapy has been effective.
Untreated, dogs affected with malignant lymphoma live an average of only six weeks once a
diagnosis has been made. With chemotherapy, dogs can survive for 6-10 months with an excellent
quality of life. Dosage of chemotherapeutic agents for the cat is the same as for the dog except
when Adriamycin is used. While dogs may receive Adriamycin every 21 days at a dosage of 30
mg/m2, cats appear to be more sensitive to the drug and many of them can only tolerate a dosage
of 20 mg/m2 given every 21 days. Anorexia and renal failure have been reported as significant side
effects in cats.
 Malignant lymphoma is one of the most responsive forms of cancer presented to the practitioner.
With appropriate chemotherapy protocols, nearly 90% of animals placed on therapy should reach
complete remission. Of those that reach remission, approximately 80-90% will maintain a

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 reasonable (>6 mos) timeframe of excellent quality life. Cost is not inexpensive; however, it is
within reasonable financial reach of many clients, thus allowing therapy to be possible.
 Although marginally effective, prednisone is inexpensive and often used in combination with
other drugs to treat lymphoma. With prednisone therapy, the average pet lives 2 months. One-third
of the dogs and cats treated with prednisone will go into complete remission, one-third will go into
partial remission, and one-third will not respond at all.
 Adriamycin is one of the most effective single agent treatments for lymphoma in dogs. Of the
dogs treated with adriamycin, 81% developed a complete and partial remission. The duration of
remission is approximately 9 months. Dogs treated with Adriamycin and then switched to COP
(cyclophosphamide, Oncovin, prednisone) had a higher second remission rate compared to those
started on COP and then switched to Adriamycin.

COP PROTOCOL

 The COP protocol is effective.

 A median duration of remission of 6 months
 The addition of adriamycin to the COP regiment resulted in longer remission time (7 months vs 6
months).
 Table 1. COPA protocol for Dogs+

Drug Dose (mg/m2) 1 2 3 4 5 6 7 8 9 10 11 12 13 52

Cytoxan 250 PO X X X X
Adriamycin* 30 IV X X
Vincristine 0.75 IV X X X X X X
Prednisone** 30 PO > > > > > > > > >

SIDE EFFECTS

 Whisker or Hair Loss (Alopecia)

 Reduction in the Number of White Blood Cells (Neutropenia)
 Stomach or Intestinal (Gastrointestinal) Discomfort
 Vomiting
 Loss of appetite
 Diarrhea
 Tissue Damage
 Allergic Reactions
 Heart Damage
 Increased Drinking of Water, Urination and Appetite

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 2. EMERGENCY MEDICINE AND CRITICAL CARE
EMERGENCY MANAGEMENT OF CASES

The following should be evaluated and treated accordingly.

 Airway
 Breathing or respiratory depression or respiratory failure
o A patent airway should be established with cuffed endotracheal tube.
o Mechanical ventillation or oxygen should be used
o Centrally acting respiratory stimulant should be used if necessary Doxapram – 1
mg / kg b.wt i/v) excessive dose cause seizures or the animal may relapse to coma.
o Nalaxone – 0.04 mg/kg .wt. i/v, i/v, s/c – for respiratory depression caused due to
opiate exposure.
o Cardiac arrhythmias of several types can occur.

Types of Poison Treatment

arrhythmia
Sinus Bradycardia  Opioid  Atropine : 0.01 – 0.2 mg/kg b.wt i/v or
 Carbamate i/m
 Β – blockers  Glycopyidate : 0.005 – 0.01 mg/kg b.wt.
 Phenothiazine i/v or i/m
Atrio ventricular Digitalis  Atropine – 0.01 – 0.2 mg/kg b.wt. i/v or
block i/m
 Dopamine – 3-5 mg/kg b.wt / min
 Iroproterenol – 0.01 mg/kg b.wt / min
i/v
Atrial stand still Hyperkalemia  Saline i/v
 Sodium bi carbonate
 Insulin with dextrose
Ventricular Lidocaine Hydrochloride – 2-3 mg/kg b.wt.
Tachycardia slow i/v

Shock

 Signs:
o Tachycardia
o Hypotension (prolonged capillary refill time, weak pulse)
o Rapid respiration
o Hypothermia
o Weakness, restlessness, depression

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 o Reduced urine output
o Coma, papillary dilatation
 Steps
o Ensure patent airway (intubate)
o Haemorrhage – direct pressure / bandage / tourniquet / ligation
o Fluid therapy – maintain PCV between 20 & 50 %, add 50 ml of 50% dextrose to
each time of fluid.
o Whole blood, colloids: eg: Dextran – 20 – 40 ml/kg b.wt. for 24 hrs.
o Glucocorticoids
 eg. Hydrocortisone sodium succinate – 8-20 mg/kg b.wt. i/v
 (Onset of action:- 1-4 minutes)
 Prednisolone sodium succinate – 20-25 mg/kg b.wt i/v
 Dexamethasone – 1-4 mg/kg b.wt (i/v or s/c)
o Vassoactive substances
 eg. Dopamine – 5 mg in 250 ml 5% dextrose i/v
 Sodium bicarbonate – 0.3 x body weight x base deficit
 1-2 meq / kg b.wt. i/v
 1-2 meq added in each litre of solution
o Broad spectrum antibiotics
o Diuretics
 Eg; Frusemide – 2-4 mg/kg b.wt i/v or s/c
 Heparin - 100 – 200 IU/kg b.wt i/v

CNS Dysfunction

 Seizures may be associated with hypoxia, vomiting, hypothermia and acidosis. It should
be controlled before the specific cause is known.
o Diazepam – 0.5 mg/kg i/v as it has short half life and must be re-administered
every 10-15 min for up to several treatment.
o Phenobarbitone– 6 mg/kg b.wt i/v
o Pentobarbitone – used carefully to induce light anaesthesia
 Recently proposed concept
o Proposal – 3-5 mg/kg b.wt. i/v administered after diazepam. These phenoarbitolne
or pentobarbitone opiod anaesthesia.
 Analeptics
o To treat CNS depression
o Dexopram / Nalaxone used
o Phenothiazine tranquilizers
o Prolonged vomition and diarrhea – CNS cause
 Hypothermia / Hyperthermia
o Hypothermia – use of blankets, warm water bottles, heating pads, warm i/v fluids
intraperitoneally.
o Hyperthermia – cold pack, ice pack, cold i/v fluids.

ANAPHYLACTIC SHOCK

 This is the immediate type of hypersensitivity reaction. Anaphylactic shock rarely

develops without the interference of man. An exception is the condition that is a result of
bees/wasp sting. The main signs are attributed to the effect of activation of
complementary system which induce dilatation of smooth muscles which releases
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 histamine, serotonin, acetylcholine and bradykinin in dogs, sphanchnic viscera and other
major organs are involved.

Signs in Dogs

 Restlessness, diarrhora (reddish), circulatory failure, epileptic form of seizures, coma and
death.

Signs in Cats

 Respiratory signs are predominant, pruritis, ptyalism, vomiting, incoordination, broncho

constriction, pulmonary haemorrhage, laryngeal odema and death.

Agents Causing Anaphylactic Shock

 Penicillin, streptomycin, tetracyclines, chloramphenicol, Erythromycin, vancomycin,

insulin, oxytocin, penicillin, procaine, lidocaine, salicylate, tranquilizers, antihistamines,
heparin, stinging insects.

Treatment

 Severe Cases
o Administer 1 in 1000 of Epinephrine – 0.01 ml/kg BW, if indicated repeat after
20-30 minutes.
o Infiltrate subcutaneously at the site of allergant entry, with 1 in 1,00,000
Epinephrine – 0.3 ml/kg b.wt.
o Ensure clear air passage and administer oxygen by face mark or endotracheal tube.
Establish an IV line and administer Ringer’s lactate, saline or Dextrose (5%)
solution.
 Mild / Moderate Cases
o Administer 0.2 – 0.5 ml of epinephrine subcutaneously and another 0.2 – 0.5 ml
subcutaneously elsewhere. Administer another 0.5 ml, if symptoms not subsided.
o Administer an rapidly acting steroid intravenously.
 Hydrocortisone - 100 to 500 mg/kg b.wt
 Prednisolone - 15 to 30 mg q 6 hrs.
 Dexamethasone Phosphate - 4 mg / kg b.wt q 4 hrs.
o Hospitalise and monitor the patient. If recovery occurs within 5-10 minutes,
following intensive treatment, then the prognosis is good.

SEIZURES

 Not seizing at the time of presentation – perform complete physical examination.

 Complete profile – hematology, biochemical including urogenital examination
 Start Potassium Bromide 450 – 600 mg /kg p/o (loading) dividing 4 doses and
administer in food.
 Maintenance: 40-50 mg / kg q 24 hours.
 If seizing (status epileptics). Primary aim: stop seizing.

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 o Diazepam: 1 mg/kg i/v. If seizure does not subside within 1-2 minutes repeat Dz
(1-2 times it can be repeated). Restore and maintain homeostasis, airway, oxygen,
temperature, glucose and vital signs.
o Diazepam: Inline burette 0.5 – 1 mg /kg/hour. Prepare only requirement for 1-2
hours. If no seizure occurs during 4-6 hours reduce by 25% every 4-6 hours.
o If more than or equal to 2 seizures during Dz therapy can increase dose upto 1-5
mg/kg/hour.
o Add phenobarbitone 15 mg/kg i/v in addition to above and see for seizure. If still
seizure is present give propofol 1-3.5 mg/kg to effect followed by constant rate
infusion 0.01-0.25 mg/kg/min for 24-48 hours.
 If the above method fails, induce GA using propofol 4-6 mg/kg i/v followed by 0.1-0.3
mg/kg/min to effect or Isoflurane or pentobarbital 2.5 mg/kg i/v to effect followed by 5
mg/kg/hour for several hours.
 Oral Antiepileptic drugs:
o I choice: Potassium Bromide: 40-50 mg/kg q 24 hours. Contraindicated in renal
insufficiency.
o II choice: Phenobarbitone: 2.5-4 mg/kg q 12 hours. Contraindicated in liver
disorders. Increase by 50% in case of puppies. No seizure occurs for 6-12 months
slow weaning over a period of few months. If seizure occurs, 1 per 6-8 weeks
resume therapy.
 For cats:
o I choice phenobarbitone: 2-2.5 mg q 12 hours.
o II choice: Dz: 0.5-1mg/kg q 24 hours
o III choice: KBr: 30-40 mg/kg q 24 hours.
 Contraindications: Accpromazine, Ketamine, Aminophylline, Xylazine as they lower the
seizure threshold.

ANTIEPILEPTIC DRUGS

Anticonvulsant Therapy

 Phenobarbital Phenobarbital (PB) remains one of the first-choice drugs for use in dogs
with seizures and is also the preferred anticonvulsant drug for cats. The proposed
mechanisms of action of PB include increasing neuronal responsiveness to gamma-
aminobutyric acid (GABA), antiglutamate effects, and decreasing calcium inflow into
neurons. PB is metabolized by hepatic microsomal enzymes, with a serum half-life (t½)
of elimination between 40 and 90 hours in the dog, and approximately 40 to 50 hours in
the cat after oral administration. It takes approximately 10 to 15 days to reach steady-
state kinetics with oral dosing at a maintenance level. PB is a potent inducer of hepatic
microsomal enzyme activity (eg, cytochrome P450), The maintenance dose range used by
the author for PB in dogs is 3 to 5 mg/kg of body weight administered orally every 12
hours.
 In cats, a similar dose range is used, but the initial dose is 2.5 mg/kg of body weight
administered orally every 12 hours. Commonly reported side effects of PB in dogs and
cats include sedation, polyuria/polydipsia (PU/PD), polyphagia (PP) with weight gain,
and ataxia. These side effects usually subside dramatically within the first several weeks
of treatment. An uncommon but potentially life-threatening consequence of PB use is
hepatic failure. Less commonly reported side effects attributable to PB use in dogs
include bone marrow necrosis (with attendant blood dyscrasias) and superficial
necrolytic dermatitis.
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  Blood dyscrasias (eg, leukopenia, thrombocytopenia, anemia) are likely to resolve after
PB discontinuation. Chronic (>3 weeks) PB administration at standard therapeutic doses
has been shown to cause a significant decrease in total (TT4) and free (FT4) serum
thyroxine levels. Serum chemistry values should be checked every 6 months in patients
receiving PB. Increased serum alkaline phosphatase (ALP) is expected in dogs receiving
PB. Increases in serum alanine aminotransferase (ALT) are cause for concern. It is
generally thought that serum ALT increases represent hepatocellular damage, whereas
serum ALP elevations reflect PB-induced hepatic enzyme production.

Bromide

 Bromide (Br) is a halide salt that has been used primarily as a second-line (ie, add-on to
PB) drug in dogs but is gaining popularity as a first-choice anticonvulsant in this species
Br has been shown to be an effective add-on therapy for dogs receiving PB; side effects of
Br therapy are similar to those of PB when compared as sole anticonvulsant agents. Br is
usually administered as the potassium salt (KBr). The sodium salt form (NaBr) contains
more Br per gram of drug; therefore, the dose should be approximately 15% less than that
calculated for KBr.
 The anticonvulsant mechanism of Br is thought to be attributable to its competition with
chloride ions; the Br ion is thought to hyperpolarize neuronal membranes after traversing
neuronal chloride channels Br is renally excreted, and is thus a good choice for patients
with hepatic disease (eg, porto-systemic shunt). The t½ of elimination for KBr is 24 days
in dogs; initial maintenance dose for oral KBr is 35 mg/kg of body weight divided into
two daily doses. A loading dose is often administered over a 5-day period to dogs to attain
steady-state kinetics sooner.
 The loading dose used by the author is 125 mg/kg of body weight divided into two daily
doses. Side effects of KBr include pelvic limb stiffness and ataxia, sedation, vomiting,
PU/PD, PP with weight gain, hyperactivity, and skin rash. Less commonly, aggressive
behavior and pancreatitis have been associated with KBr use Pancreatitis has been
suggested to be more likely when KBr is used in conjunction with PB. persistent cough
that seemed to be associated with Br therapy.

Benzodiazepines

 Benzodiazepine drugs used in dogs and cats with seizure disorders include diazepam,
clonazepam, clorazepate, midazolam, and lorazepam. Benzodiazepines exert their
anticonvulsant effects by enhancing GABA activity in the brain. Diazepam is ineffective as
an oral maintenance anticonvulsant in dogs because of its short t½ of elimination (2–4
hours) and the tendency for dogs to develop tolerance to its anticonvulsant effect. In
contrast, diazepam is an effective oral anticonvulsant in cats
Clonazepam is an oral anticonvulsant drug of limited use in dogs because of the rapid
development of tolerance to the drug's anticonvulsant effects. Clorazepate has an
elimination t½ between 3 and 6 hours in dogs after oral administration, and the dose
range is 0.5 to 1 mg/kg of body weight administered every 8 hours.

Felbamate

 Felbamate is a dicarbamate drug that has demonstrated efficacy for focal (partial) and
generalized seizures Proposed mechanisms of action include blocking of N-methyl-D-
aspartate (NMDA)–mediated neuronal excitation, potentiation of GABA-mediated
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 neuronal inhibition, and inhibition of voltage-sensitive neuronal sodium and calcium
channels Approximately 70% of the orally administered dose of felbamate in dogs is
excreted in the urine unchanged; the remainder undergoes hepatic metabolism. For adult
dogs, the author recommends an initial felbamate dose regimen of 15 mg/kg of body
weight administered every 8 hours.
 A major advantage of felbamate over more standard anticonvulsant drugs is that it does
not cause sedation. Because felbamate does undergo some hepatic metabolism, liver
dysfunction is a potential side effect Aplastic anemia (caused by bone marrow
suppression) reversible bone marrow suppression mild thrombocytopenia, and mild
leukopenia. In dogs with evidence of preexisting hepatic disease, felbamate should be
avoided. Because of the potential for hepatoxicity.

Gabapentin

 Gabapentin, a structural analogue of GABA, has been suspected to exert its antiseizure
effects via enhancing the release and action of GABA in the brain as well as by inhibiting
neuronal sodium channels. More recent evidence, however, suggests that gabapentin's
anticonvulsant activity is due primarily to inhibition of voltage-gated calcium channels in
the brain. Despite undergoing some hepatic metabolism in dogs, there is no appreciable
induction of hepatic microsomal enzymes in this species.
 The recommended dose range of gabapentin for dogs is 25 to 60 mg/kg of body weight
divided into doses administered every 6 to 8 hours The author recommends an initial
dose regimen of 10 mg/kg of body weight administered every 8 hours. dogs experienced
mild sedation or mild polyphagia and weight gain associated with gabapentin use,
sedation and pelvic limb ataxia.

Levetiracetam

 Levetiracetam is a new piracetam anticonvulsant drug that has demonstrated efficacy in

the treatment of focal and generalized seizure disorders in people as well as in several
experimental animal models The mechanism of action for levetiracetam's anticonvulsant
effects is unknown; There is some evidence that levetiracetam may inhibit high voltage–
activated neuronal calcium currents.
 It has recently been discovered that the binding site for levetiracetam in the brain is an
integral membrane protein called synaptic vesicle protein 2A (SV2A); the interaction of
levetiracetam with this protein appears to be associated with the drug's anticonvulsant
effect. In dogs, approximately 70% to 90% of the administered dose of levetiracetam is
excreted unchanged in the urine; the remainder of the drug is hydrolyzed in the serum
and other organs. initial dosing schedule of 20 mg/kg of body weight administered every
8 hours

Zonisamide

 Zonisamide is a sulfonamide-based anticonvulsant drug efficacy in the treatment of focal

and generalized seizures in people, Suspected anticonvulsant mechanisms of action
include blockage of T-type calcium and voltage-gated sodium channels in the brain,
facilitation of dopaminergic and serotonergic neurotransmission in the central nervous
system, scavenging free radical species, enhancing actions of GABA in the brain,
inhibition of glutamate-mediated neuronal excitation in the brain, and inhibition of
carbonic anhydrase activity. Zonisamide is metabolized primarily by hepatic microsomal
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 enzymes, initial oral zonisamide dose schedule of 10 mg/kg of body weight administered
every 12 hours.

Therapy for Cluster Seizures and Status Epilepticus

 Cluster seizures and status epilepticus hold the unfortunate role of being the most life-
threatening and difficult to treat types of seizure activity. Cluster seizures to include two
or more discrete seizure events within a 24-hour period. A discrete seizure implies that
the patient fully recovers before experiencing a subsequent seizure episode. Status
epilepticus is continuous seizure activity lasting more than 5 minutes or recurrent
seizures between which the patient does not fully recover.
 Unabated seizure activity can lead to severe consequences, such as hyperthermia,
aspiration pneumonia, disseminated intravascular coagulation, and permanent brain
injury It is vitally important in such severe cases to halt seizure activity, treat any seizure-
associated problems (eg, brain edema), and provide attentive monitoring and nursing
care. many cases of cluster seizures, and most cases of status epilepticus, require
measures that produce heavy sedation or anesthesia; these patients typically require
tracheal intubation and close monitoring in an intensive care unit setting. Intravenous
diazepam (0.5–1.0 mg/kg) is the preferred initial choice to halt seizure activity because of
its rapid onset of action and safety.
 Despite this, diazepam often results in temporary cessation of seizure activity or fails to
halt seizure activity entirely. If seizure activity is repeatedly ceased with intravenous
diazepam boluses, a diazepam intravenous CRI at a dose of 0.5 to 2.0 mg/kg/h may be
successful. Other intravenous benzodiazepine drugs have been suggested for emergency
treatment of seizures in dogs and cats,. These drugs include clonazepam, midazolam, and
lorazepam Intravenous.
 Clonazepam: 0.05 to 0.2 mg/kg of body weight intravenous Midazolam intravenous or
intramuscular administration. 0.066 to 0.22 mg/kg of body weight
 Lorazepam: An intravenous dose of 0.2 mg/kg of body weight
 Potential disadvantages of intranasal administration of drugs versus intrarectal drug
administration include technical factors (eg, drug loss attributable to swallowing or
sneezing) and increased risk of an owner being inadvertently bitten by a pet during a
seizure episode. Diazepam (0.5 mg/kg of body weight) and lorazepam (0.2 mg/kg of body
weight) have been demonstrated to reach serum levels in dogs within the suspected
therapeutic range within minutes after intranasal administration
 Diazepam has been shown to be well absorbed after intrarectal administration in dogs
and effective as an at-home treatment of dogs with cluster seizures; the recommended
dose range is 1 to 2 mg/kg of body weight
 Intravenous barbiturate therapy is commonly used when intravenous benzodiazepine
therapy fails to terminate seizure activity or if repeated dosing of intravenously
administered benzodiazepine is necessary to control seizures. Because of the potential for
respiratory and cardiovascular depression with barbiturates, these drugs should be given
to effect, with meticulous patient monitoring
 Pentobarbital is usually successful in abolishing motor manifestations of seizure activity
within several minutes of intravenous administration but is not generally considered an
anticonvulsant drug. The dose range for intravenous pentobarbital is 2 to 15 mg/kg of
body weight. Compared with diazepam, it may require several minutes for pentobarbital
to take effect If seizure activity is recurrent, an intravenous pentobarbital CRI can also be
administered at a dose range of 0.5 to 4.0 mg/kg/h In addition to lacking anticonvulsant

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 activity, pentobarbital is often associated with paddling activity during recovery; such
activity may be confused with continued seizure activity
 Intravenously administered phenobarbital (2–6 mg/kg of body weight) requires
approximately 15 to 20 minutes for clinical effect, so it is important not to give an
overdose during this lag period.. For patients not already receiving PB therapy,
intermittent bolus injections (eg, 3–6 mg/kg of body weight) can be cautiously
administered every 15 to 30 minutes to attain a serum PB level within the therapeutic
range Alternatively, an IV CRI of PB (2–4 mg/kg/h) can be instituted.
 Propofol is a phenolic injectable anesthetic agent that has been demonstrated to have
GABA agonistic activity in the brain; propofol also decreases intracranial pressure (ICP)
and brain metabolic activity. Propofol has the advantageous properties of being rapidly
acting and quickly metabolized Propofol has proven to be useful in the treatment of
cluster seizures and status epilepticus in human and small animal patients. A bolus dose
of 1 to 6 mg/kg should be administered slowly to effect. Because transient apnea is a
commonly reported effect of bolus propofol administration, the clinician should be
prepared to intubate the patient and assist with respirations. propofol CRI can be
initiated (0.1–0.6 mg/kg/min). Clonic motor activity, similar to that seen with
pentobarbital use, can occur with propofol
 Etomidate is an imidazole injectable anesthetic drug that has GABA-ergic activity in the
brain and also decreases brain metabolic activity. Etomidate also may protect neurons
from hypoxic damage and decrease ICP. 1 to 3 mg/kg of body weight. transient apnea
may occur after injection of etomidate, this drug has minimal effects on the respiratory
and cardiovascular systems
 Fosphenytoin After intravenous or intramuscular injection, fosphenytoin is rapidly
converted to phenytoin (the active drug) by serum and tissue phosphatases. Unlike
injectable phenytoin, fosphenytoin use is not associated with severe phlebitis and pain at
the injection site. An intravenous dose range of approximately 10 to 20 mg/kg of body
weight, potential side effects of fosphenytoin use reported in people include hypotension,
cardiac arrhythmias, nystagmus, ataxia, and somnolence
Ineffective and Contraindicated Drugs
 There are a number of older drugs that are generally ineffective in dogs, primarily
because of their extremely short elimination t½ in this species. These drugs are known or
suspected to be toxic to cats as well. They include phenytoin, carbamazepine, valproic
acid, and ethosuximide. More recently introduced drugs that have been suggested for use
in dogs include vigabatrin, lamotrigine, oxcarbazepine, tiagabine, and topiramate.
vigabatrin hemolytic anemia
 Lamotrigine cardiotoxic compound.
 Tiagabine cause marked sedation and visual impairment

Submission of Samples for Toxicological Investigation and

Management of Various Poisoning

CHEMICAL EXAMINATION OF SAMPLES

 The report which accompany materials for toxicological analysis should include full
history, clinical signs, necropsy findings, particularly the result of search of environment
for access to poisoning.
 If the animal has been treated, drug used and date of administration should be given.
 The poison / group of poisons should be defined.

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  Specimens should include poison’s source and gastrointestinal contents.
 List Suspects
o Arsenic - kidney, skin, hair
o Lead - kidney, bone, blood
o Phosphorous - kidney , muscle
o Mercury - kidney
o Copper - kidney, blood
o Sodium chloride- Alimentary tract and its contents
o Flourine - Bone, teeth, urine
o Hydrogen cyanide - Ingesta in air tight container
o Nitrate & Nitrite - Ingesta in chloroform or formalin in air tight container or blood.
o Strychnine - Blood, kidney, urine
 Careful packing of specimen is necessary to avoid loss of poison by escape of gas or
convertion by bacterial fermentation and to prevent contamination.
 No preservative should be added except in cases suspected nitrate poisoning. If a
preservative is necessary, because of distance from laboratory, packing in dry ice /
ethanol 1 ml/gram of tissue is advisable.
 In the later instances, a specimen of alcohol should be sent.
 Ingesta and tissues must be kept separate because diffusions may occur.
 Specimens should be packed in glass or plastic to prevent contamination.
 Metal tops or jars should be also separated by a layer of plastic or other impervious
material.
 Suitable amount of material should be sent for analysis (1 kg of ingesta, 1 kg of liner,
proportionate amount of others).
 If there is a strong suspicion or criminal poisoning/litigation duplicate specimens
collected in preserve of witness.
 A complete set of specimen should be available in both parties for independent analysis.
 Veterinarian should make clinical, pathological, epidemiological investigation.
 Take photographs and document the same.

TOXICOLOGICAL EMERGENCIES

 Amitraz:It affects the peripheral alpha1 an d alpha2 adrenergic site in CNS system
 Toxicity: Oral or dermal route
 History: Ingestion, vomition, polyurea, ataxia, depression that may progress to coma.
 Signs: Hypotension, hypothermia, mydriasis, bradycardia, hypopesistalsis, vomiting,
diarrhea, polyurea, ataxia, sedation, disprientation, coma.
 Note: Atropine sulpate contraindicated

Treatment

 Spontaneous recovery in mildly affected animals. In comatosed animal, attempt to

remove by gastric lavage.
o Administer activated charcoal 2-5 g/kg b.wt PO (in slurry), 1g / 5 ml, repeat after
3-4 hrs.
o Cathartic: osmotic or saline cathartic after 30 min of administration of charcoal.
o Sorbitol – 4g / kg b.wt PO as 7% preparation
o Mix 200 – 500 mg of magnesium sulfate in water and give at the rate of 5ml –
10ml / kg b.wt. PO.

12
 o Yohimbine – 0.11 mg/kg b.wt. slow i/v competitively inhibit alpha2 receptor and
removes depression, hypotension and bradycardia.
o Atipamazole – 50 mg/kg b.wt i/m q 3-4 hrs. can also be combined with yohimbine
at dose rate of 0.1 mg/kg b.wt 8 hrs.

Organophosphorous Compounds and Carbamate Poisoning

 Clinical Signs
o Muscarinic signs – SLUD, bradycardia
o Nicotinic signs – muscle tremor, twitching, paresis, paralysis
o Depression, seizures
 Treatment
o Dermal exposure – wash
o Ingestion – emesis, lavage
o Death due to cardiac arrhythmia, dyspnoea caused by excessive pulmonary
secretion.
o Atropine – 0.1 – 0.5 mg/kg .wt, ¼th i/v q 6 hrs (if muscarnic signs returns) and
wait 5 min ¾th s/c or i/m. Atropine counteracts only muscarinic sings.
o Antidote – 2 pralidoxine chloride (2PAM).
 Small animals – 20 mg/kg .wt twice daily i/v slowly, i/m q 8-12 hrs
 Horse - 2g slow i/v TID
 Cattle - 20-50 mg/kg b.wt i/v

Organochlorine Poisoning

 Clinical Signs
o Nervous system – severity of clinical signs not corretated with prognosis.
 Earlier:- Salivation, nausea, vomiting, nervousness, tremors,
hyperexitability, incordination.
 Advanced:- clonic, tonic spasms, seizures, opisthotonus, paddling,
champing of jaws.
o In cattle:- abnormal posture, lick excessively, walk backwards.
 Treatment
o Dermal - wash
o Ingestion - Activated charcoal, phenobarbitone, pentobarbitone, diazepam,
propofol.
o Supportive therapy and place the animal in comfortable place.

Pyrethrin Poisoning

 Clinical Signs
o Mild:- Mild hypersalivation, ear twitching, depression, vomiting, diarrhea.
o Moderate:- hyperaesthesia, incoordination, muscle tremor
o Severe:- seizure and death
o Emergic reaction: pruritis, hyperaemia, shock, urticaria, death (rare)
 Treatment
o Topical decontamination
 Detergent bath (hand wash)

13
  Adverse reactions are mild and self limiting
 Maintenance of body temperature is critical.
o Tremous:- Diazepam – 0.5 mg/kg b.wt i/v to effect
o Phenobarbitone – 2-4 mg/kg b.wt i/v to effect
o Atropine sulfate contraindicated

Ivermectin Poisoning

 Clinical Signs
o Ataxia, vocalization, disorientation, aggression, blindness, head pressing, loss of
menace reflex, incomplete PLR.
o Severe cases: Bradycardia, hypothermia, respiratory depression, multifocal
impairment of thalamus, coma, death.
 Treatment
o Symptomatic and supportive care
o CNS depression may last for a week, institute nutritional care.
o Affected animal remain recumbent for long period. Physiotherapy with frequent
turning and nursing care.

Rodenticide or Anticoagulant Poisoning

 Clinical Signs
o Bleeding through nose, bowel, gums, wounds
o Pale mucosa, depression, lethargic, haematuria, melena
o Lameness, haemrrhage in cavity, hypovolemic shock
 Treatment
o Phythomenodione – 2.5 – 5 mg / kg b.wt P/O, i/v, i/m, s/c, 5 days – 6 weeks
o Bioavailability enhanced by fat.
o Fresh blood or plasma transfusion. Anaphylactic reaction may occur during
vitamin K administration.

Cyanide Poisoning

 Sodium nitrate - 22 mg / kg b.wt i/v

 Sodium thiosulfate - 660 mg/kg .wt i/v

Nitrate Poisoning

 Methylene blue - 4-15 mg/kg b.wt i/v as 1% solution

 Repeat dose at 6-8 hrs.

OXYGEN THERAPY

Indications

 For severe acute respiratory diseases causing hypoxia and hypoxemia

 For ventilation- perfusion mismatch (Eg. Pneunconia and air by respiration)
 Supportive care for animals in shock
 For any disease causing hypoxia
 Animals with poor ventilation require tracheal intulation and pressure intulation.
14
  → Hyperventillation is not an indication for nasal oxygen.

Procedure

 With nose pointing upwards, 1 ml Lignocaine is instilled into the nostrils. Repeat this
after a minute. Measure tubes from external nares to the inner canthus of the eye.
Lubricate the catheter with sterile lubricant. Insert it into the ventral nasal meatus to
distance already marked on catheter.
 Apply suture on the skin near the nostrils. Position the tube between the eyes and secure
it at forehead and top of the head. Connect the extension tubing with nasal catheter,
liquefy the passage, start administering oxygen.

Rate of Administration of Oxygen

 50 – 100 ml / min / kg body wt or 4 litres/min in small animals

 12 litres / min in large animal
 0.5 litres / min in birds

ACUTE ABDOMEN

 It is a multietiologic clinical syndrome characterized by the sudden onset of intense

abdominal pain and associated signs which include: shock, vomiting, diarrhea, changes in
gastrointestinal peristaltic activity, fever, anorexia and dyspnea.
 Immediate supportive therapy is often indicated to preserve the life of the patient while a
diagnosis is pursued. Decisions about the overall management of the patient can only be
made after establishment of an accurate diagnosis. Even with a searching history and
physical examination the etiology may tax the diagnostic acumen of even the most
experienced practitioner. Diagnostic laboratory and radiographic procedures are
essential.
 An acute abdominal problem can usually be classified into one of three categories, each
dictating its own course of management:
o Intra-abdominal lesions usually requiring urgent surgical intervention after a
period of resuscitation and stabilization.
o Primary medical conditions or surgical conditions not usually requiring immediate
surgical intervention.
o Medical and Surgical Conditions Simulating the Acute Abdomen.

HISTORY

Immediate Patient Evaluation

 The clinician should be able to quickly determine whether immediate intervention is

required. At presentation, the complaint should be noted and a brief history taken while
carrying out a rapid evaluation of the patient. This evaluation should include the patient's
attitude, mucous membrane color, heart rate, pulse quality, respiratory effort, and
response to abdominal palpation. If the patient is in shock or bleeding, supportive
therapy should be initiated and a more detailed history obtained at a later opportunity.

History
15
 This is always the first, and often the most important aid to diagnosis. The age, breed,
sex, environment, onset, course, nature and duration of signs should all be considered. It
is important to note if the onset is spontaneous or follows trauma.
 The presenting complaint for an animal with an acute abdomen may include acute
abdominal pain or distension, vomiting, diarrhea, anorexia, weakness or collapse. The
signalment may indicate the likely cause of the problem; for example, young animals are
more likely to ingest foreign bodies, develop intussusceptions or contract viral enteritis.
 Acute abdominal diseases in the adult include: decompensated chronic infections,
pancreatitis, vascular occlusive disease and intestinal obstruction or abdominal organ
displacement caused by a tumor. Older obese female dogs may have an increased risk of
pancreatitis. Cats tend to ingest linear foreign bodies whereas deep chested dogs such as
great Danes, Wolfhounds and Irish setters are more likely to develop gastric dilatation
volvulus. German shepherds and Labrador and golden retrievers are commonly affected
with splenic neoplasia.
 Knowledge of the previous medical history such as exposure to infectious disease, trauma
or previous abdominal surgery (which may suggest a paralytic ileus or obstruction from
adhesions) is often helpful. Chronic weight loss may suggest an intra-abdominal tumor.
Over-eating or the ingestion of spoiled or frozen food may precipitate acute gastric
dilatation or acute hemorrhagic gastroenteritis. A history of mast cell tumors or
corticosteroid or non-steroidal anti-inflammatory drug therapy increases the risk for
gastrointestinal ulceration. The potential for toxin exposure can be a crucial part of the
history.

PHYSICAL EXAMINATION

 The patient should be assessed for mental attitude (alertness), posture, and ability to
walk. Dogs with abdominal pain may stand with an arched posture or "praying position"
that alleviates abdominal pressure. Cats may stand with their heads extended and elbows
abducted, signs that may be confused with respiratory distress.
 Points to be noted during the evaluation include the patient's body temperature,
hydration status, heart rate and rhythm, pulse quality, mucous membrane color, and
capillary refill time. The thorax should be carefully auscultated and a thorough oral
examination performed, including looking under the tongue. Oral examination may
require sedation or anesthesia. Patients unwilling to allow an oral examination are often
the ones that need it most.
 A rectal examination is also important. The prostate should be carefully evaluated in male
dogs and the urethra palpated in both males and females. A rectal examination may also
be indicated in cats but should be withheld until the animal is sedated or anesthetized. It
is important to evaluate the character of the feces during the rectal examination.

ABDOMINAL EVALUATION

 This is one of the most important parts of the physical examination and has to be a
thorough exploration of each organ system. Visual inspection of the abdomen may tend to
localize signs of trauma or of distension which can be symmetrical or asymmetrical.
Abdominal distension may be caused by the six F's (fat, food, fluid, flatus, feces, fetus) or
by a tumor.
 Depending upon the quantity of gas, percussion may yield signs of tympany indicating
mechanical obstruction or acute gastric dilatation. Free peritoneal fluid may be identified
16
 by ballottement. Palpation may be difficult because of protective spasm of the abdominal
muscles in response to pain. Spinal cord trauma and other, nonsurgical, conditions also
result in a rigid abdomen.
 Foreign bodies, intussusception, calculi, enlarged organs and abdominal masses may be
palpated in the cooperative patient. Other important findings include identifying fluid or
gas filled bowel loops, a plicated or thickened intestinal segment, or a mass (tumor,
intussusception or foreign body).

DIFFERENTIAL DIAGNOSIS

 Each of the patient's problems should be considered and differential diagnoses identified
and ranked according to their probability based on the signalment, history and physical
findings. A complete list of differential diagnoses is listed in Table 1.

Table 1. Differential Diagnosis of Acute Abdominal Pain

 Digestive system
o Gastric or duodenal ulcers
o Gastritis, gastroenteritis
o Gastric dilation, volvulus
o Intestinal obstruction (foreign body, intussusception, incarcerated strangulated
hernia)
o Intestinal perforation, volvulus
o Pancreatitis, pancreatic abscess
o Gastroenteritis
o Inflammatory Intestinal Disease (parvovirus, panleukopenia, hemorrhagic
gastroenteritis, hookworm infection)
o Portal hypertension
o Ruptured bile duct, necrotic cholecystitis
o Ruptured diaphragm with gastrointestinal tract compromise
 Urinary system
o Obstructive calculi in ureter or urethra
o Urethral obstruction with or without hydronephrosis
o Uroperitoneum (ruptured bladder, urethra, ureter)
o Acute nephritis (acute renal failure)
o Pyelonephritis
o Urethral obstruction, feline lower urinary tract disease
o Neoplasia
 Reproductive system
o Ruptured Pyometra
o Metritis (post partum)
o Labor/dystocia
o Uterine torsion
o Testicular torsion
 Peritoneal Cavity
o Hemoabdomen
 Trauma
 Vascular Neoplasia
 Coagulopathy
 Diapedesis
17
 o Septic Abdomen
 Gastrointestinal tract perforation (ulcer, tumor,
 Loss of blood supply, foreign body)
 Splenic torsion
 Ruptured pancreatic abscess
 Trauma
 Blunt trauma (tissue necrosis, infection)
 Penetrating trauma (bite, knife, gunshot wound)
 Ruptured pyometra
o Hydroabdomen
 Ascites (not usually painful)
 Feline infectious peritonitis, cholangiohepatitis
o Uroabdomen
 Bladder , urethral rupture
 Infectious disease
o Infectious canine hepatitis
o Leptospirosis
 Musculoskeletal
o Intervertebral disc disease
o Ruptured abdominal muscle
 Trauma--abdominal traumas can result in
o Ruptured viscus
o Fractures
o Shock
 Miscellaneous
o Ruptured tumor
o Poisoning (lead, thallium and arsenic can cause abdominal pain)

CLINICAL PATHOLOGY

 The number of laboratory tests utilized depends upon a selection made in the light of the
history and physical findings. Some studies should be carried out on all patients; others
are indicated only to confirm a provisional diagnosis.
 Studies that should be considered routinely include: the packed cell volume and total
solids (PCV/TS), red cell count, total and differential white cell count, creatinine or BUN,
glucose, urinalysis and fecal examination. Hypoglycemia may suggest sepsis. A low PCV
may indicate hemorrhage, although anemia can result from other disorders. Anemia from
hemorrhage may not be immediately evident because of splenic contraction or volume
depletion. A low protein suggests decreased production or losses due to gastrointestinal,
renal or peritoneal disease. Azotemia may also be due to renal failure, shock or sepsis.
 If available, a full serum chemistry profile can help evaluate abdominal disease, although
many abnormal results are non-specific. Hepatic enzyme activities may be increased
because of hepatic injury, sepsis, hypoxia or pancreatitis. A complete white blood cell
count helps determine if inflammation is present which can be associated with sepsis, or
peritonitis. The WBC differential count may suggest an acute, chronic or degenerative
response. Urinalysis may provide information about the patient's urine concentrating
18
 ability and hydration status, the presence or absence of urogenital hemorrhage or trauma,
or the potential source of infection e.g., pyelonephritis.
 Paracentesis and abdominal lavage are valuable diagnostic aids in the evaluation of
abdominal disease and should be considered in patients which have had abdominal
trauma or have ascites. Cytological evaluation of any fluid obtained often provides
valuable clues to diagnosis.

RADIOGRAPHIC EXAMINATION OF THE ABDOMEN

 Radiographic examination of the abdomen often plays a valuable and important part in
the early diagnosis, prognosis and management of the patient with acute abdominal
disease.
 Survey radiographs of the thorax and abdomen may reveal pathologic anatomy with a
minimum of manipulation of the patient and with results available in a much shorter
period of time than data from many laboratory tests.

Contrast Radiography

 Upper GI series--this can define obstructions, perforations or inflammatory changes.

 Pneumocystogram or cystogram defines and determines the integrity of the bladder and
urethra.
 An IVP or renal arteriogram determines the integrity of the kidneys and ureters.
 A pneumoperitoneum can outline the borders of otherwise poorly defined abdominal
organs.

ULTRASOUND EXAMINATION AND EXPLORATORY LAPAROTOMY

Ultrasound Examination

 Ultrasonography is another very useful imaging technique. An ultrasound examination

can help distinguish surgical from non surgical disease.

Exploratory Laparotomy

 The decision to perform surgery in the patient with an acute abdomen can be challenging.
Sometimes the results of diagnostic testing fail to yield a clear diagnosis and exploratory
laparotomy must be considered a diagnostic test. There are a number of intra-abdominal
lesions that are difficult to recognize or positively define without abdominal exploration.
This is particularly true when the signs are obscure or if they recur with an increase in
severity or frequency.

TREATMENT

 Treatment of the patient with the acute abdomen should always be predicated on
correction or amelioration of the underlying disease. There are nevertheless, certain
fundamental principles that must be applied to all patients. These are the treatment of

19
 shock, antimicrobial therapy, ensuring adequate tissue oxygenation and protection of the
gastric mucosal barrier.
 Fluid loss or sequestration is common in many patients with acute abdominal disease and
fluid therapy and correction of electrolyte disturbances are critical. Diseases that
compromise gastrointestinal integrity can increase the likelihood of bacterial
translocation from the gut, decrease venous return, or cause portal hypertension or
septicemia that predispose the patient to endotoxemia and shock. Intravenous fluid
therapy with a balanced electrolyte solution containing supplemental potassium is critical
in many if not all patients. The administration of blood products or colloids may also
benefit critically ill patients.
 While culture and antimicrobial sensitivity testing are always indicated in instances of
infection, it is prudent to begin empirical antibiotic therapy in a systemically ill patient
while awaiting test results. Appropriate choices of antibiotics include cefazolin sodium or
amoxicillin trihydrate clavulanate potassium. Combination therapy with ampicillin
sodium and enrofloxacin or ampicillin sodium and amikacin sulfate may be used for more
coverage of gram-negative infections. Metronidazole or clindamycin can be used for
expanded anaerobic coverage.
 The gastric mucosal barrier can be disrupted in many patients with acute abdominal
disease. This can occur as a result of hypovolemia or of sepsis which both cause decreased
gastric mucosal blood flow. Portal hypertension can cause a congestive gastropathy with
similar results. The end result is diffuse gastric erosion or ulceration with loss of blood
and tissue fluid. This can be minimized with aggressive prophylactic therapy early in the
disease process. Intravenous ranitidine is a good initial choice with an oral proton pump
inhibitor in severe disease. Oral sucralfate is also beneficial since it forms a protective
shield over the eroded mucosa.

BLEEDING

20
 Bleeding is a common clinical presentation in small animal practice. Bleeding disorders
occur more commonly in dogs than in cats. Clinical manifestations of bleeding disorders
may range from mild and self-limited to life-threatening hemorrhage requiring
immediate medical attention. Animals may bleed due to vascular injury caused by any
trauma, surgery, ulcer, and tumor. In case of hemostatic disturbances, the hemorrhagic
tendency is exaggerated as exemplified by spontaneous, multifocal, and unexpected
severe bleeding.

COAGULATION CASCADE

 The coagulation cascade is a series of enzymatic reactions involving coagulation factors.

This complex biochemical pathway plays three pivotal roles in the formation of fibrin
from fibrinogen:
o Acceleration of fibrin generation >10 million-fold
o Regulation of fibrin plug size appropriate for injury
o Localization of fibrin clot formation to site of injury
 The coagulation cascade can be divided into an extrinsic and intrinsic system which
merge into the common pathway. When blood vessel walls are injured, the extrinsic
coagulation system is initially activated by tissue factor (thromboplastin produced in the
subendothelium), which combines with factor VII. The small amount of thrombin
produced through Factor VIIa appears sufficient to activate factor XI to factor XIa and
also to activate other cofactors (factors V, VIII, XIII). Through the action of factor XIa on
factor IX, thrombin formation is maintained. The other contact phase coagulation factors
(e.g., factor XII) are in vivo of lesser importance in the activation of the intrinsic system.
The above described coagulation process explains why hemophilic (Factor VIII and IX
deficient) or Factor VII deficient animals bleed, whereas Factor XII deficient animals do
not.
 Coagulation factors are enzymes, cofactors, or substrates of particular reactions of the
coagulation cascade. Most factors are given roman numerals from I-XIII, but the
numbering is not sequential and there is no factor VI. Calcium (factor IV) is required for
most reactions and is the reason why chelators, e.g., citrate and EDTA, are used for blood
collection and processing, where plasma or blood cells are analyzed. All coagulation
factors are synthesized in the liver and circulate as inactive precursors in the plasma.
21
 They need to be activated at the site of vessel injury. Vitamin K is needed for the
functional synthesis of the coagulation factor II, VII, IX, and X. The half-lives of the
coagulation factors vary from hours (Factor VII) to a few days (Fibrinogen). Following a
fibrin plug formation, plasminogen will be activated and plasmin, an unspecific protease
will commence breaking down fibrinogen as well as fibrin which results in fibrinogen lysis
and fibrin (-ogen) split product (FSP) as well as D-dimer formation.

DIAGNOSTIC APPROACH

 Signalment & Family History: Although hereditary coagulopathies may occur in any
breed, each coagulopathy has thus far only been reported in certain breeds. Hemophilia A
and B occur in many different breeds and are X-chromosomal recessively inherited; thus,
only males are generally affected and females are asymptomatic carriers. Signs of
bleeding typically occur at an early age and are often recurring, but may not be recognized
until adulthood.
 History: Bleeding may be induced (trauma, surgery) or appear spontaneous. Careful
history taking may reveal exposure to toxins (rodenticides, mushrooms) and drugs
(warfarin, heparin). It is important to identify the specific product, as e.g., different
rodenticides have quite varied potency. Any evidence of other diseases, e.g.,
hepatopathies and cancer, may be responsible for the hemorrhage.

PHYSICAL EXAMINATION

 Careful clinical evaluation may differentiate between primary and secondary hemostatic
defects. Surface bleeding is typically seen with primary hemostatic disorders. Petechia
and ecchymosis are hallmark features of thrombocytopenias and thrombopathias.
However, von Willebrand disease (vWD) is causing bleeding at sites of injury (trauma,
dental disease, estrus, gastrointestinal) rather than petechia or ecchymosis.
Coagulopathies may be associated with single or multiple sites of bleeding characterized
by cavity bleeding such as hematoma, hemarthrosis, hemomediastinum,
hemoperitoneum, and hemothorax, but gastrointestinal hemorrhage and bruising may
also occur. Signs of other underlying diseases may be recognized.

Hemostatic Test

 Hemostatic tests are indicated:

o whenever an animal is bleeding excessively
o prior to surgery when an increased bleeding tendency is suspected
o to monitor therapeutic interventions
o for genetic screening in certain breeds or families with a known bleeding disorder.
 Hemostatic abnormalities should be assessed prior to instituting therapy whenever
possible or at least appropriate blood samples should be collected pretreatment. Excellent
venipuncture with discarding of the first few drops of blood (to avoid platelet activation
and tissue factor) and extended compression over jugular, saphenous or femoral vein is
required. The cuticle bleeding time crudely assesses overall hemostasis, but is not
standardized and painful and is, therefore, not recommended. A minimal database
includes a packed cell volume and total protein evaluation. Evaluation of a blood smear
can provide a platelet estimate and identify platelet size and clumping as well as

22
 schistocytes. The results can provide some measure of the extent of blood loss and red
blood cell transfusion requirement.

PRIMARY HEMOSTASIS: PLATELETS & VWF

 Since 8-15 platelets are normally found per high power oil emersion microscopic field, an
absence to low number of platelets suggests a severe thrombocytopenia. Hemorrhage is
generally not observed unless the platelet count is <40,000/µl (normal 150-500,000/µl).
Detection of platelet-associated antibodies further supports an immune-mediated
thrombocytopenia, but this test is rarely available. Serum titers or PCR tests for tick-born
and other infectious diseases are indicated in certain countries or areas.
 The presence of schistocytes and thrombocytopenia suggests intravascular disseminated
coagulation, where intravascular fibrin strands fragment erythrocytes. Because von
Willebrand disease is such a common mild primary hemostatic defect in dogs, plasma
vWF measurements by ELISA are indicated. Alternatively, DNA testing is available in
some canine breeds for breeding purposes.
 Finally, in light of normal platelet count and plasma vWF values, a prolonged buccal
mucosal bleeding time (BMBT) indicates a thrombopathia. Disposable devices are
available that facilitate making 1-2 standard 1mm deep mucosal incisions. The platelet
function analyzer (PFA100) is a simple tool to functionally assess primary hemostasis.
Electron microscopic and platelet aggregation and nucleotide studies allow further
characterization of platelet dysfunctions in specialized laboratories.

SECONDARY HAEMOSTATIC TESTS: COAGULATION TESTS

 Whereas the whole blood clotting time test is insensitive and inaccurate, there are several
standardized coagulation screening tests that are useful to define coagulopathies in
clinical practice. The screening tests assess coagulation in vitro, which is helpful, but is
now known not to be identical with the in vivo coagulation process. Nearly all coagulation
tests assess the function of certain parts of the coagulation system in fresh whole blood or
fresh (frozen) plasma to generate fibrin in a fibrometer; recalcified citrated plasma is
used and many tests are comparing a patient sample directly with a simultaneously
obtained control or pool plasma (plasma from 10 animals). Generally coagulation times,
the time to clotting (fibrin formation), are much shorter in small animals than in humans;
thus, tests need to be validated for the animal species.
 The intrinsic and common pathways are assessed by either the activated coagulation time
(ACT) or activated partial thromboplastin time (PTT). Factor XII of the intrinsic cascade
is activated by diatomaceous earth (celite) in the ACT test and by kaolin or other contact
phase substrates in the PTT test.
 The extrinsic and common pathways can be assessed by either the prothrombin time (PT)
or the protein induced by vitamin K antagonism or absence (PIVKA) test. Different tissue
factors (thromboplastins) are activating factor VII, which in turn will lead to fibrin
formation. It should be noted that the PIVKA test is not specific for the detection of
anticoagulant rodenticide poisoning, but detects any coagulation factor deficiency of the
extrinsic and common pathway and does not add information to the generally run PT
test.
 Until recently the ACT tube test was the only point of care test available for clinical
practice, whereas PTT and PT tests were performed in reference laboratories. There are
now new point of care coagulation instruments (e.g., SCA2000) introduced that are
23
 capable of determining without delay on small amounts (50µl) of fresh citrated whole
blood the PTT and PT, thereby making the chilling, rapid separation of citrated plasma
and shipment of frozen plasma on dry ice to the laboratory for initial coagulation
screening unnecessary.
 In fact, a reasonable and simple approach for a bleeding animal to be screened for a
coagulopathy would be to measure the ACT or PTT first as either test detects all
coagulopathies (except for hereditary factor VII deficiency in Beagles). If the PTT (or
ACT) is prolonged, a PT test would be indicated to differentiate between an intrinsic and
common pathway defect or a combined coagulopathy involving several coagulation
factors.
 Although hereditary coagulopathies can be suspected based upon the pattern of
coagulation test abnormalities, specific factor analyses are needed to confirm a diagnosis.
A bleeding male animal with a prolonged PTT (or ACT) and normal PT likely has
hemophilia A or B (factor VIII or IX deficiency), an X chromosomal recessive disorder.
However, factor XI deficiency is associated with the same test abnormalities and is
inherited by an autosomal recessive trait (e.g., Kerry blue terriers). Finally, factor XII
deficiency, particularly common in domestic shorthair cats, and prekallikrein deficiency
causes marked PTT (ACT) prolongations but no excessive bleeding tendency.
 Rodenticide poisoned animals that are bleeding or are at risk for bleeding will have
prolongations in all of the above coagulation tests, but would have a normal thrombin
time (TT). The thrombin time is independent of vitamin K-dependent coagulation factors
and is a functional assay for fibrinogen to form fibrin. The PIVKA test is not diagnostic,
but a toxicological investigation (product identification, blood toxicology analysis) may
confirm the rodenticide poisoning. Moderate thrombocytopenia may be associated with
rodenticide poisoning.
 All liver diseases may result in varied coagulopathies due to impaired coagulation factor
synthesis and vitamin K malabsorption. Similarly, disseminated intravascular
coagulopathies (DIC), due to many different disorders is associated with variably
prolonged coagulation times. More helpful to the diagnosis of DIC are the recognition of
schistocytes, thrombocytopenia, low antithrombin III levels, and increased D-dimers and
fibrin split (degradation) products.

Hemostatic Tests in Clinical Practice

Test Normal Dog Disorder

PCV % 37-55% Anemias; May not be evident in
first few hours
Total Protein 5.5-7.5 g/dl Hypoproteinemias with external
blood loss
Platelet estimate 8-15 per oil field Thrombocytopenias also
Platelet count (1/15,000 per µl) schistocytes
150-400,000/µl
Buccal mucosal < 4 minutes Thrombopathias vWD
bleeding time (BMBT)
von Willebrand factor (vWF) 65-150% also mutation von Willebrand disease
tests for breeding

24
Activated clotting <110 seconds (tube assay) Intrinsic and common
time (ACT) coagulopathies
Partial Thromboplastin Time PTT) 12-16 seconds (Lab*) Intrinsic and common
54-94 seconds (SCA coagulopathies
2000)
Prothrombin time (PT) 10-14 seconds (Lab*) Extrinsic and common
12-16 seconds (SCA 2000) coagulopathy
Protein Induced by Vitamin K <25 seconds Like PT, not specific for warfarin
Antagonism/Absence (PIVKA)
Thrombin time (TT) 10-12 seconds (Lab*) Hypofibrinogenemia functional
Fibrinogen 100-300 mg/dl Hypofibrinogenemia
(precipitated)
Fibrin split products <1:5 (Lab*); <5µg/dl Fibrin(-ogen) degradation in
(FSP/FDP) (Lab*) DIC
D-dimers <250µg/dl; Fibrin degradation in DIC
-/+ with kit
Antithrombin III 90-120% (Lab*) Low levels with thrombosis, DIC

TREATMENT OF BLEEDING DISORDERS

 Hemostatic disorders can be conveniently classified into vasculopathies,

thrombocytopenias, thrombopathias, von Willebrand disease (vWD), and coagulopathies
realizing that some disease processes cause combined hemostatic defects (e.g.,
disseminated intravascular coagulopathy [DIC]). A high suspicion of a hemostatic
dysfunction based upon signalment, history, clinical signs, and laboratory tests, as well as
definitive identification of the specific hemorrhage defect is important in order to
institute promptly the most effective and safe treatment. Whereas the diagnostic
approach to the bleeding patient was discussed in the previous presentation, this lecture
will cover the treatment modalities for hemorrhage focusing on transfusion medicine.
o Depending on the severity of the hemorrhage conservative prevention of further
hemorrhage to intensive care and transfusion support may have to be instituted.
There are several general therapeutic principles to consider:
o Provide local hemostasis with wound pressure, ligations, and topical agents.
o Rehydrate the patient in case of rapid blood and other fluid losses with
electrolytes; avoid plasma expanders as they can induce a bleeding tendency.
o Collect diagnostic blood samples prior to treatment as blood components and
drugs can affect results.
o Transfuse packed red blood cells as needed for the correction of severe anemia.
o Administer other blood components to replenish deficient or consumed
coagulation factors and rarely platelets.
o Remove triggering agents such as toxins in a household and infectious agents with
antimicrobial therapy.

25
 o Treat underlying disease whenever possible, including vitamin K supplementation,
immunosuppression, and other specific therapy.
o Monitor the patient's bleeding tendency and overall well-being, prevent
reexposure to toxins, delay any harmful surgical interventions, and avoid exposure
to drugs that impair hemostasis (e.g., aspirin, acepromazine).

TRANSFUSION THERAPY

 Only blood type compatible blood should be administered. Thus, patient and blood
donors should be typed with simple in practice or laboratory methods, and previously
transfused animals also need to be crossmatched to assure compatibility and prevent
transfusion reactions. As canine blood donors should not have received any blood
products previously their plasma should not contain any alloantibodies. However, cats do
have naturally occurring alloantibodies and a particularly plasma from any type B cats
contain very strong anti-A antibodies. Thus plasma transfusions should also be blood
type matched.
INDICATION OF BLOOD COMPONENT THERAPY

Disease FWB SWB PRBCs PRP FFP CRYO

Anemia x x ?
Thrombocytopenia/ Thrombocytopathia x ?
Coagulopathies Acquired & inherited x ?
Von Willebrand D. & Hemophilia A x ?

Legend: ? = best component, x = other options, FWB = fresh whole blood, SWB = stored whole
blood, PRBCs = packed red blood cells, PRP = platelet-rich plasma, FFP = fresh frozen plasma,
CRYO = cryoprecipitate

 For routine transfusion, it is not necessary to warm blood after removal from the
refrigerator. Care should be taken to not overheat the blood products while thawing them
(<37C). Blood components that have been prewarmed cannot be refrozen/refrigerated.
Blood bags are connected to blood infusion sets that have an in-line microfilter. A long
(85 cm) blood infusion set with a dripping chamber and a short infusion set (30 cm) for
small dogs and cats to connect with syringes are available. Use a latex-free infusion set for
platelet administration to avoid platelet aggregation.
 Microfilters with 170µm pores are commonly used to remove clots and larger red cell and
platelet aggregates. Finer filters with 40µm pores will remove most platelets and
microaggregates.
 Blood components are best administered intravenously. Ideally, an indwelling catheter
(16-22 gauge depending on size of animal) is placed into the cephalic or saphenous vein
on extremities may be used. In case an intravenous access cannot be obtained, red blood
cells and plasma may be administered by intramedullary (or intraosseous) infusion at the
trochanteric fossa (or other site). Avoid concurrent administration of drugs or fluids other
than physiologic saline through the same catheter in order to prevent lysis of erythrocytes
and blood coagulation.

26
 RATE OF TRANSFUSION

 Rate of transfusion depends on the hydration status, degree of anemia, and general
health condition of an animal. Initial rate is slow, starting with 1-3 ml over the first 5
minutes to observe for any transfusion reactions, even with blood typed and/or cross
matched transfusions. This is followed by a rate of about 10-20 ml/kg/hr. In animals with
cardiac failure, do not exceed 4 ml/kg/hr. Transfusion of a single bag should be
completed within 4 hours.
 The transfusion trigger varies widely depending on the rapidity of anemia onset and
degree of the anemia as well as severity of clinical signs; there is no specific PCV at which
to transfuse, but at a PCV of <15-20% oxygenation of tissues becomes drastically reduced.

VOLUME OF TRANSFUSION

 Volume of blood component to be administered depends on the degree of anemia and the
size of the animal.
 Volume (ml) of whole blood = 2 x PCV rise desired (%) x body weight (kg), or in other
words, Administration of 2 ml whole blood/kg body weight raises the PCV by 1%.
 PCV rise desired is the aim for PCV after transfusion minus the recipient's actual PCV;
this formula assumes that the PCV of the blood bag is >40%. Monitor response to
transfusion by obtaining PCV/TP readings prior to, immediately, and 6 and 24 hours post
transfusion, and consider continued blood loss and/or hemolysis.
 In thrombocytopenia or thrombopathia, one unit of PC, PRP or FWB will increase the
platelet count by 10,000/µL in a recipient weighing 30 kg. In animals with serious or life-
threatening bleeding, the platelet count should be increased to above 40,000/µL. Platelet
counts are monitored prior, 1 hour, and 24 hours after platelet transfusion.
 In coagulopathies and von Willebrand's disease, FFP at 6-10 ml/kg is an initial dose to
stop bleeding or avoid excessive bleeding during surgery. In some cases, larger volumes
and repeated administration of FFP may be needed to control bleeding. Cryoprecipitate at
a dose of 1 CRYO unit/10 kg or 2-4 ml/kg body weight twice daily is ideal to treat
hemophilia A and von Willebrand's disease. Plasma support should be provided for an
additional 1-3 days after the bleeding has been controlled to allow for healing and prevent
rebleeding.

IMMUNE - MEDITATED THROMBOCYTOPENIA

 Platelets in the form of platelet rich plasma, platelet concentrate, or fresh whole blood,
are only transfused when the patient has severe uncontrolled or life-threatening bleeding.
In fact transfused platelets given to IMT patients have a very short survival of a few
minutes to hours and thus do not generally increase the blood platelet count despite
providing transiently improved hemostasis.
 Beside treating the underlying disease, such as ehrlichiosis, babesiosis, and drug allergy,
immunosuppressive agents are used to impair the macrophage system and production of
platelet antibodies. Glucocorticoids are the first choice either in the form of prednisone at
1-2 mg/kg or dexamethasone at 0.2-0.3 mg/kg BID; the initial dose is slowly tapered after
the recognition of a response by no more than one third the dose every 2 weeks.
Vincristine at 0.02 mg/kg strictly IV once may accelerate the platelet count recovery by
impairing the macrophage system, stimulating platelet release from the megakaryocytes
and platelet production. Other immunosuppressive agents such as cyclosporine,
27
 azathioprine, and intravenous immunoglobulin may also be considered, but their efficacy
and safety have not been documented. Finally, splenectomy is highly effective in
corticosteroid refractory IMT in human patients, but has not been adequately evaluated
in dogs

VON WILLEBRAND DISEASE (VWD)

 Cryoprecipitate, a product rich in vWF, is the blood component of choice. The dose is
approximately 2-4 ml/kg or about 3-4 units of cryoprecipitate per Doberman pinscher.
The cryoprecipitate or FFP transfusion may have to be repeated every 8-12 hours
depending on the control of hemorrhage.
 In cases of mild hemorrhage or in order to prevent excessive bleeding during minor
surgeries, desmopressin at a dose of 1 µg/kg once subcutaneously may provide adequate
hemostasis for a few hours. Desmopressin may improve vascular integrity as the observe
increase in plasma vWF following desmopressin injection is very minimal. The effect of
cryoprecipitate, FFP, and desmopressin can be monitored with the buccal mucosal
bleeding time one hour after the injection.

VITAMIN K ANTAGONISM (RODENTICIDE POISONING) AND

DEFICIENCY

 Only if the rodenticide has just been ingested should emesis be induced. When critically
bleeding, vitamin K-dependent coagulation factors can be replaced with fresh frozen
plasma at 10 ml/kg q 8-12 hours or with 20 ml/kg fresh whole blood, if also anemic.
Vitamin K1 at an initial dose of 3-5 mg/kg per os or subcutaneously at several spots is
followed by 0.5-4 mg/kg per os once daily depending on PT or PTT/ACT response. The
dose and duration of treatment depends on the type and amount of the ingested
rodenticide. In cases of malabsorption or biliary obstruction low parenteral doses of
vitamin K are effective.

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

 Without being able to remove the trigger and treat the underlying disease (infection,
cancer, IMHA, heat stroke), any therapeutic intervention seems futile. Administration of
electrolyte fluids to maintain tissue perfusion and attempts to correct acidosis and hyper-
/hypothermia are considered important supportive measures. However, the approaches
to stop intravascular coagulation and supplement coagulation factors are highly
controversial. No controlled studies in human patients and animals have documented
their benefit.
 Heparin at a dose of 50-250 IU/kg either every 4 hours or by constant infusion have been
recommended; the goal has been a 1-2 fold prolongation of the PT time above normal, but
direct serum drug concentration measurements may also be helpful. Low molecular
weight heparin has also been used, but cannot be monitored by the routine PTT. Other
anti-thrombotic agents are also being investigated. Despite the assessment of various
therapeutic strategies none have been documented to be effective in clinical practice in
animals with DIC.

28
 BLOOD TRANSFUSION

Rationale for therapy

 Whole blood is a mixture of cellular constituents suspended in a liquid transport medium.

The cells have different functions. Erythrocytes carry oxygen and participate in host
defense by surface adsorption and absorption of many materials, phagocytes control
bacteria, platelets are required for hemostasis, and lymphocytes mediate immunity. The
liquid medium also contains an array of dissolved substances: albumin, globulins,
coagulation proteins, metabolic intermediates, electrolytes, organic anions, and trace
elements. Practical techniques for separation and concentration of some of the cellular
constituents of whole blood are within the capabilities of all major veterinary blood donor
centers. Modern transfusion therapy should be based upon use of components to treat
specific defects with concentrates of the deficient blood constituent.

Consideration of the limited resource

 The most cogent argument supporting component therapy is that blood is a precious
resource considering its therapeutic potential and the logistics and costs required in
obtaining and delivering blood products. Separation into components permits a single
donation to meet the individual needs of more than several patients. Blood donor
screening eligibility criteria should be sufficient to obtain a safe donation.

Kinetic Considerations

 Following hemorrhage, homeostatic mechanisms restore the various blood constituents

at differing rates, depending on the capacity for synthesis, endogenous consumption,
degradation, and distribution in various physiologic compartments. The half inactivation
time of canine and feline red cells is in terms of months whereas the half-life of albumin is
just three to four days. Surgical blood loss may require restoration of red cells. Albumin
29
 may not be required as it will be restored within several days. Another consideration is
tolerance. Loss of fifty percent of red cell mass is well tolerated in a healthy individual
whereas loss of fifty percent of blood volume can be fatal unless rapidly corrected.

Consideration of Adverse Effects

 Other rationale for supporting the use of blood components include the myriad of
possible adverse effects that can result from transfusion of unnecessary blood
constituents. Any transfusion reaction means that the transfusion is not doing the
intended job and, importantly, has burdened a patient already burdened by the
physiologic state requiring transfusion. Sensitization to blood cells can result in refractory
results in subsequent transfusions. Transfusion of multiple units of whole blood
sequentially in order to achieve a certain hematocrit may also produce pulmonary edema
due to volume overload.

Blood Donor Screening

 All blood donors should be given thorough physical examinations at each donation and be
annually screened hematologically, biochemically, and serologically. Donors should be
healthy, receiving adequate nutrition, and be parasite free. All donors should be blood
typed and be current on appropriate vaccinations. Female donors should not have had
pups or kittens and preferably not be intact. In addition, all canine donors should be
screened for brucellosis, heartworm microfilaria, ehrlichiosis, Rocky Mountain spotted
fever, trypanosomiasis, and systemic mycoses. Feline donors should be house cats not
allowed to roam. Cats should be screened for retroviruses, heartworm microfilaria,
toxoplasmosis, and hemobartonellosis.

BLOOD TYPING

 The feline AB blood group system consists of three blood types: type A, type B, and type
AB. All type B cats have strong alloantibodies against type red blood cells. Type A cats
have weak but potent anti B alloantibodies in terms of the life expectancy of transfused
type B cells. These alloantibodies are responsible for transfusion reactions and neonatal
isoerythrolysis in cats and can be detected by crossmatch procedures. Feline patients
receiving blood products should receive donor products of the same blood type as the
patient and have had crossmatch testing which indicates compatibility. Cats with the rare
AB blood type should receive AB blood (often quite difficult to obtain) or type A blood
which is compatible or only slightly incompatible in the minor crossmatch. There are no
feline "universal" donors.
 A simple "in-house" card test for feline red cell antigens A, B, and AB and canine DEA 1.1
has The dog has eight different blood types identified as dog erythrocyte antigens (DEA)
1.1, 1.2, 3, 4, 5, 6, 7, and 8. The use of DEA 1.1 and 1.2 positive blood products that are
crossmatch incompatible may cause hemolysis. Controversy exists as to whether DEA 7 is
an important determinant in canine transfusion reactions. Ideally canine blood negative
for DEA 1.1, 1.2 and 7 should be used as it conforms with the concept of "universal" donor
blood. In random source, first time canine transfusion of non-crossmatched or typed
blood the transfusion reaction rate is approximately fifteen percent. Again, transfusion
reaction indicates that the materials transfused are not effective and are causing a
physiologic burden on an already burdened patient--reasons to blood type and
crossmatch. Recently there has been suggestions that the only significant canine antigen
30
 is DEA 1.1. Donors blood products negative for DEA 1.1 that are crossmatch compatible
have a much reduced chance of transfusion reaction. Recently, card tests to detect feline
blood types A, B, and AB and canine blood type 1.1 have become available.

CROSSMATCH OF BLOOD

 Crossmatching reveals the presence of naturally occurring isoantibodies or antibodies

generated in response to a previous incompatible transfusion. Crossmatching does not
prevent sensitization of the patient to future transfusions. In fact, even though a specific
blood donor is crossmatch compatible with the patient, if five or more days have elapsed
since the first transfusion, another crossmatch must be performed if more blood products
are to be administered and especially when the same donor blood products will be used.
 Crossmatching is a simple technique that can be performed with standard laboratory
equipment. A major, minor, and autocontrol crossmatch should be performed although
the minor crossmatch is rarely used in dogs. The major crossmatch should always be
compatible at room temperature and at 37 degrees Celsius (°C).
 The following is a simple (nonpurist) major crossmatch protocol (donor red cells and
patient serum or plasma):
o Centrifuge EDTA or citrated DONOR blood at the LOWEST centrifugal rate
possible on your centrifuge...for about 10 minutes.
o Remove 0.2 mLs of packed and place in 4.8 mLs of normal (0.9%) saline. Mix.
(There are now 5.0 mLs in the tube; this essentially replaces washing step.)
o Place 0.1 mL of this mixture into three small test tubes.
o Place 0.1 mL of PATIENT serum or plasma into each of the three tubes described
above. Each tube will now have 0.1 mL of the donor red cell-saline mixture and 0.1
mL of patient serum or plasma, a total of 0.2 mLs each.
o Incubate-for 15 minutes-one tube at 37 degrees C, one at room temperature (25
degreesC), and one at refrigerator temperature (4 degrees C).
o Centrifuge briskly for one minute.
o Examine the supernatant for any hemolysis. Any hemolysis indicates crossmatch
incompatibility.
o Examine the cell button. Flick or swish the test tube. The fluid in the tube should
redden as red cells disperse. If the button is agglutinated or microagglutinated
(examine a drop under low microscopic power), this indicates crossmatch
incompatibility. To complete the minor crossmatch, use patient red cells & donor
serum or plasma. To complete the autocontrol use patent red cells and patient
plasma. In dogs the minor crossmatch is useful for a patient receiving multiple
plasma product transfusions.

BURNS

 Burnt small animals are trauma patients with many complications over them. There are
many different sources of burn lesions: electrical, chemicals, direct heat, fire, fireworks,
etc. A common cause of burn in small animals is the use of electrical heating pads during
surgery or in cage hospital management.
 The care of burn patient will therefore be divided into 3 stages:
o From arriving to 36 hours
o Early period: 36 hours after arrive to 5 days
o Inflammation-Infection period, after the first week

31
 Burn injuries are extremely complex, with compromise of respiratory, cardiovascular,
dermatological systems, and require a proper understanding and management of
physiology, endocrinology, nutrition and immunology status of the patients, to give them
appropriate treatment.
 Burns affect primarily the skin, and the degrees of injury are related to the depth and
extension surface affected. The skin have many different roles in the normal physiology of
the body: is the primary barrier against invasive infection, help to maintain the body
temperature controlling the evaporation of fluids, adapts to aggressions or changes in the
environment like pain, cold and heat. All these functions are impaired in burned animals
and have been related as secondary cause of death.
 Affected surface can be approached by burned body segments: Each forelimb means 9%
each rear limb means 18%, head and neck 9%, Trunk and abdomen 18%. Burn depth has
been classified according the degrees of injury:
 Superficial or first degree involves the epidermis layer, partial-thickness or second degree
involves the epidermis and mid to deep amount of dermis, and the full-thickness or third
degree there is complete destruction of the skin and compromise structures of the
subcutaneous.

I STAGE CARE : FROM ARRIVING TO 36 HOURS

 The initial assessment should start with the general physical condition, systemic
compromise, amount of body and surface affected, plus degree of local injury. If the lost
area of skin are large enough, euthanasia can be recommended.
 People involved in fires have respiratory injury due to the inhalation of air heated to a
temperature higher than 150°C that results in burns into the mouth, oropharynx, and
upper airway. Pulmonary damage due to smoke inhalation, is the major cause of
mortality in human beings. Deaths are associated to the fall of oxygen concentration in
the environment, inhalation of carbon monoxide and dioxide during combustion and
cyanide toxicity. This mechanism is more rare in small animals, apparently because they
walk almost at floor level.
 Animals affected by smoke inhalation should be placed on 100% oxygen early after arrive
to ICU. Inhalated heat produces upper airway obstruction due to airway edema. Early
endotracheal intubation is crucial, and must be performed if physical exam shows signs of
airway burn damage or if patient shows respiratory distress. It is important consider that
pulse oximetry cannot evaluate the severity of hypoxia because its lacking capability to
differentiate between oxygenated hemoglobin and carboxyhemoglobin.
 The initial therapy is oriented to pain relief with cold direct application in the burn area:
chilly water, soak towels, cold tap water are good alternatives. Oxymorphine alone or
combined with Acetylpromazine in neuroleptanalgesia is indicated for pain control in
dogs. Cats can be treated with Diazepam plus Ketamine.
 Oxygen 100-150 ml/Kg/ per minute should be initiated, as soon as possible and a central
catheter into jugular vein should be placed. Give fluid replacement at 4 ml/Kg per hour in
dogs and 2 ml/Kg per hour in cats. Isotonic balanced electrolyte solution like Lactated
Ringer's or normal Saline is the first choice. Free glucose fluids must be avoided because
hyperglycemia and glucosuria will occur after deep burns.
 Potassium levels should be monitored because during the first 24 hours it will be a rise
with severe hyperkalemia associated to cells destruction into the burned tissues.
Solutions with contents of 4-5 mEq/L of potassium are recommended during this phase.
 Check out serum protein levels, urine production, hematocrit level, hemoglobin,
electrolytes and blood gases. If total protein drops below 3 gm/dl, fresh plasma or
32
 colloids should be added. Acidosis can be corrected with Sodium bicarbonate 5 mEq/Kg
of body weight, every hour or 30 minutes. If hematocrit falls below 20% or, hemoglobin
falls below 7 g/dL, whole blood or washed red blood cells must be added to the treatment.
Hct above 30% is the goal.
 After start analgesia treatment the hair must to be clipped, burn wound can be washed
with antiseptic solutions as povidone iodine or chlorhexidine. Necrotic tissues, foreign
material and debris must be removed.
 Burn wounds of first or second degree should be topically treated with antibiotic
medication; (Silvadene is the first choice) and bandaged. With third degree burns, eschar
must be removed soon and in a daily frequency. That is a very painful procedure, so
anesthesia or proper analgesia should be considered. Eschar remove must to show
healthy underlying granulation tissue.
 Systemic antibiotics do note penetrate eschar, so topical therapy is always indicated with
antibiotic ointments and creams. Gentamycin, Polymyxin, Neomycin, and bacitracin are
very effective against the contaminant flora in burn wounds, as well as fluoroquinolones.
 Last reports with Aloe vera shows certain antiprostaglandin effects that can help to
maintain normal dermal vasculature.

II STAGE CARE : 36 HOURS AFTER ARRIVE TO 5 DAYS

 This period of time is a transition from flow phase of shock to the hypermetabolic phase.
The main problems in this stage are:
o Pulmonary problems
o Hemodynamic stability
o Proper care of burn wounds
o Pain and anxiety control
 The main pulmonary problems come up from airway obstruction due to thermal or
chemical burn of the airway mucosa. Adequate laryngoscopy is very helpful to assess the
real damage. Long term intubation should be considered, if mechanical ventilation is
available.
 Cough and increased mucous production are very common in this period, related to
mucosal irritation. However, the damage and impairment of ciliary function, leads to
infections as: bacterial tracheobronchitis, pneumonia or bronchopneumonia. Proper
antibiotic selection trough culture of secretions are the first choice for this complications.
 Evaporation is a major source of water loss within the burn wounded areas. An
estimation of the loss must be obtained to perform proper fluid therapy. Anemia is
another complication caused by red cells destruction plus bone marrow impaired
production.
 Fluid therapy is a keystone during this period of time. Fluids with 5% glucose with small
amount of sodium are indicated because there are no major losses of sodium during this
stage. No aggressive fluid therapy are currently indicated: 60-70 mmHg as mean arterial
pressure, checking urine production around 1-2 ml/Kg/ hour. Albumin level around 2,5
g/dL is the goal, with hematocrit should be kept over 30%, considering whole blood
transfusion.
 It is important to remember that burn animals has major effects over the immune system,
associated to impaired cell mediated immunity, decrease in the neutrophil function, and
compromise of the humoral immune response. With all these effects, infection should be
a major complication in the wounds care. Culture, biopsy analysis and antibiotic studies
must be performed in order to specific control over infection. Wound cleaning, excision

33
 and escharotomy are regular that procedures, can be used to obtain proper samples for
culture.
 Careful handling of stress, anxiety and pain are extreme important in the small animal
burn patient: narcotics as morphine, oxymorphine, butorphanol and low doses of
benzodiazepines are indicated. Phenothiazines must be avoided because their
extrapyramidal side effects in burn patients.

III STAGE CARE

Inflammation-Infection period, after the first week

 Sepsis, SIRS and septic shock are common during this period. Adequate nutritional
support are very important for clinical outcome. Feeding tubes are first choices in
starving animals.
 Pulmonary infections and RADS (Respiratory Acute Distress Syndrome) remains as
major causes of mortality during this period.
 Partial ventilatory support could be useful if necessary.
 Treatment in human patients commonly include anabolic agents, in order to attenuate
catabolism during this phase. There is no information available in small animals patients
to support this management.

SEPTIC SHOCK

 Septic shock is a common complication in small animal practice and the most common
cause of shock in most humans ICU. Many pathologic conditions can result in spread
infection and associated Shock. The overuse of corticoids, immunosuppressive therapies,
the wide spread use of IV catheters are some of the reasons that septic shock has become
more familiar for Veterinary practitioners.
 Effective management requires prompt recognition of early clinical signs related to
systemic inflammation: mental depression, hyper or hypo body temperature, elevated
heart rate, respiratory impairment in addition to a potential source of infection.
 Shock has been defined as a critical imbalance of cellular energy production because
failure in the delivery of oxygen and nutrients to the cell and utilization of oxygen and
nutrients by the cell. More than 90% of the energy that the cell spends is about to survive
from an aggressive environment. Shock may be result from any syndrome, diseases state,
or injury that leads to a critical decrease in effective blood flow to the tissues, leads to
derangement in cellular metabolism and ultimately cell death.

SEPSIS

 Sepsis is defined as the systemic inflammatory response to infection. Therefore systemic

inflammatory response syndrome (SIRS) is a complicate syndrome that may occur as a
result of trauma, burn, sepsis and is currently defined as patients that show two or more
of the following criteria:
o Temperature > 39.7 or < 37.8 oC
o Respiratory rate > 30 bpm or PaCO2 < 32 mm Hg.
o Heart rate > 160 bpm (dog) or > 250 bpm (cat)
o White blood cell count > 19,000 or < 4,000 or > 10% band neutrophils

34
 Septic shock is actually a combination of the 3 types of Shocks: hypovolemic, cardiogenic
and distributive. In early stages of septic shock (hyperdynamic phase), patients may show
dark red mucous membranes with a short capillary refill time (CRT<1 second), elevated
heart and respiratory rate, fever, bounding pulses and signs associated to peripheral
vasodilation. In more advanced stages mucous membranes may see grey and dry,
Increased CRT, weak pulses. These patients need a Emergency Team approach, because
the different procedures and exams that such a patient require.
 Data about of septic patients should be collected to determine if they have any
predisposing factor in history as immunosuppressive therapy or chemotherapy, as well
metabolic diseases such as Cushing's Syndrome, Diabetes mellitus or viral infections as
Parvovirus.
 Blood samples should be obtained for culture, complete blood count, prothrombin time,
partial thromboplastin time, clinical chemistry panel and blood gas evaluation. In the
same way, urine sample must be obtained by centesis for urinalysis and culture.

TREATMENT

 The aim of treatment in septic shock is care, improve and maximize oxygen delivery to
the tissues to address their demands. Two or three largest possible catheter should be
placed for fluid administration and if possible, a jugular catheter for asses central venous
pressure.
 The adequate fluid and administration rate choice for fluid therapy remains as a very
controversial issue. Initially you can start with a crystalloid fluid at 70-90 ml/kg in dogs,
45-60 ml/kg in cats, looking forward a hemodynamic stability (Blood pressure, Capillary
refill time, Central Venous Pressure, Good quality and rate Femoral Pulse, Mucous
Membrane Color, Peripheral temperature).
 If there is not adequate response to therapy, the remainder volume can be given as a
colloid such as Haemacell, Dextran or Hetastarch (10-20 ml/kg/day). Therefore, colloids
should also be considered if the total protein is less than 3.5 gm/dl. In cats, the best
response is achieved with colloid bolus 5-10 ml per cat. If there is a glucose level less than
60 mg/dl, a bolus of 50% dextrose should be given at a volume of 0.5-1 ml/kg, diluted
with and equal volume of saline, IV.
 If the microorganism source can be identified, samples should be aseptically obtained and
submitted for culture and sensitivity. While wait for the culture results, antibiotic therapy
should be instituted. Broad-spectrum antibiotics should be selected based on the
suspected pathogen organism.
 Intravenous empirical antimicrobial therapy directed to all potential infections sources
should be given as early as possible. Coverage should always include Staphylococcus,
Streptococcus and E. Coli.
 Infectious process requiring surgical drainage or debridement should be treated
promptly. Cardiopulmonary unstable function is not an acceptable reason to delay
surgical treatment if sepsis is the cause of instability.
 Frequent complications associated to the Septic Shock patients are sepsis and GI
ulceration. Use of Famotidine, Ranitidine may help to reduce the risk of ulceration. If
there is evidence of GI hemorrhage, Sucralfate is indicated by oral tube if needed.
 Nutrition is the key to maximize the likelihood of healing in septic patients, and enteral
nutrition is the best choice to feed both to the patient and to the enterocytes. If the patient
do not eat despite adequate GI protective and antiemetic drugs, a pharyngei-esophageal
tube can be placed for short-term enteral nutrition. Otherwise, total parenteral nutrition
(TPN) is very expensive and does not provide nutritional support of the enterocytes.
35
  Finally, good hospital care is very important for the patient's well being, like prevention of
decubital ulcers keeping patients on soft padded surfaces covered with absorbent material
to prevent scalding by urine and feces. Catheters must to be checked daily and the
entrance point must be routinely disinfected.

ANTIBIOTICS AND DOSES RECOMMENDED IN SEPTIC PATIENTS

Drug Dosage Route Freq Gram Spectrum

Ampicillin 20-40 mg/kg IV TID G+, G-, some anaerobes
Penicillin G, 20,000- IV, IV, TID G+, G-, anaerobes
aqueous 100,000 U/kg SC
Cefazolin1 20 mg/kg IV TID G+, some G-, some anaerobes
Cephalothin1 20-30 mg/kg IV QID G+, some G-, some anaerobes
Cefotaxime3 20-80 mg/kg IV, IM TID G+, some G-, some anaerobes
Cefoxitin2 20 mg/kg IV TID some G+, some G-, some
anaerobes
Trimethoprimsulfa 15 mg/kg IV, IM BID some G+, G-, some anaerobes
Enrofloxacin 5-10 mg/kg 5-20 IV IV SID some G+, G-
mg/kg
Ciprofloxacin 5-15 mg/kg 10-20 PO PO SID some G+, G-,
mg/kg
Amikacin 10-15 mg/kg IV SID few G+, good G-,
Gentamicin 6-9 mg/kg IV, IM, SID few G+, good G-,
SC BID
Tobramycin 2-4 mg/kg IV TID few G+, good G-,
Clindamycin 10-12 mg/kg IV BID some G+, few G-, anaerobes
Metronidazole 10 mg/kg IV as CRI TID Anaerobes, protozoa

 Note: 1first, 2second, 3third generation

FEEDING TUBES

Goals of nutritional support

 Minimize metabolic derangements

o Maintain hydration
o Attenuate acid-base disorders
o Attenuate electrolyte disturbances

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 o Provide disease-specific nutrients
 Provide nutrients to facilitate recovery
o Suppress hypermetabolic response
o Restore or reverse protein catabolism and negative nitrogen balance
o Maintain gastrointestinal tract integrity and function
o Optimize immune function
 Maintain lean body mass and body weight
 Avoid complications associated with refeeding

TYPES

 There are 2 main "Golden Rules" of nutrition: 1. If the gut works, use it, and 2. Keep it
simple.
 There are several different techniques available that facilitate "using the gut". These
include forced feeding, appetite stimulation, and tube feeding. Feeding tubes offer a
means to provide nutrition to an animal that is unable or unwilling to consume food.
Placing a tube within the gastrointestinal tract may provide enteral feeding. Such tubes
include orogastric, nasoesophageal, pharyngostomy, esophagostomy, gastrostomy, and
enterostomy tubes.

OROGASTRIC AND NASOESOPHAGEAL FEEDING TUBE

Orogastric feeding tube

 These tubes are often used to provide nutrition to orphaned puppies and kittens. They are
not left in, but are inserted at each feeding.

Nasoesophageal feeding tube

 Nasoesophageal feeding tubes are technically easy to place, and can be used safely in
many animals. Do not use if the patient is comatose or lacks a gag reflex because of risk of
aspiration. Nasoesophageal feeding tubes should probably not be used in animals with
esophageal motility disorders. These tubes may be placed without general anesthesia.
Complications of nasoesophageal feeding tubes include rhinitis, dacryocystitis,
esophageal reflux, vomiting, aspiration, pneumonia, inadvertent tube removal, and
obstruction of the tube. Placement of a nasoesophageal feeding tube is accomplished as
follows:
o An 8 French tube may be used in most dogs and cats; however, in small dogs and
small cats, a 5 Fr tube should be used.
o To place the tube, instill 2-4 drops of topical anesthetic into the nasal cavity, and
tilt the head back. Do this 2 times.
o The distal end of the tube may terminate in the thoracic esophagus or stomach. To
accomplish this, measure the tube to the last rib. I usually place a small piece of
tape as a butterfly to mark the tube and to provide a means of securing the tube
once it is passed. Lubricate the end of the tube.
o Pass the tube into the nasal cavity. In cats, pass the tube ventromedially. In dogs,
pass the tube in 0.5 to 1 cm and then push up on the planum nasale while passing
the tube in a ventromedial direction. Once it has been inserted a little further, flex
the head ventrally to promote passage of the tube into the esophagus and not the
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 trachea. When the animal swallows, continue passing the tube into the esophagus
to the level of the butterfly piece of tape.
o If it cannot be passed beyond the level of the medial canthus, it is probably in the
dorsal meatus. Withdraw and redirect.
o Secure tube using 3-0 nylon and the butterfly tape. Dogs usually require
Elizabethan collars to prevent dislodging.
 Nasoesophageal feeding tubes are easy to place and maintain. Many dogs and cats will
leave them alone as long as there is no tension placed on the skin of the face. Prior to
feeding, you should insure that the tube is still within the esophagus. This can be done by
infusing 5-10 ml of warm tap water and observing for coughing, or by injecting 5-10 ml of
air while ausculting over the abdomen for "gurgling" as air moves into the stomach.
Complications of nasoesophageal feeding tubes include irritation at the nares,
dacryocystitis, inhibition of voluntary food intake, and migration of the tube into the
respiratory cavity. If an 8 French tube is placed, convalescent therapeutic diets may be
blended and administered; however, if a 5 French tube is placed, then only liquid diets
may be administered.

PHARYNGOSTOMY AND ESOPHAGOSTOMY FEEDING TUBE

Pharyngostomy feeding tube

 These tubes are not routinely used.

Esophagostomy feeding tube

 Esophagostomy tubes are easy to place, and a large bore (> 12 French) feeding tube may
be placed in most animals. The advantages of an esophagostomy feeding tube are that
there is no interference with voluntary consumption of food, and that gruels may be used
because of the size of the tube used. Furthermore, because the tube exits caudal to the
oropharynx, esophagostomy tubes provide a means of bypassing the oral cavity and do
not interfere with voluntary food consumption when the animal recovers. Esophagostomy
tubes must be placed under heavy sedation or general anesthesia. It can be placed
surgically, or by using a blind percutaneous gastrostomy feeding tube applicator such as
the ELD PGFTA (Jorgenson Laboratories). In all placement methods, the tube is fixed in
place with a friction suture or tape "butterfly". The tube is capped and bandaged so that
the feeding port exits behind the animal's head. Many cats do not tolerate bandages that
encompass their neck; therefore, I do not wrap esophagostomy tubes in cats. The ostomy
site is allowed to heal by granulation and epithelialization when the tube is removed.
Esophageal has not been reported to occur unless the distal tip of the tube terminates in
the stomach, which may cause gastroesophageal reflux and esophagitis. They should not
be used in dogs with esophageal motility disorders.

GASTROSTOMY FEEDING TUBE

 Gastrostomy feeding tubes may be placed surgically through a small laparotomy incision
or at time of abdominal surgery, or non-surgically using an endoscope (percutaneous
endoscopic gastrostomy tube) or non-endoscopically (blind placement using an ELD
PGFTA, the gastrostomy introducer (Cooke Veterinary Products), or using a stomach
tube).
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 Advantages of a gastrostomy tube are that they can be used in animals with esophageal or
higher disease, a large bore feeding tube (16 to 24 French) can be used so pet food gruels
may be administered, they can be used for extended periods of time (months to years),
and there is no mechanical inhibition of voluntary food consumption.
 A gastrostomy tube placement device can be prepared by purchasing a length of vinyl or
stainless steel tubing from a hardware store. The length of the tubing is determined by
measuring the distance from the nasal planum to the iliac crease and adding 15 cm. The
outer diameter of the tube ranges from 1.2 cm (patients weighing <12kg) to 2.5 cm for
dogs weighing >25kg. The distal tip of a stainless steel tube can be flared and deflected
45o to the long axis of the tube to help displace the lateral body wall. The lubricated tube
is passed through the mouth and into the stomach.
 The tube is advanced until the end of the tube displaces the stomach laterally. Positioning
the animal with its head over the edge of the table and lowering the proximal end of the
tube will facilitate identifying the tube tip through the body wall. A percutaneous needle
is introduced into the lumen of the tube while the assistant firmly holds the distal tip of
the tube between two fingers.
 A skin nick is made over the end of the tube and a 14G over-the-needle catheter is
advanced into the lumen of the tube. Proper positioning of the catheter is confirmed by
moving the hub from side to side and feeling the catheter tip strike the inside of the tube.
 A guide wire prepared from a banjo string or cerclage wire is threaded through the
catheter, into the tube, and out of the mouth of the patient. The tube and catheter are
removed and the wire is attached to a gastrostomy tube, which is secured. The tube is
then pulled into the stomach and through the abdominal wall by placing tension on the
wire at the abdominal wall exit site.
 Gastrostomy tubes can also be placed by using commercially available devices (the ELD
PGFTA or the Cooke gastrostomy introducer). The ELD PGFTA is the only device that
utilizes an internal trocar, whereas the Cooke gastrostomy introducer contains a wire that
is threaded through an introduction needle. Dogs and cats tend to tolerate gastrostomy
feeding tubes well.
 In addition, a low profile gastrostomy feeding tube device may be used for extended
periods of time. Complications with use of gastrostomy feeding tubes include vomiting
with risk of aspiration pneumonia (often associated with administering cold food or food
too quickly), dislodgement of the tube which may result in peritonitis or cellulitis,
peristomal infections, and difficulties in maintaining bandages on dogs and cats.
 Additionally, penetration of the spleen, stomach, or omentum may occur if the stomach is
not insufflated with air prior to positioning the tube against the lateral abdominal wall.
When managing a gastrostomy feeding tube, it is important for the ostomy site to be
observed and cleaned daily. Contraindications to using the blind techniques include
severe obesity, ascites, and esophageal disease.

ENTEROSTOMY FEEDING TUBE

 Enterostomy feeding tubes are usually 5 French tubes that are placed directly into the
duodenum and/or jejunum.
 An advantage of an enterostomy feeding tube is that they bypass the stomach and so can
be used in animals undergoing gastric surgery or in dogs with pancreatitis. However, they
must be placed surgically, and only liquid enteral diets may be used through a 5 French
feeding tube.
 Placement of an enterostomy feeding tube can be done at the time of surgery; therefore,
careful planning is necessary to avoid a second surgery.
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 An enterostomy feeding tube should be placed in the descending duodenum or jejunum.
 The tube should travel in the wall of the small intestine for a few centimeters before it
enters the lumen of the small intestine. T
 he distal end of the tube should be 20-30 cm from the site of entry into the small
intestine.
 The feeding end of the tube should exit the lateral abdominal wall. Usually, liquid diets
are administered through enterostomy feeding tubes.
 It is difficult to pulverize medications into a fine enough powder to prevent them from
occluding enterostomy tubes; therefore, administer only liquid medications.

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