CHAPTER 4. Critical Care

C HA P T E R 4
Critical Care
Samuel D. Hurcombe*
Y INTRODUCTION horses admitted for gastrointestinal disease, administration of

antibiotics, and fasting are such examples.2
The development of critical care in equine medicine has truly In addition to dedicated stalls and personnel, some key
evolved over the past 20 years to deliver high-level care to the equipment for diagnostic and therapeutic purposes are neces-
sickest patients, both adult horses and foals. To this end, criti- sary to deliver optimal care. Fluid pumps, electrocardiographic
cal care has developed into a specialty stream of medicine in (ECG) capabilities, ultrasonography, and point-of-care clini-
its own right in which many of the leading hospitals and foun- copathologic testing capabilities are a few examples. However,
dation criticalists have pushed the envelope in advancing care there is no greater asset in an ICU than methodical, detail-
to our equine patients with improved outcomes. The develop- oriented personnel that serially evaluate their patients and are
ment of the American College of Veterinary Emergency and in tune with even subtle changes.
Critical Care (ACVECC) large-animal group was formed and There are no randomized, controlled studies that advocate
has somewhat legitimized equine critical care as a specialty for the provision of critical care medicine and improved sur-
in its own right. Both members of ACVECC, many of whom vival outcomes. The precedent has been set time and again in
are also specialists in internal medicine or surgery, and other human medicine where, in many instances, dedicated person-
like-minded clinicians around the world, are skilled to run an nel, personalized care, early goal-directed therapies, and novel
intensive care unit (ICU) and deliver urgent and immediate therapies result in greater survival, shorter duration of stay in
care. However, there are still significant challenges and clinical the hospital, decreased morbidity, and lower hospital costs.
obstacles to overcome, yet this exciting field of study is chang- More studies are needed in veterinary medicine to support
ing rapidly and will surely continue to do so. similar outcomes in equine practice.
Critical care is provided to an animal whose condition is The provision of critical care to horses is at the purview of
typically severe, life-threatening, and acute. Early recognition equine clinicians; however, certain criteria appear to be uni-
of a disease state or complex condition is needed to execute versal among specialists, which include horses with parenteral
a diagnostic or therapeutic plan, which oftentimes has a sig- fluid requirement to support the cardiovascular system, sys-
nificant impact on the outcome. For example, in human temic inflammatory response syndrome ([SIRS]; both septic
emergency departments, the administration of antimicrobials and nonseptic causes), (poly)trauma, hemorrhage, cardiovas-
within 60 to 180 minutes of sepsis diagnosis is significantly cular collapse, malignant dysrhythmia, respiratory distress
associated with improved survival.1 (notably lower respiratory dysfunction), acute abdominal dis-
Intensive care is a dynamic process. Patient condition ease (surgical and medical), seizure disorder, and acute neuro-
can change minute to minute, and oftentimes these patients logic decompensation, to name a few.
require fine-tuning of a therapeutic plan over several days. As Therapeutic goals for all patients include providing appro-
such, this is time-consuming, detail oriented, tiring, and often priate care for the primary problems, anticipating complications
physically demanding. Therefore a team of personnel includ- and initiating appropriate preventive therapy, and providing
ing clinicians, technicians, and barn staff is best suited to the appropriate supportive care for all vital body systems.
ICU setting to optimize patient care. In this chapter, salient features of the critically ill patient
Patients in the ICU setting are better suited segregated from profile, diagnostic options, and immediate life-saving thera-
a general hospital population. There is a twofold positive effect. peutics for specific body systems will be provided. Additional
First, ICU patients are often sick, immunocompromised, and specific information on select medical conditions will be cov-
may be at risk of developing opportunistic infection. Second, ered in Chapter 20.
certain ICU populations may be at higher risk of shedding
infectious organisms like salmonella. For example, juvenile Y EQUINE INTENSIVE CARE UNIT
*The editors and authors acknowledge and appreciate the contributions of J. Equine ICUs are becoming increasingly prevalent in clini-
Hardy, P. Marsh, P. Mooresey, B. Barr, B. Waldridge, and Y. Nout as previous cal practice. Common features include housing of patients
contributors to this chapter. Some of their original work has been incorpo- according to type or severity of illness with appropriate biose-
rated into this edition. curity precautions; readily available equipment for diagnosing,
158
CHAPTER 4 Critical Care 159
monitoring, and treating the seriously compromised horse; and

24-hour staffing with professionals who have the knowledge BOX 4.1
Equipment List for Different Levels of Equine
and experience to treat these patients. The goals of the ICU are Intensive Care Units
to provide comprehensive care and improve patient outcomes
while using tools and resources that promote efficiency. BASIC
Several studies describe the general case population and • Fluid administration system: coil sets and fluid hooks
commonly performed procedures and treatments of patients • Electrocardiogram
admitted on an emergency basis to large university referral • Centrifuge
centers.3,4 Because equine emergencies are relatively com- • Refractometer
mon among patients requiring critical care, such information • Glucose meter
provides an initial database for understanding population • Lactate meter
dynamics and the required expertise when staffing the ICU. • Urinalysis strips
Colic or acute abdominal pain is the most common type of • Microscope for cytologic examination/Gram stain
case encountered in emergency/critical care centers, and stud- • Ultrasound including Doppler capability
ies show that expertise is required that can handle both medi- • Oxygen tank and regulator
cal and surgical needs. However, the fact remains that a variety • Biosecurity equipment and personnal protective equipment
of other problems present as emergencies, and the required
skills to deal with these include experience with dysfunction INTERMEDIATE
of most all body systems. Each ICU population will reflect the • Blood gas/electrolyte/glucose analyzer
local horse population type, and regular review of hospital • Complete blood count capability
populations is useful to appropriately allocate resources (staff • Coagulation profile testing
and equipment) to meet the unique needs of the region. • Blood pressure monitor (direct and indirect)
Human ICU treatment requires a multidisciplinary team • Intravenous fluid pump delivery systems
that includes intensivists (i.e., physicians who specialize in criti- • Sling and hoist for down horses
cal illness care), nurses, respiratory care therapists, dieticians,
pharmacists, and other consultants from a broad range of spe- ADVANCED
cialties, such as surgery, internal medicine, and anesthesiology. • Pulse oximeter
Because of patient numbers, costs of therapy, and limitations of • Mechanical ventilator
certain aspects in equine practice, the range of specialists is often • Colloid osmometer
consolidated to fewer, multiskilled, broadly trained individuals. • Capnograph
Integral to the ICU are licensed veterinary technicians who • Continuous electrocardiogram telemetry
provide intensive and continuous care. Generally, good nurs- • Syringe infusion pumps
ing care is pivotal to successful outcomes. The technical staff
are the “eyes and ears” of the ICU and are trained to identify
early subtle changes in patient status and feel comfortable using and drug bags/packs strategically located around the hospital
a range of equipment. The ability to perform common tech- are advisable. Drug expiration dates should be regularly moni-
niques and to recognize changes in condition early is essential. tored and expired medications replaced. Table 4.1 lists several
Box 4.1 lists basic, intermediate, and advanced equipment emergency drugs and dosages used in adult horses. Having
that may be used in the ICU. Again, based on patient popula- emergency drug cheat sheets located in several key areas with
tions, if a practice rarely sees critically ill foals, purchase of a volumes, routes, and indications listed helps all ICU personnel
mechanical ventilator would be a poor economic choice. Regu- deliver safe, appropriate care in an emergency situation.
lar review of equipment to ensure it is in working order as well In addition, assembling packs for specific anticipated emer-
as training for all personnel on new equipment are essential. gency situations, such as all the necessary items for delivering
Commonly performed procedures include patient moni- supplemental oxygen or supplies to perform an urgent trache-
toring, fluid administration, and attention to and provision otomy, and placing these packs in key areas is recommended.
of appropriate analgesia. Monitoring includes close, astute Essential monitoring equipment commonly used in the ICU
observation and serial physical examinations. Use of diag- includes an ECG, a blood pressure monitor, a point-of-care glu-
nostic techniques and laboratory support are adjunctive mea- cometer and lactate meter, a point-of-care electrolyte and chem-
sures that complement competent observation to monitor istry analyzer, an ultrasound unit, a centrifuge for hematocrit
the systemic health of the patient. Parenteral fluid adminis- determination, a refractometer for determining total protein and
tration encompasses routine administration of a wide range urine specific gravity (SG), and urine test strips for urinalysis.
of products, including crystalloids, synthetic colloids, blood, Other monitoring tools to consider are a hemocytometer, micro-
and blood components. Choosing analgesia in the ICU will scope with 100× magnification, equipment for cytologic exami-
depend on the type and severity of pain experienced by the nation (including Gram stains), and a blood gas and electrolyte
patient (e.g., inflammatory pain versus neuropathic pain). The monitoring unit. A colloid osmometer is useful for determining
clinician needs to consider potential adverse effects that also colloid osmotic pressure (COP) in hypoproteinemic horses.
may influence the primary disorder (e.g., limiting morphine Advanced imaging is becoming more common, and the use
use in the abdominal patient to minimize ileus). Multimodal of ultrasound has become an essential component of diagnos-
analgesia techniques are being used that have the purported ing and monitoring critically ill patients. Ultrasound can be
benefits of analgesia being delivered through several mecha- used for identifying and monitoring effusions, intestinal dis-
nisms of action while using lower total doses to the patient. tention, and motility; identifying umbilical structures; moni-
Emergency drugs should be readily available and accessible toring pregnancy; and visualizing ocular structures, among
within seconds to minutes in any hospital. Mobile crash carts other anatomic areas. To enable imaging of a wide variety of
160 PART 1 MECHANISMS OF DISEASE AND PRINCIPLES OF TREATMENT
TABLE 4.1 Emergency Drugs Used for Adult Horses

Drug Dose Dose per 1000 lb Route Comment
Atropine 0.01–0.02 mg/kg 0.3–0.45 mL IV Bradycardia; rescue therapy for
severe bronchoconstriction
Dobutamine (positive 2–10 μg/kg/min (1 vial 900–4500 μg/min IV Use diluted solution within 24 h; it
inotrope) [250 mg] in 1000 mL = is compatible with most IV fluids;
250 μg/mL) do not mix with alkaline solution
calcium chloride/gluconate
Doxapram (respiratory 0.2 mg/kg 4.5 mL IV or topical Do not mix with alkaline drugs/
stimulant) under tongue fluid
Epinephrine 4.5–9 mL IV/IM/SC/ Do not give with bicarbonate, hy-
For anaphylaxis 0.01–0.02 mg/kg Intratracheal pertonic saline, or aminophylline
For asystole 0.1–0.5 mg/kg It does not need to be diluted
when given IV to adults
Double volumes when given
intratracheally
Furosemide 0.5–1.1 mg/kg 5–10 mL IV Pulmonary edema, diuresis,
congestive heart failure
Glycopyrrolate (for 0.001–0.005 mg/kg 2.25–11.25 mL IV/IM/SC Do not mix with alkaline drugs/
bronchodilation and fluids
bradycardia)
Lidocaine (treatment of 1.3 mg/kg loading Loading: 30 mL IV Ensure that product does not
ileus) slowly over 5 minutes Infusion: 67 mL/h contain epinephrine
0.05-mg/kg/min
infusion
Lidocaine (treatment of Bolus: 0.25–0.5 mg/kg Bolus: 5–10 mL IV Ensure that product does not
arrhythmias) (slowly) Infusion: 30–60 mL/h contain epinephrine
Infusion: 20–50 μg/kg/min
Aminophylline 5 mg/kg 2.5 g Nebulized

IV, Intravenously; IM, intramuscularly; SC, subcutaneously.
structures, access to a variety of transducers ranging from 2.5 be routine, large foaling stalls should be available. These stalls
to 10 MHz, as well as a rectal probe, is recommended. may feature mobile separators to facilitate treatment of foals
Oxygen provision for supplementation through nasal while allowing them access to their dams.
insufflation, demand valve access, or for mechanical venti- A central office facilitates oversight of the entire unit. A
lation should be available. Compressed gas cylinders can be central viewing station with either cameras or direct visual-
used but must be stored and handled appropriately to prevent ization of stalls is ideal. The ICU should have adequate stor-
injury. Oxygen cylinders can be fitted with a diameter index age and be uncluttered. Hand sanitizer, wash sinks, and boxes
safety system for connection to a demand valve. At peak flow, of gloves should be easily accessible. Hand washing between
a demand valve can provide up to 160 L/min of oxygen. For patients is essential to prevent spread of nosocomial infection.
each cylinder type, knowledge of the capacity of the cylinder Food preparation areas should be separate, and operators
and the flow rate enables calculation of the amount of time should be diligent in washing hands to prevent cross-contam-
provided. The small portable E cylinders contain 655 L of oxy- ination of pathogens in feed.
gen when full and can provide oxygen for 260 minutes when In the ICU, strict disinfection and isolation protocols
set at a flow rate of 5 L/min. Adult horses may require flow should be in place to prevent nosocomial infections and the
rates of 10 to 15 L/min to have any significant effect on the spread of infectious disease. In addition to hand washing,
fraction of oxygen inspired (Fio2). Larger G or H cylinders hand rubbing with an alcohol-based solution is more effec-
containing 5290 or 6910 L, respectively, allow oxygen supple- tive than hand washing with an antiseptic, probably because it
mentation for longer periods. does not require rinsing and drying of hands.5
The design of the ICU should accommodate the care of Guidelines and standard operating procedures (SOPs) can
horses with a wide variety of problems. All stalls should have the be applied to a variety of aspects of the ICU; for example,
equipment necessary for hanging large-volume fluid bags. Stalls guidelines for the use of antibiotics, guidelines on how to han-
should be free of objects that could cause injury. In addition, the dle multidrug-resistant pathogens, SOPs for personnel inju-
design should include one or two stalls for easy unloading of ries, and so forth. It is recommended that each ICU establish
down horses, and the structure must be able to withstand hoist- “best practice regimens” to optimize care, minimize complica-
ing. A track system to hoist horses off a trailer and transport to tions and mistakes, and maximize patient survival and per-
a surgical table or ICU stall would be a welcome feature. Com- sonnel safety.
mercially made glides are also essential to facilitate safe move- The overarching goal of critical care is to support and
ment of down horses. If care of neonatal patients is expected to treat the patient such that normal homeostatic mechanisms
become fully functional and independent of exogenous sup-

port. Treating and preventing shock, in all its various forms, is Adult Horse: Basic Procedures in
a common theme among patients. Provision of care that main- Critical Care
tains oxygen and cellular metabolic substrate delivery to meet
the unique demands of the patient is key. The clinician often Samuel D. Hurcombe
focuses on a specific disease process or even organ system.
However, because of the systemic consequences of several Expedient acquisition of important physiologic and physical
pathologic processes (e.g., inflammation, neoplasia), methodi- findings in the critically ill horse is essential to formulating
cal and serial evaluations of the entire patient are important. an initial diagnostic and/or therapeutic plan. Regardless of the
This allows the practitioner to identify problems early with nature of the particular condition presented to the clinician,
hopes of instituting early intervention and avoid morbidity. expertise in a variety of technical procedures is required to
Severely ill patients require special attention. Their condition facilitate diagnostic and therapeutic efforts.
is dynamic and can change quickly. These patients may require
rechecking key indices such as coagulation panels or ionized
electrolyte concentrations as frequently as each hour. Cardiac Y VASCULAR ACCESS AND
rhythm reassessment or direct blood pressure measurement ADMINISTRATION OF FLUIDS
may be required on a minute-by-minute basis (continuous
telemetry is particularly beneficial in these patients). Establishing venous access is often crucial in critical care.
Expected and unexpected problems can be encountered Generally, using large veins (i.e., jugular veins, lateral thoracic
in the ICU patient. Horses with focal disease (e.g., injection veins, cephalic veins, and rarely saphenous veins) for access
site abscess) that by itself is unlikely to be life-threatening makes it easier to catheterize and deliver medications, fluids,
can develop multisystemic consequences that jeopardize the parenteral nutrition (PN), and perform blood draws for clini-
patient (e.g., hemolytic anemia, fever, anemic hypoxia, and copathologic monitoring. IV catheters are available in vary-
pigment nephropathy). Oftentimes, the development of seri- ing materials, constructions, lengths, and diameters (Tables
ous problems can be a consequence of a ramped up immune 4.2 and 4.3). In choosing a catheter, the practitioner should
system and SIRS. In health, inflammatory pathways can be consider the desired fluid rate, fluid viscosity, the length of
regulated by antiinflammatory pathways. When the balance time the catheter will remain in the vein, the severity of the
tips in favor of inflammatory pathways, overwhelming acti- systemic illness, and the size of the animal. Determinants
vated systemic inflammation ensues and downstream effects of catheter flow rate follow the Poiseuille-Hagen law: larger
can be observed, such as coagulopathy or acute respiratory lumen diameter (r), shorter length (L), and higher pressure
distress syndrome (ARDS), which may be seemingly unrelated differences (ΔP) between flow into the catheter versus flow out
to the primary disease process. of the catheter result in greater volumes per unit time through
Medication mistakes can be categorized in two main cat- the catheter (Poiseuille-Hagen equation of flow through a tube
egories: therapeutic-related unexpected adverse effects in the [e.g., catheter]):
patient and administration mistakes made by the ICU staff. 4
An example of an adverse effect would be the development of Flow α Pressure gradient (ΔP) × radius (r) /viscosity (η)
antibiotic-associated colitis (AAC). Horses with acute gastroin- × length (L)
testinal disease represent the most common admission to the
ICU. In many instances, these patients are stressed, inappetent In cases in which volume provision is critical, placement of
(often forcibly), and often require intestinal surgery, all of which short, large-bore catheters using a pressurized fluid bag would
are considered to be selection pressures for intestinal dysbio- optimize fluid delivery. Viscosity (η) of the fluid administered
sis.2 These horses also are frequently treated with antibiotics in also modulates a flow rate in which higher viscosity fluids (i.e.,
the perioperative period, which, with preexisting pressures, can natural colloids, blood, blood products) result in slower rates
lead to life-threatening colitis. It is prudent for the clinician to of fluid administration. Cautious use of high flow rates may
exercise good judgment on antibiotic usage and try to institute be more traumatic to the vascular endothelium, increasing
early enteral feeding where possible to help avoid AAC. thrombotic risk.
Medication administration mistakes can also occur. A Catheters are generally made of Teflon or polyurethane. The
recent article highlighted that poor compliance to medication thrombogenic properties of each material should be taken into
recommendations occurs more frequently than anticipated.6 consideration with the patient’s clinical condition. Polyurethane
Mistakes can be minimized by having clear medical records catheters (i.e., MILA International) are considered to be less
that list the generic name of the medication, the dose (e.g., thrombogenic than Teflon; therefore, it is recommended to use
number of milligrams), the amount of units delivered (e.g., this material in patients with clinical coagulopathy or “at risk
milliliters), route of administration, and frequency of dos- for” clinical coagulopathy. Typically these patients are horses
ing: for example, gentamicin, 3000 mg (30 mL), intravenously with hypoproteinemia; SIRS; those requiring blood products,
(IV), q 24 h. PN provision, endotoxemic/hemorrhagic shock, septicemia/
ICU orders should be reviewed by a supervising clinician bacteremia; and horses with inherited or acquired coagulo-
and signed off on as a check and balance, especially when pathic disease. Teflon catheters should be changed every 3 days,
multiple users may be following and carrying out these orders. and polyurethane catheters can remain in the vein for up to 2
Daily rounds with ICU personnel on the patient condition, weeks. Regardless of the type of catheter, the site of vascular
current treatment and monitoring plan, and a discussion of access should be closely monitored several times daily for signs
potential complications is highly informative for ICU staff and of flow disturbance, thrombosis, and/or infection.
helps maintain an open line of communication to ensure that For most applications, over-the-needle catheters are easi-
the orders are clearly understood. est and faster to place and achieve therapeutic goals in adult
TABLE 4.2 List of Available Catheters (by Material Type)

Material Example Comment
Polypropylene Polyethylene tubing, Medicut Highly thrombogenic not recommended
Teflon Angiocath Less thrombogenic
Polyurethane MILA Much less thrombogenic
Silastic Centrasil Least thrombogenic

TABLE 4.3 Commercially Available Catheters (by Construction Type)

Type Description Advantage Disadvantage
Butterfly Needle attached to tubing Ease of use Laceration of vessel; vessel
puncture and extravascular
administration
Over-the-needle Stylet inside catheter for venipunc- Available in large diameter, ease of Limited length of catheter, not
ture insertion flexible, break at catheter and
hub junction
Through-the-needle Short needle inserted; catheter All lengths available, flexible, Technically more difficult to
threaded through needle peel-away needle insert
Over-the-wire Needle serving as guide to insert Flexible, long catheters avail- More technical expertise
wire, which serves as guide for able, ensures proper catheter required to place catheter,
catheter placement expensive

horses. Over-the-wire (OTW) catheters are more technically Provision of an antithrombotic such as clopidogrel (4 mg/kg
challenging to place; however, they are often better tolerated PO once, then 2 mg/kg PO every 24 hours) has been used
long term and are less traumatic to the vascular endothelium. to help prevent thrombotic catheter complications despite
OTW catheters come in single-lumen and multilumen models proven efficacy.
and are often placed in foals and adult horses at high risk for Injection caps should be changed daily or sooner if exces-
thrombotic complications or patients in which multiple solu- sively perforated with multiple injections. Before inserting a
tions may be administered, especially hyperosmolar/hyper- needle, injection caps should be wiped with 70% isopropyl
tonic solutions. OTW catheters are recommended for lateral alcohol and allowed to dry.
thoracic vein catheterization caused by the acute angulation Catheters and extension sets may be secured using adhe-
that the vessel travels into the thorax. Ultrasound guidance sive glue for short-term catheters or directly sutured to the
can assist in catheter placement at this location, particularly in skin using 2-0 nonabsorbable suture material. Care should be
obese and edematous horses. taken to ensure that no part of the catheter is exposed when
Short- and long-extension sets are available as well as being secured.
small-bore and large-bore diameters. Using an extension set Each line can be labeled and the utmost care should be
with a Luer lock that screws into the hub of the catheter is exercised to never break the circuit of any solution contain-
best to prevent dislodgment. In horses with low central venous ing glucose (e.g., supplemented crystalloid solutions or PN)
pressures (CVPs), disconnection of the line can result in sig- to help prevent catheter and line sepsis. Some practitioners
nificant aspiration of air and cardiovascular collapse, notably apply triple antibiotic ointment to insertion sites to prevent
from jugular venous catheters. Moreover, one-way hemostatic infection, although evidence is lacking about the efficacy of
valves are also available to help prevent backflow of blood and this practice. If infection is suspected, the catheter should be
aspiration of air. removed and the catheter tip should be cultured (aerobic and
Horses receiving multiple infusions (i.e., crystalloid flu- anaerobic).
ids and continuous rate infusions [CRI’s]), may benefit from Coil sets are used for stall-side fluid administration for
double extensions in which each fluid/medication type has most adult horses. These are advantageous because they allow
an individual port entering a central line catheter rather than the horse to move around, lie down, and eat without restraint.
“piggybacking” fluids into each other. An overhead pulley system with a rotating hook prevents fluid
lines from becoming tangled.
Catheter Maintenance and Care Solution administration sets are used for short-term fluid
Before using any placed catheter, drawing back on the cath- or drug administration and typically deliver 10 drops/mL.
eter to ensure intravascular placement is advised. Cath- Long coiled extension sets can then be used to connect fluids
eters should be flushed frequently with heparinized saline to the horse.
(10 units/mL) before and after each medication administered Calibrated pumps allow continuous even delivery of solu-
and every 4 to 6 hours after catheter placement. For some cath- tions at designated flow rates (CRI). When using a calibrated
eters that are infrequently used, a “heparin lock” comprised of fluid pump, one should take care to use the appropriate set cal-
20 units/mL heparinized saline instilled in the catheter, fol- ibrated for the brand of pump. These pumps have alarms that
lowed by line clamps, may help preserve the integrity of flow. signal air in the line, an empty fluid bag, or catheter problems.
TABLE 4.4 Parameters Used for Estimation of Dehydration in the Horse

Heart Rate (Beats
% Estimated Dehydration per Minute) CRT (Seconds) PCV/TP (%/g/dL) Creatinine (mg/dL)
6 40–60 2 40/7 1.5–2
8 61–80 3 45/7.5 2–3
10 81–100 4 50/8 3–4
12 >100 >4 >50/>8 >4

CRT, Capillary refill time; PCV, packed cell volume; TP, total protein.
The maximal fluid rate that most commercial pumps can of liters of enterogastric reflux) or estimates of ongoing fluid
deliver is 999 mL/h, which is insufficient for crystalloid deliv- losses to calculate a total volume deficit/requirement for the
ery in most adult horses. Infusion pumps are useful for PN, first 24 hours.
multimodal analgesia, prokinetic therapies, and cardiovascu- The rate of fluid administration depends on the severity of the
lar drugs, to name a few. Some clinicians advocate CRI antibi- critical illness. Horses with profound deficits and cardiovascular
otic administration for time-dependent drugs (i.e., β-lactams) compromise require expedient delivery of resuscitative fluids.
to minimize peak-trough pharmacodynamics and potential The type of fluid also varies, depending on the critical
periods of subtherapeutic (sub–minimum inhibitory concen- nature. Replacement crystalloids typically have higher sodium
tration) drug delivery. and chloride concentrations than maintenance solutions
For large-volume fluid delivery, peristaltic or oscillation that have lower sodium and higher calcium, potassium, and
infusion pumps are available that can deliver up to 40 L/h. One magnesium concentrations. Hyperosmolar solutions and/or
must supervise these pumps constantly when in use because colloid solutions may also be indicated, and, together with iso-
they continue to run even if fluids run out. Large-bore cath- tonic crystalloids, all three types should be considered.
eters should be used to prevent trauma resulting from the jet Special circumstances to consider when delivering fluid
effect on the endothelium of the vein. therapy include patients with renal failure. Both volume and
content of fluid choice should be considered depending on the
Y FUNDAMENTALS OF FLUID THERAPY clinical disease process—for example, anuric renal failure ver-
sus acute tubular necrosis of the proximal convoluted tubule
The provision of fluid therapy to adult horses is a pivotal (PCT) and abnormal fractional electrolyte clearances. Horses
modality in treating the critically ill equine patient. Dehydra- with decreased oncotic pressure may not tolerate high-volume
tion is detectable clinically when the deficit comprises 5% or crystalloid therapy without adjunctive colloid support.
greater. Fluids can be delivered in several methods but most Cardiopulmonary arrest, while dire in nature, is the ulti-
commonly enterally and IV. Intraperitoneal and intraosseous mate form of congestive heart failure, and judicious limited
delivery is less commonly used but possible with specific indi- fluid therapy to allow for enough circulation of cardioactive
cations. Parenteral fluids should be administered to horses who therapies is indicated without excess loading of the vascular
cannot tolerate enteral fluids (i.e., gastrointestinal obstruction, circuit.
esophageal trauma, dysphagia, and/or dehydration estimates
exceeding 5%). Enteral fluids are often more cost-effective and Maintenance Requirements
indicated in cases with mild volume deficits (≤5%) and may In the adult horse, maintenance fluid requirements have been
be more effective for certain conditions than parenteral fluid estimated at 40 to 60 mL/kg per day. This volume likely overes-
delivery (e.g., colonic impaction) and maintenance therapy. timates the actual needs of a resting, fasted animal but appears
to be safe in most situations. Smaller breeds may be more
Rational Fluid Therapy Planning appropriately dosed at 60 mL/kg per day, and heavier breeds
An understanding of fluid types and properties as well as the (e.g., draft horses) are more appropriately dosed at 40 mL/
needs of the patient are essential to design a fluid therapy plan. kg per day. In horses with renal failure, monitoring of body
The clinician should consider several key questions that facili- weight, CVP, and ideally urine output is indicated. If weight
tate developing a fluid regimen: gain, edema, or increased CVP (>12 mm Hg) is evident, the
1. What volume of fluid is required? fluid administration rate should be decreased if not stopped
2. What rate of fluid is required? and other renal replacement therapy (RRT) considered.
3. What type of fluid is required?
4. What specific circumstances (physical and physiologic) do Fluid Deficit
you need to consider? Practical evaluation of hypovolemia caused by dehydration is
The volume of fluid required is determined based on the a subjective estimate using both clinical and clinicopathologic
clinical and clinicopathologic data gleaned from a thorough findings. Table 4.4 lists useful parameters for evaluating acute,
clinical examination and minimum database laboratory work. extracellular dehydration.
Skin turgor, heart rate, mucous membrane color and texture, After obtaining an estimate of dehydration, the clinician
eye position, neurologic status, serum creatinine concentra- can calculate the amount of fluids to be given as follows
tion, and packed cell volume with total protein estimates help (Table 4.5):
the clinician determine a deficit, often expressed as a percent-
age of body weight. Maintenance fluid requirements should Volume (Liters) = Body Weight (kilograms)
be combined along with either quantification (i.e., number × Percent Dehydrated (expressed as a decimal)
TABLE 4.5 Commonly Used Equations in Critical Care normalize. Additional means of monitoring adequate fluid
delivery may include measurement of CVP, arterial blood
Maintenance fluids pressure, and urine output.
requirement (mL) 40–60 mL/kg/day The fundamental basic principle of establishing a fluid
Fluid deficit calculation Body weight (kg) × percent dehy- therapy regimen centers on choosing an appropriate volume
(L) drated (expressed as a decimal) as follows (see Table 4.5):
Electrolyte deficit for Body weight (kg) × 0.3 (ECF ∑
monovalent electro- coefficient) × ([Electrolyte]desired Fluid requirement (initial 24 hours) = (fluid deficit
lytes in abundance in − [Electrolyte]measured) + estimated losses + maintenance needs)
the ECF space (e.g.,
bicarbonate) This is a starting point and subject to change based on clinical
Shock rate of isotonic 80–100 mL/kg in the first 60–90 response of the patient.
crystalloid (mL) min
Fluid Choices
Blood transfusion ([PCVdesired − PCVpatient] × body
Isotonic crystalloid fluids almost always constitute the
volume (L) weight [kg] × 0.08 [blood vol-
foundation of any parenteral fluid therapy regimen. The
ume coefficient])/PCVdonor
type of crystalloid fluid to administer depends on the
Osmolarity (mOsm) 2 × [Na] + glucose/18 + BUN/2.8 results of a chemistry evaluation and disease of the patient.
(when glucose and BUN are Generally, an appropriate volume is most critical. How-
measured in mg/dL) ever, when several options are available, one should decide
Mean arterial pressure 1
⁄3 × (SAP − DAP) + DAP between a balanced electrolyte solution (BES) or isotonic
(mm Hg) saline (0.9% NaCl) as the baseline fluid. Additives can then
Pulse pressure (mm Hg) SAP − DAP be added à la carte to treat specific electrolyte and/or meta-
Cerebral perfusion pres- MAP − ICP bolic derangements.
sure (mm Hg) Table 4.6 lists the composition of various commercially
Abdominal perfusion MAP − IAP
available fluids. Generally, BESs are chosen when serum
pressure (mm Hg)
electrolytes are close to normal or when chemistry analysis
is unavailable, because BESs are generally considered more
Content of oxygen in (1.34 × [hemoglobin] × Sao2) + physiologic.
arterial blood (Cao2 (0.0031 × Pao2) Physiologic saline might be preferable in conditions in
[mL O2/dL]) which potassium restriction is indicated (e.g., hyperkalemic
Delivery of oxygen (mL/ Q (cardiac output) × Cao2 states, such as hyperkalemic periodic paralysis, uroperito-
minute) neum, renal failure) because BESs all contain some potassium.
Oxygen extraction ratio (Cao2 − Cvo2)/Cao2 or BESs, by their nature, also have buffering ability. Lactate in
(Sao2 − Svo2)/Sao2 lactated Ringer’s solution (LRS) requires hepatic metabolism;
Alveolar Po2 (Pao2) Fio2 × (Patmosphere − PH O) − thus, LRS may not be an ideal choice in horses with liver dys-
2
Paco2/0.8 function. In cases of long-term fluid maintenance therapy
A-a gradient PAo2 − Pao2 (greater than 4–5 days), if the oral route is not available, the
practitioner should consider half-strength basic fluids (e.g.,
ECF, Extracellular fluid; PCV, packed cell volume; BUN, blood urea nitrogen; 0.45% NaCl and 2.5% dextrose) to which potassium and cal-
SAP, systolic arterial pressure; DAP, diastolic arterial pressure; MAP, mean cium are added. Long-term fluid therapy with routine BESs
arterial pressure; ICP, intracranial pressure; IAP, intraabdominal pressure. can result in hypernatremia, hypokalemia, hypomagnesemia,
and hypocalcemia.
Routine electrolyte supplementation often includes cal-
Continued Ongoing Losses cium, potassium, and magnesium provision. This is particu-
Objective quantification of ongoing losses is ideal but sel- larly important when the horse receives limited or no enteral
dom truly reflective of all volume deficits. Even measuring intake (e.g., gastrointestinal disease). These electrolytes are
enterogastric reflux volume still does not account for the third important for smooth muscle function, vascular tone, and
spaced volume of fluid within the bowel that remains. This intestinal smooth muscle activity.7,8
remaining volume does not contribute to effective circulat- Suggested doses of calcium depend on ionized calcium
ing volume and, as such, quantification of reflux in the bucket concentrations. Routine supplementation with 10 mL of
underestimates the true volume deficit. Horses with high- 23% calcium gluconate per liter of fluids is used by the
volume diarrhea can also lose significant volumes as well as author as a starting point. Potassium chloride can be sup-
third space volume within the large reservoir of the large colon plemented at up to 0.5 mEq/kg per hour maximum paren-
and cecum. teral rate. The author starts at 0.05 mEq/kg per hour for
Regardless of the nature of ongoing losses, frequent clinical routine supplementation and 1 g magnesium sulfate per
and clinicopathologic reassessment of the patient is imperative liter of fluids.
to minimize further deterioration. Heart rate, measurement Horses with high anion gap metabolic acidosis (e.g.,
of packed cell volume, total protein, and l-lactate concentra- lactic acidosis) are often hypobicarbonatemic because of
tion are clinically useful every 2 to 6 hours, depending on the increased buffering of organic acid production. In most
nature of critical illness. instances, this represents a type A lactic acidosis, such as
Daily creatinine concentration assessment and urinalysis perfusion-mediated hyperlactatemia. As such, volume res-
are indicated in patients with azotemia until laboratory values toration to optimize systemic perfusion should be the first
TABLE 4.6 Crystalloid Solutions Available for Fluid Therapy

Product Approximate pH mOsm/L Na (mEq/L) K (mEq/L) Ca (mEq/L) Mg (mEq/L) Cl (mEq/L) Buffer (mEq/L)
Lactated Ringer’s 6.5 273 130 4 3 — 109 Lactate 28
solution
Lactated Ringer’s 5 525 130 4 3 — 109 Lactate 28
solution and 5%
dextrose
Plasma-Lyte A 7.4 294 140 5 — 3 98 Acetate 27
Gluconate 23
Plasma-Lyte 148 7.4 294 140 5 — 3 98 Acetate 27
Gluconate 23
Plasma-Lyte 148 5.5 294 140 5 — 3 98 Acetate 27
Gluconate 23
Plasma-Lyte 56 and 5 362 40 13 — 3 40 Acetate 16
5% dextrose
5% dextrose 4 252 — — — — — —
0.9% NaCl 5 308 154 — — — 154 —
7% NaCl — 2400 1196 — — — 1196 —
5% dextrose and 4 560 154 — — — 154 —
0.9% NaCl
5% dextrose and 4 280 77 — — — 77 —
0.45% NaCl
5% NaHCO3 8 1190 595 — — — 595 —
8.4% NaHCO3 — 2000 1000 — — — 1000 —
1.3% NaHCO3 (must — 308 154 — — — 1541 —
be mixed)

step in treating the acidosis; however, in extreme cases, option. The deficit is calculated and the number of milliequiv-
supplemental bicarbonate (NaHCO3) treatment may also alents converted to a weight (in grams):
be required.
Horses receiving bicarbonate therapy should have their 1 g NaHCO3 = 12 mEq NaHCO3
respiratory function assessed because carbon dioxide (CO2)
generated from carbonic anhydrase activity requires nor- The total number of grams is divided into several admin-
mal alveolar ventilation for effective CO2 removal. Respi- istrations per day. Orally administered NaHCO3 may cause
ratory compromise will result in worsening of acidemia minor caustic injury to the gingival mucosa. Mixing NaHCO3
caused by mixed metabolic and respiratory acidosis. with Karo syrup or molasses and washing the mouth after the
For horses with a pH ≤7.2 caused by metabolic derange- horse swallows may help prevent injury.
ments (nonrespiratory) following shock crystalloid dosing (80
mL/kg in 1 h), isotonic bicarbonate (1.3%) therapy is indi- Rate of Administration
cated. First, administer 50% of the bicarbonate deficit (see For patients in severe shock, the clinician should strive to
later) rapidly over 1 to 2 hours followed by the remaining 50% administer a shock dose of isotonic crystalloid fluids in the
over 12 to 24 hours. first hour (80 mL/kg), which can be done only with pressur-
Note that parenteral bicarbonate solutions are incompat- ized bags, a fluid pump, and/or multiple catheters.
ible with calcium-containing solutions. The 1.3% sodium In other situations, the volume calculated accounting for
bicarbonate solutions are isotonic, and 8.4% sodium bicar- losses, replacement, and maintenance represents a volume
bonate solutions are hypertonic (1 mEq/mL). To make a 1.3% for the 24-hour requirements and estimates as a volume per
NaHCO3 solution, remove 130 mL of water from a 1-L sterile hour. Accurate record keeping of a running tally of fluids
water bag. Add 130 mL (130 mEq) of 8.4% NaHCO3 to the provided is important to ensure that the correct amount is
sterile water bag. administered.
Bicarbonate de�cit = (Bicarbonatedesired − Bicarbonatemeasured ) Y ORALLY ADMINISTERED FLUIDS

× body weight (kilograms) × �.� (e�tracellular �uid
[ECF] compartment coeﬃcient; see Table 4.5) Oral fluids are indicated in horses with only mild volume
deficits and who can tolerate enteral fluids (e.g., no intes-
For ongoing losses of bicarbonate not associated with tinal obstruction or reflux). Oral fluid therapy should be
excessive plasma buffering (e.g., hypersecretory diarrhea, administered using the fluid composition shown in Table 4.7.
renal tubular acidosis), enteral supplementation is a suitable One should administer calcium separately because it causes
TABLE 4.7 Fluid Composition for Orally Administered Hypertonic Saline Solution (7.2% NaCl)
Fluid Therapy Hypertonic saline solution (HSS) is approximately eight times
the tonicity of plasma and ECF, and the immediate effect is
For Every L of Water, add: to rapidly expand the vascular volume by redistribution of
FOR EVERY 21 L OF WATER fluid from the interstitial and intracellular spaces. The rapid
increase in vascular volume improves cardiac output (CO)
Electrolyte Amount (g)
and tissue perfusion with rapid administration of only a rel-
NaCl 10 atively small volume of fluid. Initially, this is a roughly 1:3
NaHCO3 15 ratio—that is, for every liter of HSS administered, the patient
KCl 75 recruits up to 3 L of volume expansion. This effect is short-
K2HPO4 60 lived (estimated to be ∼20 minutes). Because the electrolytes
redistribute across the ECF, fluid redistribution occurs again
and the patient becomes hypovolemic again. Because the
principal effect is fluid redistribution, a total body deficit still
precipitation of the solution. This electrolyte solution meets exists and it must be replaced. For this reason, concurrent or
daily needs for an adult horse and can be given through a immediately following HSS administration, isotonic crystal-
small, preplaced nasogastric feeding tube or by intermittent loids must be provided to correct the total body volume defi-
intubation. cit. The duration of effect of hypertonic solutions is directly
proportional to the distribution constant, which is the indexed
Parenteral Fluids CO. The dose is 2 to 4 mL/kg, administered as rapidly as pos-
sible. Iatrogenic metabolic acidosis, hypernatremia, and hypo-
Crystalloids kalemia may occur after hypertonic saline administration;
The IV administration of isotonic crystalloids immediately therefore, plasma electrolyte concentrations should ideally be
reconstitutes effective circulating volume. Crystalloids (all evaluated in the patient before and after the administration of
types) rapidly redistribute out of the vascular space (VS) to hypertonic saline.
the entire ECF space. The ECF is roughly 30% of body weight,
and the VS is roughly 8% of body weight. As such, to maintain Maintenance Solutions
a desired expanded intravascular volume, 3 to 3.75 times as Crystalloid maintenance fluids are polyionic isotonic or hypo-
much volume is required to account for redistribution among tonic fluids formulated for long-term use in patients needing
the entire ECF. BESs are typically chosen such as LRS. Doses chronic fluid support beyond fluid volume resuscitation. They
of BESs for rapid volume expansion (not maintenance fluid contain lower sodium and higher potassium, calcium, and
requirements) are 70 to 90 mL/kg per hour with frequent magnesium concentrations. Examples include Plasma-Lyte
(every 20 minutes) reassessment of additional volume needs. 56, Normosol-M, and 0.45% NaCl/2.5% dextrose, and these
fluids should not be used for rapid volume expansion.
Replacement Solutions Colloids
Lactated Ringer’s Solution Colloid fluids contain large molecular weight particles that do
LRS has a lower sodium concentration and higher chloride not readily diffuse across healthy cellular barriers, maintaining
concentration than equine plasma. LRS should be avoided in or increasing COP within the intravascular space. These mole-
cases of hyperkalemia because of low levels of potassium and cules do redistribute to the ECF but at a much slower rate than
when administering products containing citrate or bicarbon- crystalloids; thus, the duration of effect is prolonged compared
ate, because the calcium in LRS may precipitate. Lactate in with that of crystalloids. Table 4.8 describes the different col-
LRS is metabolized by the liver and, in theory, may accumulate loids available. Critically ill patients often develop endothelial
and contribute to metabolic acidosis in patients with hepatic dysfunction, and the associated increased vascular permeabil-
dysfunction. ity may ameliorate some of the beneficial effects of colloids,
dependent, in part, on the average molecular size of the col-
Plasma-Lyte 148 and Normosol-R loid administered. For example, hetastarch (6% hydroxyethyl
Plasma-Lyte 148 and Normosol-R are similar to LRS but have starch) has an average molecular size of 450 kDa, and albu-
a more physiologic sodium:chloride ratio and contain mag- min in plasma has a molecular size of 70 kDa. Further, meta-
nesium rather than calcium. They may be administered con- analyses in humans failed to support the theory of improved
currently with blood products and bicarbonate but should be resuscitation through the use of colloids over crystalloids9;
avoided in cases where neuromuscular blockade is a concern however, colloids may be indicated in patients with hypopro-
(e.g., botulism). The alkalinizing agents in these fluids are ace- teinemia, severe blood loss, or those in need of clotting factors
tate and gluconate, respectively. or immunoglobulins.
A disadvantage of natural colloids (plasma or albumin)
Normal Saline (0.9% NaCl) is that they are more antigenic and can cause allergic reac-
Normal saline consists solely of sodium and chloride in con- tions. Synthetic colloids have a much lower antigenicity, but
centrations significantly higher than that of plasma. Saline they can cause bleeding disorders because of their tendency to
is acidifying and is useful in the treatment of patients with coat platelets or by causing a decrease in coagulation factors.
hyperkalemia and metabolic alkalosis. The use of normal In the horse Dextran 40 can cause anaphylactoid reactions.
saline in cases of hyponatremia is cautioned because overly Hetastarch administration can cause a decrease in coagula-
rapid correction of sodium concentrations may lead to exces- tion factors and prolong clotting times, particularly at high
sive osmotic draw of water from cells. doses (20 mL/kg).10
TABLE 4.8 Characteristics of Colloid Solutions Available for Fluid Therapy

Hetastarch Tetrastarch
Characteristics 5% Albumin 25% Albumin Dextran 40 Dextran 70 (600/0.75) 6% (130/0.4) 6%
Molecular weight (d) — — — — — —
Average 69,000 69,000 40,000 70,000 450,000 130,000
Number average 69,000 69,000 25,000 39,000 70,000
Range — — 10,000–80,000 15,000–160,000 10,000–3,400,000 110,000–
150,000
Solvent — — 0.9% saline or 5% 0.9% saline or 0.9% saline or 0.9% saline
dextrose 5% dextrose balanced
electrolyte solution
Maximum water 18 18 37 29 20 —
binding (mL/g)
Concentration (%) 5 25 10 6 6 6
Half-life 14–16 days 14–16 days 2.5 h 6h 25 h 12 h (human)
Plasma percentage — — 18 29 38 —
(after 24 h)
Extravascular per- — — 22 33 39 —
centage (after 24 h)
Overall survival in — — 44 h 4–6 weeks 17–26 weeks —
blood
Colloid osmotic 20 100 40 — 30 36
pressure (mm Hg)

Synthetic colloids do not register on a refractometer. Accu- of oncotic effect, the potential for adverse reactions (10%
rate evaluation of oncotic pressure requires the use of a colloid incidence),15 and the relatively high cost if given for large-
osmometer. If one is not available, the clinician must use clini- volume resuscitation.
cal evaluation (e.g., observing the presence of edema and poor
circulatory volume and pressure). Whole Blood
Whole blood can be considered the ultimate colloid replace-
Synthetic Colloids ment fluid when indicated in cases of hemorrhage.16 Blood
Hetastarch is a more cost-effective synthetic colloid. Advan- transfusion may restore circulating volume, improve oncotic
tages of hetastarch include maintenance of plasma oncotic activity, increase oxygen-carrying capacity, is a supply vehicle
effect for up to 24 hours following administration and the for therapeutic drug transport, and replenishes coagulation
ability to give as a rapid bolus.10,11 However, unlike plasma, factors. Whole blood is the ideal fluid for blood loss or plate-
there are no functional proteins present in hydroxyethyl let loss, provided that it is fresh blood and has been cross-
starch solutions and a negative effect on coagulation has matched. It is important to remember that stored blood loses
been demonstrated in healthy equids.10,12 Further, a 2013 its oxygen-carrying capacity and it can take several hours to
review of the use of colloids as volume replacement in criti- restore it after administration.
cally ill humans found an increased risk of mortality and Access to whole-blood donors that are free of erythrocyte
acute kidney injury in patients receiving hetastarch.13 As antigenic determinants, particularly Aa and Qa, and of isoan-
such, the use of hetastarch in horses with underlying renal tibodies are important hores to have available to ones practice.
insufficiency is cautioned, and its use is restricted to those The practitioner can perform a major and minor cross-match
with clinical signs of acute hypoproteinemia. Recently tet- to select an appropriate donor, provided that complement is
rastarch (6%) was evaluated and shown to have a more added to the test for hemolysin detection. Interpretation of
sustained effect on COP with fewer adverse coagulopathic the minor cross-match may be difficult if autoagglutination is
effects than hetastarch.14 Both hetastarch and tetrastarch present. If cross-matching is unavailable, use of a non-Thor-
can be dosed at 10 mL/kg. oughbred gelding is advised. Up to 20 mL/kg can be safely
collected every 3 weeks in adult horses, and whole blood can
Natural Colloids: Plasma be collected in sodium citrate using sterile technique provided
Plasma contains not only osmotically active albumin but the product will be used immediately.
a variety of essential proteins, including clotting factors, Commercial blood collection kits are also available. The
immunoglobulins, and antithrombin III. The advantage of reported incidence of transfusion reactions is 16%,17 and a
plasma over synthetic colloids is that these proteins provide recent study showed a marked decrease in transfused erythro-
carrier sites for exogenous (pharmaceuticals) and endog- cyte half-life with an incompatible cross-match (4.7 days ver-
enous (hormones) compounds. Disadvantages of plasma as sus 33.5 days).18 Complications of blood transfusion include
a resuscitation fluid in horses include the prolonged time acute anaphylactic reactions, allergic reactions, hemolysis,
required for administration, a relatively short duration fever, tachypnea, and hypocalcemia caused by citrate chelation.
Oxygen delivery to tissues depends on adequate perfusion

Critical Care Techniques of functional capillary density (FCD) of the tissues. FCD has
recently become a research interest in veterinary species in
Samuel D. Hurcombe which dark-field microscopy has been used to evaluate gin-
gival and colonic perfusion.19 Clinically, FCD quantification
techniques are impractical; thus, blood pressure is used to esti-
Y MONTORING ARTERIAL mate blood flow and tissue perfusion. MAP as a perfusion esti-
BLOOD PRESSURE mate does not account for local regulation of tissue bed blood
flow. Regional shunting, regional vasomotor tone differences,
The goal of blood pressure measurement is to identify hypo- microthrombi, and interstitial edema may all affect local blood
tension and follow the response to therapy after interventions. flow. Blood flow through a vessel is also dependent on the vis-
Mean arterial blood pressures (MAPs) of greater than 70 mm Hg cosity of the fluid (blood) and the radius of the vessel. At high
are targeted in the adult, and pressures greater than 60 mm Hg viscosity blood flow may be impaired. Severe vasoconstric-
are targeted in neonates. Table 4.9 shows expected blood pres- tion, although maintaining blood pressure, may impair flow.
sures in healthy conscious horses. Hypertension is uncommon
in horses. Pheochromocytoma, pain, and transient hypertensive Direct (Invasive) Blood Pressure Measurement
states associated with pressor agents have been described. A 20-gauge or 22-gauge over-the-needle catheter is most
Arterial blood pressure can be measured by direct catheter- commonly used to perform direct or invasive blood pressure
ization of a peripheral artery or by indirect measurements that measurement. Suitable sites for catheterization include the
depend on a cuff placed over an artery and cuff inflation until transverse facial, facial, and greater metatarsal arteries (Fig. 4.1).
blood flow is occluded. Blood pressure can also be calculated as In the standing horse the transverse facial or the facial artery
the product of CO and systemic vascular resistance (SVR). The are most practical. Catheters are placed toward the direction
MAP is a surrogate estimate of tissue perfusion but does not nec- of blood flow (i.e., toward the heart), and noncompliant tubing
essarily correlate with blood flow through the tissue. For example, filled with heparinized saline is used to connect the catheter to
a hypovolemic patient with high SVR may have a MAP within an a calibrated pressure transducer. It is important to flush all air
acceptable range; yet, the actual volume of blood per unit time from the circuit to avoid dampening of the waveform.
flowing through the tissue (e.g., perfusion volume) might be Blood pressures are measured in millimeters of mercury
inadequate. Horses can have low MAP as a result of hypovolemia, (mm Hg), which measures the force exerted by the blood
SIRS, heart failure, or any of a wide variety of disorders. against an area of the vessel wall to raise a column of mer-
Most monitoring equipment provides an estimation of sys- cury by a certain number of millimeters. Occasionally, cen-
tolic arterial pressure (SAP), diastolic arterial pressure (DAP), timeters of water (cm H2O) are used where 1 mm Hg = 1.36
and MAP. MAP is a calculated value determined by integrat- cm H2O. Continuous readings of blood pressure are most
ing the area under the pressure waveform and dividing this by useful clinically and can be graphically displayed using an
the duration of the cardiac cycle. MAP can also be calculated electronic transducer that converts a pressure signal to an
by MAP = 1⁄3 × (SAP − DAP) + DAP (see Table 4.5). electronic output. The transducer and flush device (Pressure
Pulse pressure is the difference between systolic and dia-
stolic pressure (SAP − DAP; see Table 4.5). A bounding
pulse pressure results from an increased systolic pressure, a
decreased diastolic pressure, or both. Conversely, a poor or
weak pulse quality indicates little difference between SAP and
DAP. Ultimately, pulse pressure is not a good surrogate of per-
fusion, and clinical markers of perfusion or quantitative meth-
ods of CO are required for improved accuracy.
TABLE 4.9 Hemodynamic Parameters in Adult Horses

Type of Pressure Blood Pressure Reading
Arterial pressure
Mean arterial pressure >60 mm Hg
(indirect) 106 ± 12 mm Hg
Mean arterial pressure
(direct)
Systolic (indirect) 111.8 ± 13.3 mm Hg
Systolic (direct) 142 ± 18 mm Hg
Diastolic (indirect) 67.7 ± 13.8 mm Hg
Diastolic (direct) 82 ± 12 mm Hg
Central venous pressure 8–12 mm Hg (6–18 cm H2O)

Data from Magdesian KG. Monitoring the critically ill equine patient. Vet Clin
North Am Equine Pract. 2004; 20:11-39; Hurcombe SD, Scott VHL. Direct
intraabdominal pressures and abdominal perfusion pressures in unsedated FIG. 4.1 Adult horse with an arterial catheter in the transverse facial
normal horses. J Vet Emerg Crit Care. 2012; 22(4):441-446. artery for direct blood pressure monitoring.
Monitoring Kit with TruWave disposable pressure trans- Doppler (Systolic Arterial Blood Pressure)
ducer; Edwards Lifesciences, Irvine, CA) then can be used Doppler uses a small ultrasound probe placed on a periph-
for continuous blood pressure measurement. The transducer eral artery, and a piezoelectric crystal within the probe con-
should be maintained at the level of the heart base, which is verts the pulse wave into an audible signal. The probe must be
estimated to be at the point of the shoulder. Pressure record- placed over a shaved area (usually under the tail of the horse)
ing systems should be zeroed to atmosphere before reading after application of a coupling gel. Doppler only measures sys-
from the patient. tolic arterial blood pressure.
When the waveform appears flat or dampened, the line and
catheter should be flushed to yield a “square wave.” When the Oscillometric Sphygmomanometry
flush is stopped, the arterial waveform should resume. This test Oscillometric sphygmomanometry relies on detecting changes
also evaluates the dampening status of the circuit. Immediately in oscillations generated by changes in blood flow during grad-
after flushing, wave oscillations are observed before beginning ual deflation of a cuff. Oscillations are initially detected once
the next arterial waveform. Two oscillations are considered the cuff pressure decreases to be equal to the systolic pressure.
normal. An overdamped system (e.g., clot in the catheter, air Maximal oscillations are detected when cuff pressure is equal
bubble in connection tubing) results in fewer oscillations and to the mean pressure and then disappear when the cuff reaches
lower magnitude. An underdamped system (e.g., long stiff diastolic pressure. The meter records and displays systolic, dia-
tubing) results in a greater number of oscillations. stolic, and mean pressures (Fig. 4.2).
Indirect (Noninvasive) Blood Pressure Photoplethysmography

Photoplethysmography relies on the detection of arterial vol-
Measurement ume by attenuation of infrared radiation. Photoplethysmogra-
Indirect blood pressure measurements depend on a cuff placed phy originally was designed for use in human fingers and has
around the tail (coccygeal artery) or the metatarsus (metatar- been validated for use in small dogs and cats but has not been
sal artery). The diameter of the cuff influences the accuracy evaluated for use in horses.
of the measurement, and cuffs that are too wide result in
underestimation of the blood pressure. An ideal cuff width-to-
circumference ratio of 0.25 to 0.35 has been recommended for Y CENTRAL VENOUS PRESSURE
use on the tail or limbs of horses. Cuff widths are available for
neonate, pediatric, and adult horses. Monitoring Central Venous Pressure
CVP is the hydrostatic pressure within a large central vein, typi-
cally the cranial vena cava, and is an estimate of right atrial fill-
ing pressure. The CVP is affected by vascular volume, venous
tone, and cardiac function. Monitoring CVP is most useful for
patients in which the veterinarian is attempting to maintain
adequate vascular volume without fluid overload. For example,
assessment of CVP may be useful in horses with oliguric or
anuric renal failure, horses with large-volume gastric reflux, and
horses predisposed to edema formation. The venous system has
high volume capacitance, which makes CVP quite insensitive to
subclinical volume overload. By the time CVP measurements
increase, transvenous fluid shifts, and interstitial edema and
volume overload have likely occurred.
Conversely, negative CVP values may reflect hypovolemia,
indicating a need for fluid therapy.20 As with measurements
of arterial blood pressure, the trend in CVP seen through
repeated monitoring is most informative.
CVP is measured by using an IV catheter placed in the
jugular vein and terminating in the intrathoracic portion of
the cranial vena cava. The catheter is attached via an extension
set to a water manometer positioned such that the pressure is
at the level of the base of the heart (point of the shoulder), or
it can be connected to an electronic transducer. The latter is
preferred by the author because the typical CVP waveform can
be visualized to confirm accurate location of the catheter tip.
Normal CVP in adult horses is 8 to 12 mm Hg (6–18 cm H2O).
Y EMERGENCY TRACHEOSTOMY
FIG. 4.2 Indirect oscillometric blood pressure cuff applied to the tail Acute respiratory distress referable to obstruction of the upper
(coccygeal artery) of this 27-year-old Miniature Horse. Lower left inset is a respiratory tract represents a true emergency and need to estab-
close-up of the tail cuff. Lower right inset is the electronic indirect blood lish a patent airway. It is important for the clinician to make
pressure reading. This horse had apparent blindness and was found to a rapid assessment of that patient to determine the anatomic
have hypertensive cardiomyopathy on echocardiography. location (upper versus lower respiratory tract) of obstruction
placement of chest tubes. Indwelling tubes used are typically

BOX 4.2
Materials Needed for an Emergency 20 to 32 Fr and sterile. The location for tube placement is ide-
Tracheostomy Pack ally identified by ultrasound; however, a rough guide for safe
placement is a hand span caudal to the olecranon and a hand
Local anesthetic (2% without epinephrine) span dorsal to the lateral thoracic vein. Where possible, the
20-gauge needle and 10-mL syringe most ventrally dependent location that minimizes trauma to
Sterile, disposable no. 10 surgical blade the heart and lateral thoracic vein is ideal.
Metzenbaum scissors The clinician clips and prepares the site with antiseptic,
Hemostats infiltrating it with 2% local anesthetic. An incision is made in
J-type tracheostomy tube or self-retaining tube the desensitized skin slightly cranial to the proposed point of
entry, and the trocar is inserted through the skin. The clinician
moves the incision in a caudal direction to the cranial mar-
and to decide if a tracheostomy is indicated. Box 4.2 shows the gin of the nearest rib. Using controlled pressure, the trocar is
typical equipment needed for a tracheostomy. advanced perpendicular to the chest wall and in a slight caudal
When possible, the clinician should clip and prepare the direction. Fluid is seen to fill the tube, and the tube is fed off
planned incision site and infiltrate it with 2% local anesthetic. In the trocar. A unidirectional flow apparatus should be placed
cases of true acute respiratory obstruction, the patient may be in on the free end of the tube (e.g., Heimlich valve, latex glove
such distress that surgical preparation is unnecessary. At this time, finger, condom) to allow egress of pleural fluid but preventing
the operator should not waste time and immediately perform the air entry into the chest. The tube is secured at the entry point
tracheostomy without preparation. The clinician makes an 8- using 0 or 2-0 suture with a purse-string and Chinese finger
to 10-cm longitudinal incision at midline at the junction of the trap pattern.
proximal and middle third of the neck, just above the V made by Normal pleural fluid has a protein concentration <2.5 g/dL
the junction of the sternothyrohyoideus muscles. Blunt dissection and total nucleated cell count <5000/μL.
with Metzenbaum scissors is used to expose the tracheal rings. Pneumothorax is classified as open (e.g., external wound)
Next, an incision is made between two tracheal rings, taking care or closed (e.g., bronchopleural fistula). As pleural pressure
not to damage the tracheal cartilages. This incision should be no equilibrates with atmospheric pressure, lung collapse occurs
more than 50% of the circumference of the trachea. In emergency and can be seen as a cranioventral retraction of the lung field
situations a J-type tracheostomy tube is used because of its ease of on radiographs. Tension pneumothorax develops when air
insertion. When the horse is calm, or if the situation is not critical, continuously enters the chest without evacuation and repre-
a metal self-retaining tube is preferable for maintenance because sents a most serious and life-threatening condition in which
J-tubes tend to fall out. Silicone-cuffed tubes are also available for supraatmospheric pleural pressures causes rapid cardiorespi-
closed-system ventilation. ratory demise.
The tracheostomy tube should be cleaned daily and With open pneumothorax, rapid recognition, sealing of
changed as needed. The surgical site should be cleaned with the open wound, and evacuation of air must occur. In open
dilute antiseptic, and saline with petroleum gel applied pneumothorax sealing of the chest must occur, followed by
around the incision prevents skin scalding. Generally, but evacuation of air. Clear plastic wrap (e.g., Saran wrap) makes
particularly in foals, tracheostomy tubes should be removed an ideal temporary sealant that conforms to the chest and can
as early as possible to avoid permanent tracheal deformity. be wrapped around the thorax. Application of silver sulfadia-
To help decide when to remove the tube, the clinician can zine cream around the wound before plastic wrap application
occlude the tube temporarily to see if the horse can breathe provides a secure air-tight seal.
without it. After the tube is removed, the site should be Pleural air is then evacuated via placement of a cannula
cleaned of exudate twice daily and allowed to heal by sec- or 14-gauge catheter in the caudodorsal lung field. The 12th
ond intention. It is the author’s opinion that broad-spectrum or 13th intercostal space is a suitable location. Air is gradu-
antibiotics, such as potentiated sulfonamides, should be ally removed using 60-mL syringes. Reexpansion pulmonary
administered to help prevent local cellulitis and dissecting edema is a concern and can be avoided by slow, gradual air
infection down fascial planes of the neck. The wound gener- evacuation with evacuation pressures <25 mm Hg. As the lung
ally closes in 10 to 14 days and heals in 3 weeks. expands, it begins to “tickle” the cannula end, which is seen
as a twitching of the cannula during inspiration. The cannula
Y THORACOCENTESIS is removed once the air has been evacuated satisfactorily. In
closed pneumothorax or tension pneumothorax, the catheter
Pleural fluid drainage is integral in cases of effusive disease must be kept in place until the source of air entry can be sealed.
and can be life-saving. Prolonged increased pleural pressures
can lead to pulmonary collapse; associated respiratory dys- Y NASOGASTRIC INTUBATION
function; dyspnea; and in severe cases, cardiac tamponade.
Auscultation and percussion of the chest, an increased field of Nasogastric intubation is an essential and possibly life-saving
cardiac auscultation, and transthoracic ultrasound can iden- procedure performed in cases of equine colic. Unless contra-
tify pleural effusion. Different tools can be used to facilitate indicated (e.g., dangerous patient; head, neck, or esophageal
drainage depending on the volume, shock status of the patient, trauma), failing to pass a tube may be construed as negligence.
quality and tenacity of the fluid, and likelihood of the need for The patient should be adequately restrained, with a twitch
continued drainage. Small volumes can be drained using a teat and sedation if needed. The clinician should stand on the
cannula or 14-gauge catheter with the stylet removed. Larger side of the horse, with the hand closest to the horse placed on
volumes, hyperechoic fluid (e.g., pyothorax), proteinaceous the nose, and the thumb in the nostril. With the other hand,
fluid, and horses with infectious pleuritis usually require the clinician passes the tube in the ventral meatus, using the
thumb to keep it directed ventromedially. If any resistance nephrosplenic entrapment of the large colon. Colonic dis-
is met or a hard structure is encountered (possibly ethmoid tention can exert extraluminal pressure on the stomach
turbinates), the user should stop, retract, and redirect ven- and/or duodenum.
trally. On reaching the pharynx, the practitioner should feel The clinician should note the amount of reflux obtained
a soft resistance. The tube can be turned 180 degrees to direct because this factors into ongoing losses, and the volume of
its curvature dorsally. The clinician stimulates the horse to fluids given IV must be adjusted accordingly. Horses with
swallow by gentle to-and-fro movement or by blowing in functional ileus need gastric decompression usually every
the tube. Keeping the head of the horse flexed at the poll is 2 to 4 hours. The nasogastric tube should be left in place
helpful to direct esophageal passage. Once the horse swal- only as long as required, because some horses develop pha-
lows, the clinician pushes the tube into the esophagus. Blow- ryngeal and laryngeal irritation associated with its pres-
ing into the tube to dilate the esophagus facilitates insertion. ence.22 These horses may show pain on swallowing when
If the horse coughs, the clinician withdraws the tube and they resume feeding. Sinusitis can also occur because of
repeats the procedure until the tube is positioned correctly. nasogastric tube placement.23 When tubes are left in place,
Determining correct anatomic placement in the esophagus a small-bore tube that still allows effective gastric emptying
and stomach is imperative. It is signaled by gentle suction, should be used.
which should elicit a negative pressure; shaking of the tra-
chea, which should not elicit a rattle; and visual confirmation Y ABDOMINOCENTESIS
of correct placement (typically just dorsal to the left jugular
furrow). Direct observation is the safest method. The tube is Abdominocentesis is important for evaluating abdominal dis-
advanced until it is in the stomach (14th rib). If the clinician ease, whether it is colic, weight loss, or postoperative prob-
encounters difficulty in passing the cardia, 60 mL of lido- lems. Box 4.3 provides the materials needed to perform this
caine may be injected into the tube. procedure.
Once placed, spontaneous egress of fluid may occur. If The clinician clips a 2 × 2-inch area approximately 3 cm
not, creation of a water siphon to empty the stomach can be caudal to the xiphoid and 1 to 2 cm to the right of midline
achieved by filling the tube with water using a pump or funnel or using transabdominal ultrasound to guide fluid localiza-
under gravity and then immediately directing the end of the tion.24 Various methods are described with different instru-
tube downward. One sign of an empty stomach is retrieving ments. Regardless, the procedure is performed under sterile
froth or foam that can sit on the surface of accumulated gastric technique. Use of a sterile 18-gauge 1.5-inch needle does not
fluid. It is not uncommon to lose fluid during the refluxing require local anesthetic infiltration of the skin and subcutis. If
process in horses in which no appreciable fluid accumulation a teat cannula or bitch catheter is used, local anesthesia infil-
is present. tration is necessary. The operator makes a stab incision with
Medication or intragastric fluids should never be admin- a no. 15 scalpel blade before cannula entry. Two points of
istered by nasogastric tube to a horse with colic with any net resistance will be encountered: as the device goes through the
positive volume of fluid accumulation. abdominal wall and as it goes through the peritoneum. Horses
To remove the tube, creating a fluid lock is achieved by may become agitated when the peritoneum is “tented” before
occluding the tube (putting a thumb on the end or folding it) penetration.
to prevent its contents from spilling out in the pharynx and Fluid should be collected into ethylenediaminetetraacetic
possibly the trachea as it is withdrawn. Gentle traction is then acid (EDTA) and sterile culture containers. Low-yield samples
applied in a direction parallel to the nose. If bleeding occurs, should be collected in EDTA tubes in which the anticoagu-
a towel can be placed over the horse’s nose. Epistaxis, even if lant is shaken out to avoid misinterpretation of fluid analysis.25
severe, is typically self-limiting. In rare cases of severe hem- Obtaining fluid from very dehydrated horses is often difficult,
orrhage, ε-aminocaproic acid administration, nasal packing, especially in cases of simple obstruction.
and intranasal phenylephrine (10 mg in 10 mL saline) can be Normal values and characteristics for abdominal fluid
used to help resolve bleeding. are as follows: clear, yellow in color (able to read newsprint
Nasogastric reflux is not normal. Occasionally, a small through), low turbidity, total protein concentration should
amount of reflux (≤1 L) is obtained if a horse has had a tube be less than 2.5 g/dL, and total white blood cell count
in place for a long time.21 When reflux occurs, the clinician should be less than 5000 cells/μL. On cytologic examina-
should note the amount, character, and timing in relation tion, neutrophils make up approximately 40% to 50% of
to the onset of colic. In addition, the clinician should note cells, with the remainder being lymphocytes, macrophages,
the response to gastric decompression. Reflux originating
from the small intestine is alkaline, whereas reflux com-
posed of gastric secretions is acidic. Typically, reflux refers BOX 4.3
Materials Needed for Abdominocentesis
to small intestinal ileus, functional or mechanical. Lesions
of the proximal small intestine produce large amounts of • 18-gauge, 1½-inch needle
reflux early in the onset of the colic. Inflammatory lesions • Local anesthetic (2% without epinephrine)
(e.g., duodenitis proximal jejunitis) are typically associated • Teat cannula
with copious volumes of reflux caused by the hypersecre- • Bitch catheter
tory nature of the disease process. With lesions of the distal • Peritoneal dialysis catheter
small intestine (ileum) and often mechanical obstructions, • Sterile gloves
one initially obtains no reflux, and as the condition per- • Ethylenediaminetetraacetic acid and culture tubes
sists, one obtains reflux but usually several hours after the • Sterile, disposable no. 15 scalpel blade
onset of the colic. Occasionally, large colon disease can be • Sterile gauze
associated with reflux, notably left dorsal displacement/
and peritoneal cells. l-Lactate concentration should be Subsequently, the white blood cell count remains elevated
equal to that of systemic circulation and in normal horses, for approximately 2 weeks, but on cytologic examination
with <2 mmol/L is appropriate. the neutrophils appear to be nondegenerate and no bacteria
With intestinal strangulation, total protein increases ini- are apparent. The total protein level remains elevated for 1
tially (in the first 1–2 hours) such that the fluid is clear but month after surgery.
more yellow. After 3 to 4 hours of strangulation, red blood cells
also leak, and the fluid is more orange or pink. After 6 hours or Y TROCARIZATION
more, white blood cells increase gradually, with the progres-
sion of intestinal necrosis. Serosanguineous fluid is indicative Trocarization of the cecum, or occasionally ascending colon,
of small bowel strangulation and, in concert with the rest of is useful to decompress the bowel and improve abdomi-
the examination, likely indicates a need for bowel resection if nal perfusion pressure ([APP]; see Table 4.5). By decreasing
possible. l-Lactate concentration in horses with strangulating intraabdominal pressure, APP can be improved in cases where
small bowel lesions is greater than systemic concentrations. obstructive disorders of the large intestine are diagnosed. Tro-
An l-lactate of ≥4 mmol/L or an increase in l-lactate concen- carization provides analgesic relief by reducing visceral dis-
tration on repeat assessment is highly associated with small tention and may relieve dyspnea where significant abdominal
bowel strangulation.26 bloating is apparent. Box 4.4 lists the materials needed for this
Inadvertent enterocentesis can occur, particularly in cases procedure.
with increased abdominal pressure and/or large bowel impac- Trocarization is only indicated for large bowel distention.
tions. Enterocentesis must be differentiated from intestinal Rectal palpation, abdominal auscultation and percussion, and
rupture. Cytologic features of enterocentesis include plant transabdominal ultrasound can help decipher which segment
material, bacteria, and debris but no polymorphonuclear of bowel is distended. Segments of large bowel adjacent to the
cells. Moreover, the clinical condition of the horse is not con- body wall are suitable cases. The right paralumbar fossa and
sistent with rupture (septic shock). With early rupture, clini- cecal trocarization are ideally suited because of the fixed loca-
cal evidence may not be evident for several hours. Cytologic tion of the cecal cupula in the right dorsal abdomen. Cecal
examination of abdominal fluid with intestinal rupture shows tympany commonly accompanies obstructions of the ascend-
neutrophils, bacteria, and bacteria that have been phagocy- ing colon because of cecal outflow obstruction. These are ideal
tized by neutrophils. candidates for trocarization.
Peritonitis can be classified as primary or secondary. Pri- The clinician clips and prepares the site with antiseptic,
mary peritonitis is often idiopathic or associated with Acti- infiltrating a 4 × 4-cm area of skin with a local anesthetic.
nobacillus equuli and covered in more detail elsewhere.27 With gloved hand, the clinician inserts a 14-gauge catheter
Secondary peritonitis is often associated with polymicrobial with an extension tube perpendicular to the skin. The clinician
species when fluid is evaluated cytologically and on Gram places the end of the extension in water so that gas bubbles
stain. Degenerate neutrophils (>90%), the presence of multiple are visible when the tip of the catheter is positioned correctly.
bacteria, and certainly gram-negative enteric species should When gas is obtained, the trochar part of the catheter should
alert the clinician to the possibility of compromised bowel and be withdrawn slightly or removed to keep from lacerating the
may warrant surgical exploration. bowel. It may be necessary to reposition the catheter several
Blood contamination must be differentiated from internal times when gas is not obtained. Connecting the catheter to an
hemorrhage or severely devitalized bowel. Blood from skin or extension set in water can help visualize gas egress (Fig. 4.3).
body wall vessels and inadvertent splenocentesis can cause a Occasionally, a second operator can apply gentle pressure per
bloody “tap.” When centrifuged, the sample often spins clear rectum to facilitate gas egress. After decompression, the clini-
with minor blood contamination from skin. Inadvertent sple- cian removes the trocar and infuses an antibiotic (e.g., genta-
nocentesis will result in a higher packed cell volume than micin or procaine penicillin) while withdrawing the catheter
peripheral blood, which is caused by the erythrocyte reservoir through the body wall.
of the spleen. All fresh blood contamination shows platelets, Complications with trocarization include peritonitis and
which are not present with blood older than 12 hours. In inter- local abscessation. The horse should be observed for 24 hours
nal hemorrhage blood is hemolyzed such that the supernatant for signs of peritonitis. If the practitioner suspects peritonitis,
is reddish after centrifugation; the sample has no platelets and confirmation is with abdominocentesis, and systemic broad-
shows erythrophagocytosis. Ultrasonography also reveals spectrum antibiotics should be administered to the horse until
fluid swirling in the abdomen, especially with acute internal the condition resolves. Serum amyloid A concentrations may
hemorrhage of various causes. be useful for monitoring the response to treatment and opti-
Excess EDTA in a low-volume sample will falsely increase mal time to cease therapy. If a local abscess develops, percu-
the total protein on refractometry (often by 0.9–1.0 g/dL taneous external drainage with local lavage of sterile fluids is
higher). When performing an abdominocentesis, the clinician recommended.
should shake out the EDTA from the tube to avoid this sam-
pling error.
Abdominal surgery increases the total protein level BOX 4.4
Materials Needed for Trocarization
and white blood cell count postoperatively.28 Typically, if
no enterotomy was performed, the white blood cell count 14-gauge, 5¼-inch catheter
increases for 4 to 7 days and returns to normal by 14 days. The Local anesthetic (2% without epinephrine)
total protein level may remain elevated for 3 to 4 weeks after Sterile gloves
surgery. Neutrophils appear to be nondegenerate. After an Extension tubing
enterotomy or an anastomosis, degenerate neutrophils and Small water container (syringe case works)
occasional bacteria may be seen in the first 12 to 24 hours.29
and nutrient requirements. When the cardiovascular sys-

tem fails to meet tissue oxygen demands, a state of shock
ensues. Support of cardiovascular function can be achieved
through the administration of intravenous fluids, antiar-
rhythmics, inotropes, and/or vasopressors, depending on
the nature of dysfunction.
The volume of blood, and therefore the amount of oxygen,
delivered to tissues depends on arterial oxygen content and
CO, which is defined as the amount of blood pumped out
of the heart per minute and is the product of heart rate and
stroke volume. Heart rate may be influenced by a number of
neurologic, endocrine, and physical factors. Stroke volume is
the amount of blood ejected from the heart with each contrac-
tion and is influenced by the venous return of blood to the
heart (preload), the force/duration of contraction of the heart
(inotropy), and the resistance to forward flow (afterload).
CO is not evenly distributed to all tissues in the body as a
result of varying resistance to arterial blood flow dependent on
tissue demands. Contraction of arteriole smooth muscle main-
FIG. 4.3 Cecal trocarization using a 14-gauge catheter connected to an tains a pressure gradient that allows blood to flow from arteri-
extension set in a syringe case of water. oles through tissue bed capillaries, to venules, and back to the
heart. SVR is related to blood pressure and is determined by
vasomotor tone, or degree of vessel constriction, in the systemic
Y URINARY CATHETERIZATION circulation. The greater the SVR, the less blood flow from the
heart through the systemic circulation and the greater the heart
Micturition disorders (lower motor neuron bladder, upper must work to achieve the same CO achieved at a lower SVR.
motor neuron bladder, and urethral detrusor dyssynergy)
may require manual evacuation to relieve the patient and
provide comfort. Measurement of urine output in adult Y CARDIOVASCULAR INSUFFICIENCY:
horses is indicated in horses with oliguric renal failure or SHOCK STATES
when 24-hour volumetric measurements are needed. Thor-
ough cleansing of the urethral fossa and glans penis in males When the cardiovascular system fails to supply sufficient oxy-
and the vulva and perineal region in mares is indicated gen to meet tissue demands, shock develops and cells shift
before catheter placement. Gentle soapy water or saline with to anaerobic metabolism. If left uncorrected, the shock state
roll cotton are suitable options. In mares, urine is easily col- can result in irreversible cellular dysfunction. There are four
lected by placing a Foley catheter connected to collection major categories of shock that are differentiated by underlying
tubing. A closed system can be fashioned by using a solution pathophysiology: hypovolemic, cardiogenic, obstructive, and
administration set and empty fluid bag. In geldings one can maldistributive.30
insert a male urinary catheter and suture it in place using a Hypovolemic shock is the most common type of shock rec-
Chinese finger trap pattern. If the horse is recumbent and ognized in equine patients and results from decreases in effective
thrashing, leaving as little as possible of the catheter protrud- circulating blood volume, which may occur through external
ing to keep it from being pulled out is important. Normal loss (e.g., diarrhea, reflux), third spacing of plasma volume,
horses produce 1 to 2 mL/kg per hour of urine. or hemorrhage. Decreased blood volume results in decreased
venous return to the heart (decreased preload), reduced stroke
volume, and decreased CO if heart rate cannot compensate.
Cardiovascular Critical Care The mainstay of intervention is through restoration of circulat-
ing volume via intravascular fluid administration.
Tiffany L. Hall Cardiogenic shock is associated with impaired ventricu-
lar function as a result of myocarditis, ventricular dysrhyth-
mias, or valvular pathology resulting in cardiac chamber
Y REVIEW OF CARDIOVASCULAR enlargement.31 A decrease in contractility (inotropy) results
PHYSIOLOGY in reduced stroke volume and decreased CO. Therapy is
directed at improving cardiac pumping through treatment of
The cardiovascular system functions to deliver oxygen the underlying condition and use of inotropes when indicated.
and nutrients to tissues throughout the body, as well as Obstructive shock results from lack of blood flow through
to deliver carbon dioxide to the lungs for elimination and the heart or great vessels as a result of thrombosis (atrial or
other wastes from the tissues for detoxification and excre- pulmonary), constrictive pericarditis, cardiac tamponade, or
tion from the body. It is comprised of the heart, the pul- pleural space disease (e.g., pneumothorax).32 This condition is
monary circulation, and the systemic circulation, which act characterized by decreased preload or increased afterload and
in coordination to deliver blood and its constituents to tis- results in circulatory failure.33 Therapy is directed at address-
sues. Through a complex interplay of neuroendocrine path- ing the underlying cause.
ways, the cardiovascular system is able to adapt to different Maldistributive (vasodilatory) shock is the result of abnor-
physiologic and disease states to meet the body’s oxygen mal shunting of blood through microcirculation in the face of
normal CO, leading to tissue hypoxia and metabolic derange- or dysoxic patients. If response to fluid resuscitation is inade-
ment. This may be caused by septic, anaphylactic, or neuro- quate, inotropes provide another means to increase tissue per-
genic causes.33 Central to the pathogenesis of maldistributive fusion; however, these medications increase cardiac oxygen
shock is endothelial dysfunction in response to neutrophil- consumption, so oxygenation should be monitored.31
generated cytokines, proteases, lipid mediators, and oxygen-
derived free radicals.34 Therapy is directed at addressing the Dobutamine
underlying cause, reducing systemic inflammation, and use of Dobutamine is a synthetic catecholamine that has primarily β1-
vasopressors to improve SVR. adrenergic agonist activity with weak α- and β2-affinity. Dobu-
Regardless of the inciting cause, if shock is prolonged and tamine is useful in patients with diminished CO or decreased
severe, the terminal physiologic disturbance will manifest central venous oxygen tension despite adequate fluid volume
as maldistributive shock.35 Successful management of shock restoration. Beneficial effects include increased stroke volume
depends on early recognition and aggressive intervention.36 and decreased heart rate with improved splanchnic perfusion
and urine output. Dobutamine administered to foals with
anesthesia-induced hypotension resulted in increased cardiac
Y CARDIOVASCULAR SUPPORT index, increased blood pressure, decreased oxygen consump-
THERAPIES tion, decreased oxygen extraction ratio, and apparent mainte-
nance of splanchnic perfusion.46
Principles of Management
The goal of therapy in patients with cardiovascular compro- Vasopressors
mise is to restore tissue perfusion and oxygen delivery. Thera- Vasopressors increase vasomotor tone (SVR), which is reflected
pies include fluid resuscitation to restore circulating blood as an increase in MAP. Further, decreased venous compliance/
volume, administration of vasoactive medications (inotropes/ capacitance increases venous return (preload), which improves
vasopressors) to improve CO and vascular tone, and directed CO.37,38 Careful monitoring and titration of these medications
therapies at the underlying disease condition. Fluid therapy must be performed to avoid excessive vasoconstriction, which
has been discussed earlier, and the remainder of this section would increase SVR (afterload), thus increasing cardiac work-
will focus on cardiovascular-specific therapies. load and potentially decreasing stroke volume and CO.
Vasoactive Drugs Norepinephrine
Vasoactive drugs (e.g., inotropes and/or vasopressors) may Norepinephrine (NE) has predominantly α1-adrenergic ago-
be administered if tissue perfusion is inadequate following nist activity, and it improves organ perfusion pressure during
IV fluid resuscitation. Desirable qualities of vasoactive drugs maldistributive and vasodilatory shock in patients nonre-
include a short onset of action and rapid metabolism, so they sponsive to fluid resuscitation and inotrope administration.
may be quickly titrated to effect in response to changes in Resulting vasoconstriction increases cardiac afterload, poten-
patient condition and administered as a CRI. Vasopressors tially decreasing CO; however, this effect is countered by its
and inotropes exert their effects through interaction with β1-effects, which facilitate increased stroke volume. Compared
adrenergic and nonadrenergic receptors. with dopamine, NE appears to have increased benefits in sep-
Adrenergic receptors targeted by vasoactive therapy include sis, demonstrating improved outcomes and increased splanch-
α1-, α2-, β1-, and β2-adrenergic receptors and dopamin nic perfusion in humans and increased urine output in septic
ergic receptors. α1-Adrenergic receptor stimulation results in foals when combined with dobutamine.47,48
peripheral arterial vasoconstriction and altered metabolism
as well as increased cardiac contractility.37-39 Postsynaptic α2- Epinephrine
receptor stimulation results in vasodilation.40 β1-Adrenergic Epinephrine is a strong α- and β-adrenergic agonist, mak-
receptor stimulation results primarily in cardiac effects with ing it a potent vasopressor. Splanchnic, renal, and coronary
increases in both heart rate (chronotropic effect) and con- blood flow is decreased compared with NE.49 Increased risk
tractility (inotropic effect). β2-Receptor stimulation results of dysrhythmia is associated with an increase in myocar-
in vasodilation of the arteries of coronary vessels, visceral dial irritability, and postresuscitation myocardial depres-
organs, and skeletal muscle. Slight chronotropic and inotropic sion with increased myocardial oxygen consumption is also
improvement after β2-stimulation is also seen.41 Dopaminergic reported.50
stimulation improves myocardial contractility, increases heart
rate, and results in peripheral vasoconstriction.42 Nonadren- Dopamine
ergic mechanisms include activation of vasopressin-specific Dopamine is active at adrenergic (α and β) and dopaminergic
receptors (chiefly V1) and effects on phosphodiesterase activ- receptors in a dose-dependent manner. High infusion rates of
ity.31 Vasopressin receptors (V1) are present throughout the dopamine tend to result in a predominance of α-adrenergic
vascular system and stimulation results in vasoconstriction, effects and marked vasopressor response, whereas β-adrenergic
especially at peripheral arterioles.43,44 During hypovolemic effects (inotropy) predominate at lower infusion rates. Con-
shock, markedly increased levels of V1 stimulation lead to sig- siderable controversy exists regarding the utility of dopamine,
nificant increases in vascular resistance, which is an important with mixed experimental evidence regarding its “renal protec-
mechanism for restoration of arterial blood pressure.45 tive” effects and meta-analysis data showing increased mortal-
ity in some subsets of patients.3,51-53
Inotropes
Inotropic drugs increase myocardial contractility, increasing Phenylephrine
stroke volume and CO. Cardiac workload and oxygen con- Phenylephrine is primarily an α-agonist resulting in increased
sumption are increased, which is of concern in hypoxemic SVR, MAP, and decreased CO. When phenylephrine is used as
a vasopressor, concurrent use of a β-agonist (e.g., NE, dobuta- parameters is observed or when limits to fluid resuscitation
mine) is often beneficial. (e.g., 60–80 mL/kg total volume, CVP >15 mm Hg, declin-
ing Pao2, peripheral edema) are reached. In most situations,
Vasopressin an increase in circulating volume to achieve subnormal val-
Vasopressin, or antidiuretic hormone, is a regulatory peptide ues for blood pressure are adequate to balance critical tissue
integral in regulating body water balance through promotion perfusion while limiting the risk of fluid overload, second-
of water conservation in the collecting tubule of nephrons (V2 ary compartment syndrome, and tissue edema. Once hypo-
receptor) in response to centrally mediated detection of dehy- volemia is corrected, fluids may be administered at 1 to 2
dration (osmoreceptors). In addition, vasopressin induces times maintenance to correct the remaining fluid deficits and
vasoconstriction via V1 receptors, particularly during sepsis, account for ongoing needs/losses. If limits of fluid resuscita-
and human research demonstrates beneficial effects of vaso- tion efforts are reached before perfusion parameters improve,
pressin when used concurrently with catecholamines, such as vasoactive medications may be administered to increase car-
NE.37,50,54,55 Vasopressin works through nonadrenergic mech- diac contractility or SVR.
anisms, even in the face of moderate acidosis. This is in stark
contrast to catecholamines that do not function as optimally Practical Use of Vasoactive Medications
under similar conditions. As with other vasopressors, V1 ago- When normalization of fluid volume fails to correct perfusion
nists may be unsuitable for use in horses that have not been abnormalities or limits to volume resuscitation are reached,
volume resuscitated before administration because of a reduc- the clinician should consider the use of vasoactive medica-
tion in splanchnic perfusion.56 Research in clinical equine tions (Table 4.10). Inotropes and vasopressors should not be
practice indicates that endogenous vasopressin concentrations administered in patients who are hypovolemic because of a
are increased in sick or septic animals compared with healthy risk of tachycardia, increased myocardial oxygen demand in
controls, and that nonsurvivors have higher concentrations at the face of decreased coronary perfusion, and marked vaso-
admission compared with survivors.55,57-62 constriction resulting in increased afterload and decreased
CO.53,65 The choice of which medication is most appropriate is
case dependent and sometimes patient dependent; however, all
Y CARDIOVASCULAR SUPPORT medications should be titrated to effect based on cardiovascu-
STRATEGIES lar monitoring, including serial heart rate/ECG, blood pressure,
urine volume, and, when possible, CO determination. Scientific
Practical Approach to Fluid Resuscitation data regarding inotrope/vasopressor use under clinical condi-
The goal of fluid resuscitation is the restoration of tissue per- tions is limited in horses; therefore, our knowledge is based on
fusion through increased stroke volume and improved blood human data and limited experimental research in horses.
pressure by correcting blood volume deficits. The key to fluid Administration of an inotrope, such as dobutamine, is cur-
resuscitation is, therefore, balancing rapid volume expansion rently the first-line choice of vasoactive medication in equine
with monitoring to prevent fluid overload and avoiding the patients, particularly when adequate CO cannot be confirmed.
negative effects of oversupplementation. Administration of a vasopressor in the face of inadequate car-
There is little evidence to support one fluid resuscitation diac function would result in a further decrease in CO associ-
protocol over another in horses. Therefore selection of fluid ated with increased SVR; however, if administration of low-dose
type is highly subjective in most situations, and recommenda- dobutamine (2–5 μg/kg/min) fails to improve perfusion indi-
tions are extrapolated from human critical care. Most clini- ces then a vasopressor may be added. Clinically, this situation
cians select a polyionic isotonic crystalloid fluid (e.g., LRS or is generally limited to neonatal foals with sepsis or adults with
Plasma-Lyte A) administered alone, or in combination with vasodilatory shock. NE appears to be the best vasopressor for
hypertonic saline in the presence of clinical shock symptoms. use in the horse based on the available data and clinical expe-
The use of hypertonic saline should be cautiously considered rience, and data would suggest that concurrent administration
or avoided in cases of uncontrolled hemorrhage or where with dobutamine has a favorable effect on blood pressure and
marked interstitial dehydration is likely; however, it has dem- renal perfusion while preserving splanchnic circulation.47,53,66
onstrated a more rapid return of normal heart rate and urina- If the patient’s cardiovascular status remains poor, administra-
tion in endurance horses requiring IV fluid support compared tion of vasopressin may be considered, especially in the case
with normal saline.63,64 Considering the risks/benefits of col- of septic shock, during which the body’s responsiveness to
loid administration, the concurrent administration of col- catecholamines may be reduced.37,67 Research regarding the
loids with crystalloids may be indicated where symptoms of administration of exogenous vasopressin in the equine patient
decreased plasma oncotic pressure (e.g., edema, effusions) are is limited, but preliminary data support its use.68
present or where a critical decrease in oxygen-carrying capac-
ity is detected. Therapeutic Goals and Monitoring
Ideally, volumes to be administered and administration The primary goal of the criticalist related to the cardiovascular
rates are based on estimates of fluid deficits; however, clini- system is to restore tissue perfusion and oxygen delivery. Early
cal interpretation of percentage dehydration and degree of goal-directed therapy (EGDT) outlines management proce-
hypovolemia is insensitive and may result in oversupplemen- dures to optimize global tissue perfusion and oxygenation
tation or undersupplementation. Therefore a fluid challenge in critical patients and was once considered revolutionary in
method is more commonly used in practice where a bolus human sepsis treatment to improved patient outcomes; how-
of 10 to 20 mL/kg of isotonic crystalloid is administered ever, recent clinical trials show no benefit over routine care.69
over 30 to 60 minutes with monitoring of perfusion param- Research related to EGDT in veterinary patients is limited.70,71
eters between sequential boluses. Administration of boluses Dysfunction of the cardiovascular system may be iden-
is stopped when normalization or plateau of perfusion tified clinically through abnormal mentation or weakness,
increased heart rate, weak peripheral pulse quality, cool the section Renal Critical Care later in this chapter for addi-
extremities, prolonged jugular refill time, altered mucous tional information.
membrane color or capillary refill time, and/or decreased
urine production. Clinicopathologic abnormalities reflect- l-Lactate
ing poor tissue perfusion include elevated l-lactate concen- l-Lactate is the terminal product of anaerobic glycolysis, and
trations, increases in cardiac troponin I activity, decreased increases in blood lactate concentration in the horse are most
central venous oxygenation, and increased urine SG. The often the result of inadequate delivery of oxygen to periph-
evaluation of each of these and other cardiac monitoring eral tissues resulting from hypovolemia, hypoxemia, anemia,
modalities are described in this section. or decreased perfusion pressure (type A lactic acidosis).74,75
Other causes of hyperlactatemia include abnormal tissue uti-
Physical Examination Parameters lization of oxygen, including mitochondrial dysfunction, or
Positive clinical response to therapies are indicated by abnormal clearance of lactate (type B lactic acidosis).
improved patient mentation and responsiveness to the Lactate measurement is useful clinically in monitoring the
environment, normalization of the heart rate, and the pres- response to fluid therapy and vasoactive drugs in patients with
ence of pink mucous membranes with a capillary refill time cardiovascular dysfunction. Decreases in plasma lactate con-
of 1 to 2 seconds. Further clinical indicators of adequate centration temporally follow improvements in cardiovascular
tissue perfusion include warming of the extremities, pal- performance; therefore, the trend in serial plasma lactate con-
pation of strong peripheral pulses, and improved jugular centration is most clinically useful. In situations of appropri-
refill. In the normal standing horse, the jugular vein should ate volume restoration in which lactate concentration remains
fill quickly in response to occlusion of the vein in the mid- increased, unresolved inflammatory stimulus or uncontrolled
dle of the neck. The presence of jugular pulsation may be sepsis should be considered.
a crude indicator of elevated CVP, and thus fluid overload,
when occlusion of the vein eliminates jugular pulsation.72 Arterial Blood Pressure
Other clinical evidence of fluid overload includes elevated Arterial blood pressure is the product of CO and SVR. Mean
respiratory rate, weight gain, and subcutaneous-dependent blood pressure, not systolic or diastolic blood pressure, is
edema. considered the driving perfusing pressure for tissue and
organs.73 Arterial blood pressure can be measured by direct
Urine Production (invasive) and indirect (noninvasive) means, as described
Urine production is considered a reflection of renal blood flow earlier in this chapter. Trends in arterial blood pressure, as
and hence CO and serves as an indication of adequate organ opposed to individual readings, combined with other indi-
and tissue perfusion.73 Therefore when urine production cators of perfusion (examination and urination) should be
remains low (< two thirds of fluid volume being administered) used to guide therapy.
in a euvolemic hypotensive horse, the administration of ino-
tropes/vasopressors should be considered. However, the urine Central Venous Pressure
output and glomerular filtration rate are unreliable indicators CVP is determined by central venous blood volume, muscular
of renal function in humans receiving vasopressors. Please see tone of the venous system, and the balance between venous
TABLE 4.10 Useful Drugs in Cardiovascular Critical Care

Type Dose Comments
Vasopressors
Norepinephrine 0.05–1 μg/kg/min IV —
Epinephrine 0.02–0.05 mg/kg IV —
Dopamine 1–5 μg/kg/min IV Renal dopaminergic-1 receptors
5–10 μg/kg/min IV β1-Adrenergic stimulation
>10 μg/kg/min IV α-Adrenergic stimulation
Phenylephrine 3 μg/kg/min IV over 15 min —
Vasopressin 0.4–0.8 units/kg IV —
Inotropes —
Dobutamine 1–20 μg/kg/min IV —
Plasma volume expansion —
Crystalloids
Isotonic 50–100 mL/kg IV —
Hypertonic saline (7.2%) 4–8 mL/kg IV —
Colloids —
Plasma 5–10 mL/kg IV —
Hetastarch 6% 5–10 mL/kg IV —
Tetrastarch 6%

IV, intravenously.
return and CO. CVP is an estimate of right atrial pressure and

cardiac preload. It is used to guide fluid therapy, because nor- Respiratory Critical Care
malization of CVP may reflect success of fluid volume resusci-
Tiffany L. Hall
tation, whereas elevations in CVP may reflect volume overload
and limits of fluid resuscitation. As with measurements of arte-
rial blood pressure, the trend in CVP seen through repeated
monitoring is most informative. Y REVIEW OF RESPIRATORY
PHYSIOLOGY
Venous Blood Gas
Arterial blood gas values are required to assess pulmonary gas The major function of the respiratory system is gas exchange
exchange, as described in the later section Respiratory Criti- and, in conjunction with the cardiovascular system, to deliver
cal Care; however, in patients with cardiovascular compromise oxygen to the tissues and facilitate carbon dioxide elimination.
in which severe hypoperfusion may be present, tissue level Table 4.11 shows expected arterial blood gas indices from nor-
hypoxemia, hypercapnia, and acidemia are more accurately mal horses. The respiratory control center maintains Pao2 and
represented in central venous blood. Central venous oxygen Paco2 within a narrow homeostatic range despite the body’s
saturation is a reflection of oxygen delivery and consumption wide variety of demands. Under normal conditions the pri-
by tissues and is used in monitoring the efficacy of the car- mary driving force of alveolar ventilation is changes in Paco2,
diovascular system. Decreases in venous oxygen saturation which are sensed by chemoreceptors in the brainstem.78
may reflect decreased respiratory function, decreased CO/ Changes in Pao2 are sensed by peripheral chemoreceptors
tissue perfusion, or increased oxygen demand. In goal- in the carotid and aortic bodies and also have an impact on
directed therapy, normalization of central venous oxygenation alveolar ventilation but typically alter respiratory rate or effort
serves as a therapeutic target. only in states of marked hypoxemia.78
The basic components of the respiratory system are the
Colloid Osmotic Pressure upper airways, the sequentially branching respiratory passage-
COP, also referred to as oncotic pressure, results from the ways, and the alveolar-capillary membrane. The upper airways
osmotic force created by macromolecules within the intravas- and respiratory passageways are not involved in gas exchange;
cular compartment and is essential to retaining appropriate therefore, they are referred to as anatomic dead space.78 The
intravascular volume. Proteins and colloid molecules are suf- alveolar-capillary membrane is the primary region that par-
ficiently large in mass to limit permeability across the vascular ticipates in gas exchange, although some areas may not be
endothelium and retain water within the vasculature by virtue equally perfused and ventilated, resulting in physiologic dead
of their osmotic draw. In addition, the Gibbs-Donnan effect, space.78 The alveolar-capillary membranes form a dense net-
in which sodium cations are attracted to negative residues on work within the alveoli, allowing for maximum exchange of
protein (albumin), adds further to the intravascular osmotic oxygen and carbon dioxide. Factors that affect the rate of gas
draw. diffusion include thickness and surface area of the membranes,
COP can be measured or calculated, with reasonable agree- diffusion coefficient of the gas, and the gas pressure difference
ment in healthy but not hospitalized horses. Because albumin between the two sides of the membrane.78,79
is the major contributor to COP, alterations in the albumin- In the body, oxygen diffuses down a pressure gradient
to-globulin ratio alter COP at any given total plasma protein from the alveolar space to the pulmonary capillaries to release
concentration. Direct measurement of COP is necessary after within tissue capillary beds. Oxygen in the blood is either
synthetic colloid (hetastarch) administration because these bound to hemoglobin (Sao2) in the erythrocyte or dissolved
starch molecules have considerable osmotic effect but are not (Pao2) in plasma, with approximately 97% of total blood
measurable by refractometry. oxygen content (Cao2) bound to hemoglobin under normal
conditions.78,79 The oxygen-hemoglobin dissociation curve
Electrocardiogram depicts the association between partial pressure of oxygen
Indications for ECG monitoring of equine patients with in the blood (Pao2) plotted on the x-axis and percentage (%)
cardiovascular compromise include dysrhythmias, marked oxygen saturation of hemoglobin (Sao2) on the y-axis. Fac-
electrolyte abnormalities (e.g., hyperkalemia), and during tors such as pH, temperature, carbon dioxide levels, and the
vasoactive drug therapy. The base-apex lead system is most concentration of 2,3-diphosphoglycerate alter the hemoglobin
commonly used in equine medicine, and telemetry units allow affinity for oxygen and, therefore, the ability of oxygen to be
remote monitoring of horses free in stalls. A more complete
review of the cardiovascular system and its monitoring is
TABLE 4.11 Normal Range of Arterial Blood Gas Values for
available in Chapter 9.
Adult Horses
Cardiac Output Measurements Variable Normal Range
The use of advanced technologies such as lithium dilution, indi-
pH 7.4 ± 0.2
cator dilution, bioimpedance, and pulse contour analysis for
assessment of CO has been extensively reviewed elsewhere.76 Paco2 40 ± 3 mm Hg
These techniques are impractical in the clinical setting or have Pao2 94 ± 3 mm Hg
not been validated for the horse; however, echocardiography Base excess 0 ± 1 mm Hg
(see Chapter 9) may be used in calculating CO. Volumetric Spo2 98–99%
determination (four-chamber and bullet methods) and right
ventricular outflow tract Doppler are reliable, accurate, and From Aguilera-Tejero E, Estepa JC, Lopez I, et al. Arterial blood gases and acid-
noninvasive means of determining CO in horses.77 base balance in healthy young and old horses. Equine Vet J. 1998;30:352.
carried to and unloaded at the tissue level.78,79 Disorders that If V/Q mismatch is severe, the result is a right-to-left intrapul-
affect the binding of oxygen to hemoglobin have a tremendous monary shunting of blood.78,79
impact on oxygen delivery to the tissues associated with a Hypoxemia is only one of several possible causes of oxy-
marked decrease in total oxygen content (Cao2). As such, Pao2 gen deficiency at the tissue level, such as a condition referred
is primarily an indicator of pulmonary gas exchange within to as hypoxia. Tissue hypoxia can occur in the face of normal
the lungs, whereas oxygen extraction ratios and venous oxy- respiratory function as a result of any condition that causes
gen indices are better predictors of tissue oxygenation. decreased oxygen delivery to the tissues or abnormal oxy-
gen utilization within the tissues, including decreased CO,
decreased blood oxygen-carrying capacity, peripheral arte-
Y RESPIRATORY INSUFFICIENCY: riovenous shunting, mitochondrial dysfunction, increased
HYPOXEMIA AND HYPERCAPNIA peripheral oxygen consumption, and/or hypermetabolic con-
ditions (e.g., hyperthermia, seizures, sepsis).78,79
Respiratory insufficiency leading to hypoxemia, a decrease
in oxygen content in arterial blood (low Pao2), occurs for
one of five reasons: decreased inspired oxygen content Y APPROACH TO THE PATIENT WITH
(Fio2), diffusion barrier impairment within the lungs, alveo- RESPIRATORY DISTRESS
lar hypoventilation, right-to-left shunting of blood, and/or
ventilation-perfusion (V/Q) mismatch. Hypercapnia (elevated Respiratory dysfunction may be the primary reason that a
Paco2) results from insufficient elimination of carbon dioxide veterinarian is consulted, or it may occur while a horse is
from the blood to the alveoli, or alveoli to the atmosphere, and treated for another problem. Respiratory distress is defined
is commonly observed in cases of hypoventilation and V/Q as an inappropriate degree of breathing effort based on an
mismatch. For practical purposes decreased inspired oxygen assessment of respiratory rate, rhythm, and character. Causes
is a very rare primary cause of hypoxemia because horses of respiratory distress may be respiratory or nonrespiratory
breathing room air inspire sufficient quantities of oxygen to in origin. The physiology of this condition is discussed else-
maintain adequate dissolved oxygen fractions. where (Chapter 8).
Diffusion impairment is an uncommon cause of hypox- Upper respiratory disorders that result in respiratory
emia or hypercapnia in horses at rest because pulmonary distress usually do so because of respiratory tract obstruc-
disease must be very severe before gas exchange is limited, tion (Box 4.5). Complete upper airway obstruction is a true
which is caused by a high functional residual capacity of the emergency because inspiration against a closed airway results
lungs. Diffusion is impaired because of decreased surface area in the inability to inspire and marked negative intratho-
or increased thickness of the alveolar-capillary membrane, racic pressures leading to pulmonary edema, which can be
as might occur in pulmonary fibrosis. Carbon dioxide dif- fatal.84 Diagnosis is usually based on physical examination
fuses more rapidly than oxygen (20-fold). Thus, hypoxemia is and endoscopy of the upper airway. Horses with upper air-
observed before hypercapnia. way obstruction may require an emergency tracheotomy and
Hypoventilation results in both hypoxemia and hyper- additional therapies, depending on the primary cause of the
capnia and occurs when there is a reduction in the volume obstruction.
of air entering and exiting the alveoli per minute (decreased Lower airway diseases that may be associated with respira-
alveolar ventilation), resulting in decreased gas exchange. tory distress are listed in Box 4.6. Diagnosis is based on a thor-
Metabolic production of CO2 is fairly constant under normal ough physical examination, thoracic imaging, transtracheal
metabolic circumstances, so Paco2 is primarily controlled aspirate, and arterial blood gas analysis. Treatment depends on
by its rate of elimination through the lungs and, therefore, the nature of the primary disorder and may include antimicro-
is an accurate reflection of alveolar ventilation. Hypoven- bial agents, antiinflammatory agents, oxygen administration,
tilation may occur with disorders of the central nervous or thoracic drainage as indicated. Diagnosis and treatment of
system ([CNS]; e.g., trauma, HIE, pharmaceutical drugs), specific disorders are described in Chapter 8.
thoracic cavity (e.g., pleural space disease, pain), respira- Nonpulmonary causes of respiratory distress include ane-
tory tract (e.g., obstruction), or neuromuscular disease (e.g., mia, compensation for metabolic acidosis, pain, anxiety, and
botulism).78,79 hyperthermia. Evaluation of nonpulmonary causes of respira-
Hypoxemia caused by a right-to-left shunt occurs when tory distress include a thorough history, physical examination,
blood bypasses the pulmonary circulation and is, therefore, and blood work. After the initial evaluation further diagnostic
not oxygenated within the lungs. This deoxygenated blood testing might include endoscopy, ultrasound, or radiographs.
mixes with oxygenated blood in the left heart resulting in
hypoxemia. Shunting may be extrapulmonary, such as a Oxygen Therapy
right-to-left cardiac shunt (e.g., tetralogy of Fallot), or intra- Nasopharyngeal administration of oxygen is the most common
pulmonary, such as occurs with severe V/Q mismatch (e.g., form of respiratory support in horses suffering from hypox-
ARDS). emia (Fig. 4.4). Oxygen supplementation is indicated when the
A V/Q mismatch is the most common cause of hypox- Pao2 falls below 60 mm Hg or Sao2 < 90%.80 Research demon-
emia in the horse and occurs when alveolar ventilation and strates a significant and dose-dependent increase in Pao2 and
blood flow are not closely matched, resulting in inefficient gas Sao2 with increasing flow rates of oxygen to a maximum of 10
exchange. V/Q mismatch may result from all forms of pulmo- to 20 L/min, beyond which airway irritation is observed.81,82
nary disease. A high V/Q mismatch occurs when regions of Although adequate delivery of oxygen to tissues is essential,
the lung are ventilated but not perfused, such as occurs with oxygen is also toxic when in excess through production of
pulmonary thromboembolism.78,79 Conversely, a low V/Q reactive oxygen species. Serial arterial blood gas measure-
mismatch occurs when regions of the lung are perfused but not ments will aide in determining the response to treatment and
ventilated, as with bronchopneumonia and consolidation.78,79 ability to decrease supplementation, with the goal of providing
BOX 4.5
Upper Airway Disorders That May Be Associated BOX 4.6
Lower Airway Disorders That May Be Associated
with Respiratory Distress in Adult Horses with Respiratory Distress in Adult Horses
NASAL DISORDERS PULMONARY DISORDERS

• Trauma, foreign body • Pulmonary edema (cardiogenic or neurogenic)
• Hemorrhage or hematoma • Acute interstitial pneumonia
• Neoplasia • Chronic interstitial pneumonia including equine multinod-
• Abscess ular pulmonary fibrosis (equine herpesvirus 5) infection
• Granuloma • Aspiration pneumonia
• Amyloidosis • Abscessing or coalescing bronchopneumonia
• Acute respiratory distress syndrome/acute lung injury
PHARYNGEAL DISORDERS • Silicosis
• Neoplasia • Smoke inhalation
• Subepiglottic or pharyngeal cyst • Tracheal/bronchial foreign body
• Persistent dorsal displacement of the soft palate
• Trauma, foreign body EXTRAPULMONARY DISORDERS
• Abscess • Pleural effusion (hydrothorax, pyothorax, chylothorax,
and hemothorax)
LARYNGEAL DISORDERS • Thoracic trauma
• Laryngeal paralysis • Pneumothorax (open, closed, and tension)
• Laryngeal hemiplegia
• Trauma, foreign body
• Edema
• Arytenoid chondritis
• Epiglottitis and epiglottic granuloma
MISCELLANEOUS
• Guttural pouch enlargement
• Empyema
• Tympany
• Mycosis and hemorrhage
• Head swelling: edema, cellulitis, anaphylactic shock,
bilateral jugular occlusion
the lowest flow rates (lowest Fio2) possible to achieve adequate

oxygenation.
Inhalational Therapy
Inhalational therapy is beneficial in respiratory disorders of the
lower airways, including bronchopneumonia and inflammatory
airway conditions. Mucolytics, bronchodilators, and antimicro-
bials (including amikacin, gentamicin, and sodium ceftiofur
[Naxcel]) may be administered by ultrasonic nebulization.83,84
Inhalers may be used for the administration of bronchodilators,
mast cell stabilizers, and corticosteroids (CSs) in horses with
inflammatory airway conditions such as inflammatory airway
disease or recurrent airway obstruction (RAO).85,86 Advantages FIG. 4.4 Horse with a nasal oxygen cannula. Suturing to the nostril and
of inhalation therapy include a localized delivery to the target affixing the tubing to the halter helps maintain the cannula in place.
site allowing for higher concentrations at lower doses adminis-
tered, as well as reduced incidence of adverse systemic effects.
compared with caffeine.87 Disadvantages of doxapram use
Pharmacologic Ventilation include an increase in myocardial oxygen consumption and
Hypoxemia and hypercapnia resulting from hypoventila- cost. Theophylline is similar to caffeine; however, it has a nar-
tion may respond to the administration of medications that row therapeutic index with adverse effects including colic, sei-
stimulate respiration centrally. Caffeine, doxapram, and the- zure, tachycardia, and sudden death.80
ophylline are three such medications that may benefit equine Acute bronchoconstriction and decompensation may be
patients with hypoventilation secondary to head trauma, seen with severe RAO, inhalation of noxious gases, or other
encephalitis, or hypoxic-ischemic encephalopathy. Caffeine chemical irritants and can be managed with bronchodilating
is most frequently used in practice because of ease of admin- agents. β2-Agonists (e.g., inhaled albuterol [720 μg per 450-
istration, cost, and wide therapeutic index. Doxapram has a kg horse]) and anticholinergics (e.g., intravenous glycopyrro-
short duration of action requiring frequent or CRI administra- late) are beneficial. Atropine may be used as a rescue therapy
tion, which limits use despite evidence of improved ventilation only. Bronchial inflammation can both trigger and perpetuate
bronchoconstriction and warrants the justified use of inhaled Paco2 indicates hyperventilation, the presence of which cannot
or systemic glucocorticoids in some cases. be accurately assessed based on physical examination alone.
Hypoventilation may be caused by central apnea (CNS disease),
Mechanical Ventilation obstructive apnea (upper respiratory tract disease), increased
Mechanical ventilation, when administered in a hospital set- dead space ventilation (shunt and decreased CO), reduced lung
ting by experienced clinicians, has resulted in improved out- compliance (low lung volume), respiratory muscle weakness
comes in foals80 and may be beneficial in adults.88 Indications or fatigue, poor control when mechanical ventilation is used,
for mechanical ventilation include marked hypoxemia or thoracic pain, or abdominal distention. Hyperventilation, with
hypoventilation (pHa <7.3 with Paco2 >65 mm Hg or Pao2 decreased Paco2, may result from pain, hypoxemia of any
<60 mm Hg) despite maximal medical therapy, and fatigue cause, pulmonary disease, or neurologic disease.
or excessive work of breathing. Clinical diagnoses in equine Oxygenation status is then determined by the assessment
patients that may benefit from mechanical ventilation include of Pao2 and Sao2 in light of the partial pressure of alveolar
botulism, hypoxemic-ischemic encephalopathy, or ARDS. oxygen (PAo2) and hemoglobin levels. PAo2 is influenced by
Long-term mechanical ventilation techniques in adult horses the fraction of inspired oxygen (Fio2), atmospheric pressure,
are poorly described and represent a significant challenge for and Paco2. Pao2 is typically five times the Fio2 in the healthy
equine critical care. standing horse; therefore, in a patient breathing room air at
sea level (Fio2 = 21%), expected Pao2 concentration is approx-
Therapeutic Goals and Monitoring imately 100 mm Hg with an Sao2 >93%.
The goals in supporting respiratory function are recognition Calculation of the alveolar-arterial oxygen gradient (A-a
of improved respiratory rate and effort, improved oxygen indi- gradient) is helpful in evaluating causes of hypoxemia and
ces, and normalization of oxygen and carbon dioxide blood hypercapnia.78,79 In the normal horse breathing room air,
concentrations. the Pao2 should be only slightly less than PAo2 with an A-a
difference of 5 to 10 mm Hg. In patients with a normal A-a
Blood Gas Analysis gradient, hypoxemia and/or hypercapnia are the result of alve-
Blood gas analysis is the most common method for assessment olar hypoventilation. Hypoxemia and hypercapnia in patients
of pulmonary function and acid-base status in horses that are with an increased A-a gradient may be associated with V/Q
critically ill. Arterial samples may be obtained from the facial mismatch, right-to-left shunt, or diffusion impairment; how-
artery, transverse facial artery, or lateral metatarsal artery.89 In ever, nonpulmonary causes may also be present, including an
the clinical setting, venous samples are best collected from a imbalance of oxygen demand and delivery, hypermetabolism,
catheter placed in the cranial vena cava or jugular vein. Cor- or overfeeding.
rect interpretation of the information obtained from blood The causes of hypoxemia can be further differentiated
gas analysis allows the clinician to make appropriate decisions through the administration of supplemental oxygen and eval-
regarding diagnosis, therapy, and prognosis related to respira- uation of oxygen saturation and extraction ratios. When the
tory function and acid-base status. administration of oxygen fails to increase Pao2 to 100 mm Hg,
Samples for blood gas analysis must be collected and han- right-to-left shunting or massive pulmonary thromboembo-
dled appropriately to ensure accurate results. A small amount of lism should be suspected and appropriate diagnostic testing
heparin is used to coat the hub of the needle before aspiration used. Improvement of Pao2 above 100 mm Hg with oxygen
of the sample, which should be stored anaerobically after collec- therapy suggests hypoxemia associated with V/Q mismatch or
tion by removing the needle and placing a syringe cap over the a diffusion disturbance. Venous blood gas analysis has limited
tip of the syringe. Prolonged exposure to air or bubbles in the usefulness for evaluation of respiratory tract disease; however,
syringe can result in a decrease in Paco2 and an increase in Pao2 Svo2 may be used in calculating the oxygen extraction ratio,
as the sample equilibrates with room air in the bubble.79,89 A which provides some information about tissue oxygenation
sample stored at room temperature should be analyzed within in the horse. Oxygen extraction ratios greater than 30% may
10 to 15 minutes. Delayed analysis may result in an increased reflect increased oxygen consumption (e.g., exercise, hyper-
Paco2, decreased pH, decreased glucose, and increased lactate metabolism) or inadequate oxygen delivery to tissues associ-
as blood cells continue to metabolize nutrients.90 ated with hypoxemia, anemia, or cardiovascular dysfunction.
Acid-Base Status
Blood Gas Interpretation An interpretation of blood gas analysis is not complete with-
Respiratory Function out assessment of the patient’s acid-base status. In a simpli-
A systematic evaluation of blood gas values includes consid- fied approach to acid-base status, the clinician first determines
eration of pH, Pao2, arterial and venous oxygen saturation of whether the blood pH is normal (approximately 7.40) or
hemoglobin (Sao2, Svo2), Paco2, and bicarbonate concentra- whether acidemia (pH <7.36) or alkalemia (pH >7.44) exist.
tion. The partial pressure of oxygen dissolved in arterial blood There are four primary acid-base disturbances that may occur
(Pao2) is a reflection of pulmonary oxygenating capability and in a patient based on interpretation of the blood gas: respira-
is not affected by hemoglobin-bound oxygen. Causes of low tory acidosis, resulting from hypoventilation and reflected by
Pao2 (hypoxemia) are discussed in the preceding sections. The increased Paco2; respiratory alkalosis, resulting from hyper-
partial pressure of CO2 dissolved in arterial blood (Paco2) is a ventilation and reflected by decreased Paco2; metabolic aci-
reflection of the balance between alveolar minute ventilation dosis (decreased HCO3−); and metabolic alkalosis (increased
and metabolic CO2 production.78,79,89 HCO3−). These may exist as sole disorders or in combination
The first step in interpreting the blood gas information with (mixed disorders). A complete discussion of acid-base disor-
respect to pulmonary function is to assess ventilatory status. ders and the approach to critically evaluating acid-base status
Increased Paco2 indicates hypoventilation, whereas decreased is beyond the scope of this text, and the reader is referred to
additional resources regarding the physiochemical approach mediators increase basal metabolic rate, contributing to the
to evaluation of acid-base status in animals.91,92 inefficient use of oxygen and calories, and may also modulate
the body’s response to starvation.94,95 Negative energy balance,
Pulse Oximetry in which nutritional intake does not meet the energy demands
A useful adjunct to arterial blood gas analysis is pulse oxim- of the body, depletes the body of structural and functional
etry, which is a technique that relies on the reflection of dif- proteins, impairing wound healing, decreasing immune func-
ferent wavelengths of light to differentiate oxygenated and tion, and altering many other normal physiologic functions.
deoxygenated hemoglobin reported as a percentage of oxy- The effects of an ongoing, profound negative energy balance
genated hemoglobin (Spo2). Generally, an Spo2 greater than may manifest in musculoskeletal weakness, disruption of the
91% is considered indicative of an arterial oxygen level within gastrointestinal barrier (villous blunting), sepsis, multiorgan
physiologically normal limits.79,93 Pulse oximetry has a lim- dysfunction, and even death.
ited sensitivity for determining changes in pulmonary gas
exchange at ranges above 90% hemoglobin saturation; how-
ever, Spo2 below 91% represents increasingly severe reduc- Y EVALUATION OF GASTROINTESTINAL
tions in arterial oxygen levels.79,93 The accuracy of Spo2 may FUNCTION
be influenced by several factors including pigmented skin,
hypoperfusion at the measurement site, anemia, hypothermia, Methods used to recognize gastrointestinal dysfunction in
and motion. False readings of Spo2 may occur in the presence the critically ill horse include changes in the physical exami-
of carboxyhemoglobin and methemoglobin, in which coox- nation, abdominal ultrasonography, and clinicopathologic
imetry is the preferred analytical method. Because of the limi- testing. Serial physical examinations will identify changes in
tations of pulse oximetry, response to treatment in a patient vital parameters, mentation, behavior, fecal production, and
with critical hypoxemia is best monitored with arterial blood abdominal size. Transabdominal ultrasound (2.5- to 3.5-mHz
gas analysis. transducer) can be used to evaluate the anatomic location,
contents, wall thickness, and motility of various regions of the
intestine. Classic patterns identified by ultrasound are useful
in narrowing a list of differential diagnoses for gastrointestinal
Gastrointestinal Critical Care disorders. The identification of peritoneal fluid by ultrasound
Tiffany L. Hall warrants abdominocentesis and fluid analysis to better evalu-
ate the disease process and can help guide therapy and deci-
The primary role of the gastrointestinal tract is digestion of sions regarding prognosis. Clinical pathologic abnormalities
food so that nutrients including proteins, vitamins, miner- are often nonspecific regarding gastrointestinal disorders but
als, and fluids may be absorbed into systemic circulation for may reflect the presence of systemic inflammation, major fluid
use throughout the body. Normal function of the gastroin- shifts or deficits, decreased tissue perfusion, acute protein loss,
testinal tract includes appropriate motility, balanced micro- negative energy balance (e.g., disorders of glucose and triglyc-
biota, digestion, and absorption through complex interactions erides), and/or electrolyte disturbances. See Chapter 12 for a
among the nervous system, enteric nervous system, endocrine more in-depth discussion of the use of complete blood count
system, and musculature of the gastrointestinal tract. The gas- (CBC), biochemistry, ultrasonography, and radiography for
trointestinal mucosa forms a barrier between the body and a disorders of the gastrointestinal tract.
luminal environment, which not only contains nutrients but Assessment of the nutritional status of the critically ill
also is laden with potentially hostile microorganisms and equine patient at presentation and at regular intervals dur-
toxins. Thus normal function also requires that nutrients be ing hospitalization is necessary to identify patients that would
transported across the epithelium while excluding passage of benefit from early nutritional support. The most practical
harmful molecules and organisms. methods for evaluation of nutritional status and body fat com-
position in horses are monitoring of body weight (e.g., scale
Y GASTROINTESTINAL DYSFUNCTION or weight tape) and body condition score (BCS), which is a
subjective, semiquantitative method of evaluating body fat
Complications related to the gastrointestinal tract are com- and muscle mass by visual inspection and palpation of certain
mon in the critically ill horse and include inappetence, pain, areas of the body. BCS is positively correlated to body fat but
endotoxemia/SIRS, ileus, enteritis or colitis, malassimilation not to weight or height. A nine-point scale was described by
(malabsorption/maldigestion), and protein-losing enteropa- Henneke in which 1 is extreme emaciation, 9 is obese, and 4
thy. The details of many of these conditions are discussed in to 6 are ideal.96 The appropriate assessment and monitoring
Chapter 12. Inappetence is probably the most common com- of nutritional status would include both the body weight and
plication in the critical equine patient and will be the focus of BCS.
the remainder of this section. Decreased feed intake may be
caused by a mechanical inability to eat (dysphagia) or a loss Y NUTRITIONAL SUPPORT
of appetite associated with a variety of conditions and diseases
including pain, stress, systemic infection, or loss of palatability Early nutritional support is indicated in underweight or obese
associated with medications. The regulation of appetite is an horses, those with highly catabolic disease states (e.g., pleu-
immensely complex process involving the gastrointestinal tract, ropneumonia), or in patients that are unable to eat (e.g., dys-
central and autonomic nervous systems, and many hormones. phagia, ileus). Healthy horses at rest may have feed withheld
Severe illness or injury has been associated with hyper- for 2 to 3 days without significant consequence; however, all
metabolism characterized by a pronounced catabolic state hospitalized horses may benefit from early nutritional inter-
that is made worse by a patient’s inappetence. Inflammatory vention. Numerous reports in human critical care document
the benefits of early nutritional support because it hastens with severe endotoxemia or SIRS. Hypokalemia can result
recovery, diminishes complications of the critically ill, and from decreased intake of food and the delivery of a high con-
decreases length of hospitalization.94,95,97 The goals of early centration of dextrose causing pancreatic insulin release; thus,
nutritional support are to maintain host defenses and preserve potassium should be supplemented in horses receiving PN.
lean body mass while avoiding oversupplementation.
The nutritional requirements of the critically ill adult horse
have not been determined and are influenced by size, age, dis- Y GASTROINTESTINAL MOTILITY
ease state, and metabolic stress. Maintenance requirements SUPPORT
for healthy adult horses at rest are estimated to be 30 to 40
kcal/kg per day.98-100 More research is available in critically ill The promotion of gastrointestinal motility and function in the
foals whose resting energy requirements are approximately postoperative patient is discussed elsewhere in this text (see
50 kcal/kg per day and increase as the foal’s clinical condition Chapter 12). However, maintenance of normal blood volume,
improves.101 physiologic electrolyte concentrations, and gastrointestinal
Enteral feeding is preferred to PN if the gastrointestinal blood flow will aide in maintaining gastrointestinal integrity
tract is even partially functional because local delivery of feed and function. The reader is referred to other sections of this
bulk and nutrients improves intestinal motility, maintains text for further information regarding support of normal gas-
mucosal integrity, protects against bacterial translocation, and trointestinal tract function.
supports organ and immune function.94,95,97 Even if a horse
cannot tolerate enteral feeding sufficient to meet mainte-
nance energy demands, lesser amounts of enteral nutrition are
shown to be beneficial while the remainder of energy require-
Renal Critical Care
ments are met through parenteral means (sometimes termed Samuel D. Hurcombe
trophic feeding). It can be difficult to determine caloric intake
for a horse on a voluntary feeding plan; however, weighing the Primary renal disease in horses may be underdiagnosed in
feed and hay offered compared with that left behind by the adult horses. Standard testing using blood work (blood urea
patient allows one to estimate the number of ingested calories. nitrogen [BUN] and creatinine concentrations) may only
If consumption is below 75% of the maintenance requirements increase once advanced or severe acute disease is established.
for 48 hours, or if the horse is anorexic or dysphagic, feeding Horses with critical illness are superb candidates for second-
by nasogastric tube is recommended.99,100 See Chapter 5 for a ary renal disease, which in many cases critically ill horses may
discussion of different enteral diet regimens and methods of be underperfused, in various shock states, and frequently
administration. It is recommended that enteral feeding begin administered nephrotoxic therapies.
gradually, with a goal of reaching maintenance requirements Horses with fluid deficits, severe myopathies, hemolysis,
over 3 to 7 days, because rapid changes may result in colic or and septic/endotoxemic shock are at high risk of renal disease.
diarrhea.99,100 Optimizing renal perfusion, glomerular perfusion, and tubu-
PN is indicated for aged animals off feed, pregnant or lac- lar flow should be of highest importance in supporting renal
tating mares off feed, horses with a BCS <4, critically ill breeds function. Electrolyte imbalances, acid-base disorders, urine
at risk for hyperlipidemia/hyperlipemia, and critical patients output volumes, and neurohormonal regulation of splanchnic
who cannot tolerate enteral feeding because of gastrointestinal blood flow should be evaluated and considered in the develop-
dysfunction.102-104 PN is a combination of nutrients designed ment of all fluid therapy strategies in the renal patient.
to meet the patient’s energy requirements through IV admin- Evaluation of renal function through clinicopathologic
istration and may consist of supplementation with dextrose testing of blood and urine are best performed before fluid
alone or in combination with amino acids and/or lipids. Other therapy. Provision of IV fluids may lead to changes in blood
components added to PN solutions include vitamins (A, D, E, electrolyte composition and SG findings.107
and B complex) and minerals. Macrominerals such as potas-
sium, calcium, and magnesium are best added to crystalloid Y GENERAL PRINCIPLES
fluids. The reader is referred to Chapter 5 for a complete dis-
cussion of PN. Horses with renal disease should be assessed for their ability
Complications associated with PN administration include to produce urine before fluid therapy. Low-volume resuscita-
hyperglycemia, hyperlipidemia, hypokalemia, hypophospha- tion (<40 mL/kg/day) should be used until it is known that
temia, hypomagnesemia, and thrombophlebitis.105,106 Hyper- the patient can tolerate maintenance and the previously men-
glycemia is the most common complication reported in horses tioned maintenance IV fluid rates. Monitoring body weight
and foals administered PN and may be avoided through slow and/or urine output volumes is the most practical method for
introduction of the fluid, beginning at 25% of the target rate. determining volume infusion tolerance.
This allows an appropriate endogenous insulin response to Caution should be exercised in the anuric patient and those
occur in response to dextrose supplementation. Blood glucose with low-volume oliguric renal failure. Patients with uremic
levels should be monitored every 4 to 6 hours to avoid hyper- encephalopathy and intolerance to IV fluids have a grave
glycemia, glucosuria, and osmotic diuresis. A sudden onset of prognosis.
hyperglycemia in a patient that had been tolerating PN can If the patient demonstrates volume tolerance, maintenance
indicate the presence of complications such as infection or rates (40–60 mL/kg/day) of isotonic crystalloids and/or bolus
sepsis. If hyperglycemia persists, exogenous insulin therapy infusions of hyperosmolar solutions (7.2% hypertonic saline
should be considered. Parenteral formulations containing lip- [2–4 mL/kg]; mannitol 20% solution [0.25–1 g/kg]) may be
ids should be avoided in horses with hyperlipidemia, hyperli- useful to promote renal perfusion, tubular flow, and nephron
pemia, or severe liver disease and used with caution in horses recruitment.
Specific treatment and diagnosis of acute and chronic renal Diagnostic samples to assess renal function would include
failure are discussed in greater detail elsewhere in this text. blood (CBC, serum chemistry, and leptospirosis microag-
glutination serology), urine (cytology, cast assessment, dark-
Y COMMON NEPHROTOXIC field microscopy, SG, and quantitative urine culture), and
renal tissue (histopathology with or without special stains
SUBSTANCES IN THE INTENSIVE and culture).
CARE UNIT Dilute urine (SG ≤1.012) concurrent with azotemia gen-
erally indicates decreased renal function. Azotemia with
Nonsteroidal Antiinflammatory Drugs isosthenuria (SG 1.008–1.012) indicates renal failure. Uri-
Nonsteroidal antiinflammatory drugs (NSAIDs) are com- nary indicators of tubular damage include granular casts
monly used in equine practice. Renal perfusion, notably to in urine, an increased urinary γ-glutamyl transferase-to-
the inner medulla and medullary pyramids, relies on perfu- creatinine ratio (>25), abnormal fractional clearance of
sion of the vasa recta. Intrinsic flow through the vasa recta electrolytes such as sodium and potassium,110 and increased
is affected by both volume status of the patient and vasomo- urinary glucose. The presence of white blood cells, bacteria,
tor tone. Vasomotor tone is regulated, in part, by prosta- and excess protein concentration as determined by dipstick
glandins. Prostaglandin E2 (PGE2) and prostacyclin (PGI2) or other methods as well as increased urine to protein ratio
promote vasodilation, perfusion, and health of the inner are abnormal findings in urine and should prompt more in-
tissues. These are constitutively produced via metabolism of depth investigation.
arachidonic acid shunting through cyclooxygenase-1 (COX- To understand and best prognosticate the severity of renal
1) activity.108 With the exception of firocoxib, other NSAIDs damage and chances of tissue restitution, ultrasound-guided
used in horses are not selective for COX-2, which is induced renal biopsy and histopathology are recommended.
by inflammatory stimuli.108 Therefore most NSAIDs inhibit A more complete discussion of laboratory methods of renal
activity of both enzymes to some degree, which blocks renal function assessment is found in Chapter 14.
production of prostaglandins and prevents the compensa-
tory increase in renal blood flow during dehydration, poten- Y THERAPY FOR RENAL DYSFUNCTION
tially leading to vasomotor nephropathy and renal papillary
necrosis (also termed renal ischemic necrosis). The mecha- Many cases of acute kidney injury respond favorably to
nism of action and toxicity for NSAIDs is discussed else- fluid therapy and avoidance of nephrotoxic drugs. In some
where in this text. instances, establishing a polyuric state can be beneficial when
horses are treated with the previously mentioned maintenance
Aminoglycoside Antibiotics fluid rates and can tolerate IV fluids. High tubular flow rate
Aminoglycoside antibiotics (e.g., gentamicin, amikacin) are is essential in establishing endogenous waste clearance (e.g.,
freely filtered at the glomerulus and excreted into the urine.109 creatinine) and other noxious substances (e.g., myoglobin).
In low tubular flow states (e.g., dehydration), aminoglycosides Diuresis may be induced through increased fluid rates above
are actively taken up by proximal convoluted tubular cells and the maintenance requirements (>60 mL/kg/day) of polyionic
stored in lysosomes. Drug accumulation exceeds drug disposi- isotonic solutions, administration of hypertonic solutions, and
tion and leads to rupture of PCT cells and acute tubular necro- use of diuretic therapies. Azotemia that decreases by ≥50% in
sis.109 Alternative drugs should be considered over systemic 24 hours in response to fluid therapy (usually at rates >80–100
aminoglycoside in the hypovolemic and/or azotemic patient. mL/kg/day) indicates prerenal azotemia.
If fluid therapy does not produce the expected increase in
Endogenous Toxins: Myoglobin and Hemoglobin urine output, then diuretics (furosemide, 1 mg/kg, IV) can be
Liberation of myoglobin (myopathies, e.g., rhabdomyoly- administered. Urination should be expected within 30 min-
sis, myositis) or hemoglobin (intravascular hemolysis, e.g., utes of furosemide administration. CRIs of furosemide may
immune-mediated hemolytic anemia, red maple leaf toxic- yield a more consistent diuretic response.111 Bags and infusion
ity) may lead to acute kidney injury via several mechanisms lines should be covered to prevent exposure to light because
including physical plugging of nephron tubules via polym- furosemide is light sensitive.
erization, reflexive renal vasoconstriction causing ischemia, Volume replacement should always be attempted before
and free radical injury via reduction-oxidation reactions from diuretic therapy because the resultant increase in urination
iron-containing pigments and genesis of reactive species (e.g., at blood volume expense will contribute to severe dehydra-
hydroxyl radical). free radicals. tion and reduce systemic perfusion and exacerbate renal
damage.
Y IDENTIFYING RENAL DYSFUNCTION Active treatment of refractory hypotension (hypotension
unresponsive to fluid therapy) is important to treat or prevent
Recognition of renal dysfunction is easily overlooked in criti- perfusion-mediated causes of acute kidney injury. Autoregula-
cal care patients. It is advisable to monitor serum BUN and tion begins to fail at a MAP <60 mm Hg. Maintaining an MAP
creatinine concentrations at least every 48 hours to assess ≥65 mm Hg is recommended to minimize reduced urine out-
glomerular filtration and renal function. Regular measure- put and kidney injury.53
ment of BUN and creatinine concentrations and assessment of Vasoactive therapies such as dobutamine (1–5 μg/kg/
results in light of physical examination findings (e.g., evidence min) have been advocated to improve blood pressure. Low-
of dehydration) and results of urinalysis are the most read- dose dopamine therapy (2–5 μg/kg/min) and fenoldopam
ily available methods for monitoring renal function in equine (0.04–0.4 μg/kg/min) have purported benefits in healthy sub-
critical care patients. Increases in serum creatinine concentra- jects on renal blood flow. The effects of dopamine or fenoldo-
tion as small as 0.3 mg/dL can be significant.110 pam on renal blood flow in critically ill equine patients is
unknown.110,53 Blood pressure should be measured in patients veterinary attention. Disorders of the forebrain (seizure activ-
at risk for hypotension and those that fail to produce urine ity and changes in behavior), spinal cord (ataxia and recum-
despite appropriate therapy. bency), peripheral nervous system (inability to ambulate or
In horses with oliguric renal dysfunction and certainly severe generalized weakness), and autonomic nervous sys-
anuric renal dysfunction, the CVP may be monitored to assess tem (urinary/fecal incontinence) may all require emergency
the potential for fluid overload and edema formation. Normal care. Extracranial causes of neurologic dysfunction can also
CVP in the standing horse is <12 mm Hg. Values >12 mm Hg be challenging and represent a multisystemic disorder (e.g.,
should prompt the clinician to reassess the patient’s’ tolerance hepatic and other metabolic encephalopathies).
to fluid therapy. Certain disorders may present as a neurologic disorder but
Aminoglycoside toxicity is best prevented by ensuring may be caused by other systemic causes. For example, cardio-
appropriate dosing regimens and limiting the use of amino- vascular or respiratory diseases and gait abnormalities caused
glycosides to hydrated animals without preexisting renal dys- by musculoskeletal diseases such as bone fractures, rhabdo-
function.111 Administering aminoglycoside antibiotics every 24 myolysis, or laminitis.
hours decreases the amount of time that renal tubular cells are Peripheral nerve damage in horses is not uncommon and
exposed to higher concentrations of aminoglycosides. The peak most often involves the suprascapular, radial, ulnar, femoral,
concentration (Cmax) dictates the efficacy of the drug; however, and selected cranial nerves. Occasionally, the brachial plexus
the trough concentration dictates the safety of the drug. Thera- can be injured after a collision accident. Peripheral nerve
peutic drug monitoring allows for the detection of elevated injury is commonly traumatic and associated with additional
trough (usually 24 hours after the previous dose) concentra- musculoskeletal abnormalities (e.g., fracture).
tions, which are more likely to cause toxicity. Drug-dosing Traumatic head injury with traumatic brain injury (TBI)
adjustments should be based on trough concentrations, either represents a dynamic neurologic emergency. Depending on
as a lower dose administered or a prolonged dosing interval.109 the nature of the injury, primary and secondary TBI can cause
the clinical presentation of the patient to change frequently as
Renal Replacement Therapy processes such as edema, inflammation, and changes in intra-
RRT such as peritoneal dialysis (PD) or hemodialysis is techni- cranial pressure (ICP) occur.
cally possible in horses. PD is technically easier but less effec- Abnormal neurologic function can cause secondary excite-
tive than hemodialysis. Recently venovenous hemodiafiltration ment, agitation, and stress in the patient and worry for the
was described in healthy adult horses and well tolerated.112 The owner or caretaker. Horses with alterations in the content of
need for specialized equipment and familiarity with creatinine consciousness and behavioral changes may be unpredictable,
clearance kinetics, etc., makes the application of hemodialysis in vacillating between somnolence and maniacal rage. It is pru-
clinical patients somewhat limited currently. dent to ensure safety of not only the patient to prevent addi-
PD has been described in horses as either intermittent or tional injury but also any handler or personnel. In cases of
continuous. The concept involves using the peritoneum as an unexplained neurologic deterioration, notably of inapparent
accessory kidney to dialyze blood. In one clinical report, con- causes, a thorough understanding of vaccination history of the
tinuous flow PD (CFPD) was more effective than intermittent patient and use of barrier protection strategies (e.g., medical
PD.113 LRS with 1.5% dextrose and 1 unit of unfractionated examination gloves, coveralls) should be performed. Taking
heparin per milliliter is an easy dialysate solution to obtain note of any “‘in-contact” personnel is important if potential
and use. For intermittent PD, 40 mL/kg of dialysate is infused zoonotic disease is suspected (i.e., rabies).
and left for 30 to 60 minutes and then allowed to drain. This
is repeated 2 to 6 times per day. With CFPD, an ingress cath- Y DIAGNOSTICS
eter is placed in the left flank and an egress catheter on ven-
tral midline connected to a closed bag collection system for Performing a thorough neurologic examination is critical. To
volumetric assessment. Dialysate fluid ingress is provided at come to a diagnosis, the practitioner performs a careful neu-
∼3 L/h. Eighty percent of ingress volume should be recovered rologic examination followed by appropriate ancillary diag-
in the collection system. Marked improvements in azotemia nostics. Ancillary diagnostics used in emergency situations
have been observed within the first 24 hours of starting CFPD, typically include hematology and serum chemistries, radio-
and it is continued based on creatinine clearance responses. graphs, and potentially cerebrospinal fluid analysis. When
RRT should be considered in cases where azotemia is unre- available, these patients may require further diagnostic tests,
sponsive to fluid therapy and/or diuretic medications or the notably imaging such as computed tomography, magnetic
horse is severely oliguric to anuric. Acute kidney injury would resonance imaging, endoscopy and electrodiagnostics, or a
likely yield potentially favorable outcomes using RRT com- combination of tests.
pared with chronic disease states. A neuroanatomic localization of the disease should be
made after a thorough examination,114,115 as described in
(Chapter 11). The neuroanatomic localization can be simpli-
fied by determining whether there is CNS, peripheral nerve,
Neurologic Critical Care or multifocal nerve disease. In the case of CNS disease, it is
Samuel D. Hurcombe helpful to determine whether the lesion is localized cranial or
caudal to the foramen magnum (i.e., whether there is brain
Any neurologic condition can represent a true emergency involvement). If there is brain involvement, it may be possible
requiring expedient assessment, stabilization, and targeted to further differentiate among cerebral, cerebellar, vestibular,
therapy. Severe manifestations of common diseases can be or brainstem disease. If disease is localized caudal to the fora-
challenging cases to treat, and horses that present acutely men magnum, the disease may be located in the cervical spi-
and/or deteriorate in the face of therapy require immediate nal cord or in the spinal cord caudal to T2.
Stabilization and symptomatic treatment are the primary spinal cord injury.117 Other potential beneficial effects of CSs
goals of emergency management of neurologic disease. A defin- include reduction in the spread of morphologic damage, pre-
itive diagnosis may not be known for several days following vention of the loss of axonal conduction and reflex activity,
the initial presentation of the emergent neurologic patient— preservation of vascular membrane integrity, and stabilization
for example, waiting for diagnostics for infectious agents (e.g., of white matter neuronal cell membranes in the presence of
protozoal myelitis, West Nile virus, etc.). As such, the clinician’s central hemorrhagic lesions. Furthermore, their antiinflam-
thorough neurologic examination provides a framework for a matory properties may be useful in reducing edema and fibrin
list of likely differential diagnoses. Empiric treatments, often deposition, as well as their ability to reverse sodium and potas-
for several differential diagnoses at once, are often provided sium imbalance caused by edema and necrosis.
until further testing supports a definitive diagnosis. Methylprednisolone sodium succinate (MPSS) is a syn-
thetic glucocorticoid with four times more antiinflammatory
Y TREATMENT activity and 0.8 times less mineralocorticoid action compared
with cortisol. Beneficial effects of MPSS on neural tissue
The goal of therapy should be to optimize CNS perfusion and include inhibition of lipid peroxidation, eicosanoid formation,
delivery of neurotropic substrates. Perfusion to the CNS is and lipid hydrolysis, including arachidonic acid release, main-
modulated by both the perfusing pressure (MAP) and local tenance of tissue blood flow and aerobic energy metabolism,
ICP. To promote global CNS perfusion, increasing MAP and/ improved elimination of intracellular calcium accumulation,
or decreasing ICP are desirable. reduced neurofilament degradation, and improved neuro-
Judicious use of sedation may be needed to facilitate safe nal excitability and synaptic transmission. The dose of MPSS
examination of the neurologic patient. Low-dose, short-acting used in human trials (30 mg/kg) exceeds that necessary for
drugs such as xylazine hydrochloride are recommended. How- activation of steroid receptors, which suggests that MPSS acts
ever, for more fractious and refractory patients, longer acting through mechanisms that are unrelated to steroid receptors.
continuous infusions and anesthetic agents may be required. Investigators have concluded that high-dose MPSS treatment
Stabilization of hemorrhagic and hypovolemic conditions is within 8 hours of spinal cord injury improved neurologic
necessary in trauma patients. Medical treatment of specific recovery.118,119 Controversy regarding the beneficial effects of
primary conditions is described in detail in Chapter 11. This MPSS and other steroids remains.120,121 A suggested dose for
section discusses select groups of drugs that are commonly horses is 25 mg/kg, IV bolus, then 5 to 8 mg/kg per hour for
used in horses with acute neurologic disease. 23 hours.
Analgesics Intracranial Pressure Reduction
Analgesic drugs are indicated if horses experience pain (e.g., Osmotic diuretics such as 20% mannitol (0.25–2.0 mg/kg,
in traumatic disease). NSAIDs are the mainstay drugs in administered IV over 20 minutes) and 7.2% hypertonic saline
equine medicine because of their antiinflammatory and anal- (2–4 mL/kg, administered IV as a bolus) are effective in com-
gesic properties. Flunixin meglumine (0.5–1 mg/kg, IV, every bating cerebral edema and increased ICP. These have a rapid
12–24 hours) is suitable. Opioids should be considered when onset of action (10–20 minutes) and are ideal therapies because
additional analgesia is required, or when analgesia is required they reduce ICP by drawing volume into the vascular com-
in situations of suspected NSAID toxicity, or when the risk partment and they increase MAP. Animals receiving osmotic
of developing NSAID toxicity is high (e.g., dehydration). diuretics should be adequately hydrated. Mannitol adminis-
Opioids do not have specific antiinflammatory effects and in tration is very effective in reducing ICP, although despite some
theory, κ-agonists over μ-agonists are advisable. Naloxone, technical limitations to the administration of this osmotic
μ-antagonist, has been shown to improve spinal cord blood diuretic, multiple doses of mannitol can lead to intravascular
flow. Multimodal analgesia, including the use of ketamine, dehydration, hypotension, reduction of cerebral blood flow
may offer advantages in blocking neuroexcitation through (CBF), and elevation of spinal fluid osmolarity.122,123
N-methyl-d-aspartate blockade. Hypertonic saline administered early in the treatment of
shock associated with head trauma may enhance the return of
Corticosteroids CBF and cell membrane function. Hypertonic saline may be
Corticosteroids (CSs) are potent antiinflammatory medi- the maintenance fluid of choice in head injury.124 It is associ-
cations and may be indicated in certain types of neurologic ated with significant decreases in ICP and cerebral water con-
diseases. Known inflammatory disease and acute trauma still tent compared with isotonic fluid treatment. Another study
appear to be indications for short-term corticosteroid therapy. comparing the effects of a hypertonic saline + solution and
Dexamethasone sodium phosphate is commonly adminis- mannitol on increased ICP found that the hypertonic saline
tered (0.05–0.1 mg/kg, IV, every 12–24 hours) for up to 48 hydroxyethyl starch reduced the ICP more effectively than
hours. A favorable response is expected within 4 to 8 hours mannitol alone.125 Induction of prolonged hypernatremia
after CS administration. Horses being given corticosteroid using 3% hypertonic saline administered as a continuous infu-
therapy should be monitored closely for the development of sion appears to be a promising therapy for the control of cere-
laminitis or secondary infection. If improvement in clini- bral edema.126
cal signs is observed, transition to oral prednisolone therapy Head and neck elevation at least 30 degrees above shoul-
(0.5–1.0 mg/kg, PO, daily tapered over 3–5 days) to decrease der height is also advised to minimize venous pooling in the
the chance of adverse effects is indicated. The neuroprotec- head. Increased venous pressures lead to increases in ICP via
tive effect of CSs is thought primarily to be mediated by free Queckenstedt’s phenomenon. Use of a wire and pulley system
radical scavenging.116 Recently, it has been shown that, similar connected to a halter is useful for the technique (Fig. 4.5).
to methylprednisolone, dexamethasone decreases apoptosis- Dimethyl sulfoxide (DMSO) 1 g/kg, administered IV as a
related cell death in rats that were subjected to traumatic 10% to 20% solution for 3 consecutive days, followed by three
penicillin (22,000 IU/kg, IV, every 6 hours) in combination

with gentamicin (6.6 mg/kg, IV, every 24 hours) can be used.
For anaerobic coverage, metronidazole (15 mg/kg, PO, every
8 hours) is indicated. Gentamicin and tetracyclines have poor
cerebrospinal fluid penetration.
Y SUPPORTING THE DOWN HORSE

Establishing venous access, controlling pain and anxiety of the
patient, and performing a thorough examination and frequent
repeat examinations should be done. Caution should be exer-
cised and safe handling practices are imperative when dealing
with a fractious patient and/or rabies is a concern. Manage-
ment of a recumbent horse requires intensive supportive care
and specific treatment aimed at the underlying or complicat-
ing disease processes.128,129 Supportive care is mainly directed
at protection of the animal and maintenance of adequate
hydration and nutritional status. Care of down horses is time-
consuming and more difficult if the horse is very large.
Down horses should be safely turned every 4 to 6 hours to
help prevent muscle compartmental injury, peripheral nerve
injury, and decubital ulcers. Treatment and prevention of
decubital ulcers are critical in recumbent animals,130 because
FIG. 4.5 This horse sustained head (and body) trauma. The head and prolonged or repeated unrelieved pressures to skin can result
neck are kept elevated to reduce central nervous system venous pooling in damage and ischemia to underlying tissues and subsequent
and intracranial pressure. tissue ulceration.131 Pressure ulcers usually occur over bony
prominences, and in horses the most common sites of decu-
bital ulcers are the tuber coxae, the points of the shoulder, and
treatments every other day may be of benefit in acute neuro- the caudal to the eye protuberance. Furthermore, pressure
logic disease. Reported benefits of DMSO include increased sores can occur along the distal extremities. For horses pre-
brain and spinal cord blood flow, decreased brain and spinal ventive strategies include appropriate padding and bedding,
cord edema, increased vasodilating PGE1, decreased platelet frequent changes in body positioning (i.e., turning), efforts to
aggregation, decreased PGE2 and PGF2, protection of cell mem- improve mobility, frequent examination of skin, maintenance
branes, and trapping of hydroxyl radicals. The exact mechanism of a well-balanced diet, and skin that is kept dry. Pressure
of DMSO remains unknown and remains controversial because sores generally heal well once the horse is able to stand. Rarely,
purported positive effects are unsubstantiated.127 Antioxidants infection of underlying bone can occur with prolonged severe
such as vitamin E and selenium have been shown to be benefi- decubitus and require debridement and local therapy.
cial in certain neurologic diseases. Their purported beneficial Surgical intervention may be required in some cases—for
effects include reduced lipid peroxidation and free radical scav- example, traumatic skull injury with unstable fragmentation.
enging116; however, they have not proved beneficial in cases of Successful treatment of such cases has been reported in horses.132
acute injury because of the length of time required to achieve Bedding should be absorbent, nonabrasive, and conform-
therapeutic concentrations in the CNS. able. It may be necessary to adjust the type of bedding when
the horse makes (successful) attempts to stand or is standing
Antibiotics in the sling. Once the patient begins to make attempts to stand,
Antimicrobial drugs may be required to treat the primary dis- bedding with good footing is helpful. Deep bedding in those
ease process (e.g., in bacterial meningitis) or to treat/prevent situations may hinder the horse’s attempts to stand or ambu-
secondary complications such as deep decubital ulceration, late, and straw may be slippery. Where possible, keeping the
pneumonia, and cystitis. Horses with prolonged recumbency down horse in sternal recumbency will help V/Q mismatch
or dysphagia are at high risk of aspiration pneumonia and and respiratory effort. Straw bales can assist in patient posi-
warrant broad-spectrum antibiotic therapy. tioning. Padded helmets and head bandages are advised to
Ideally, the choice of antibiotic should be based on culture help protect the head and eyes. Damage to the eyes can occur
and sensitivity testing; however, empiric coverage while await- directly by pressure to the eye or from bedding material. More-
ing results should include drugs that can penetrate the site of over, specific diseases may result in a horse’s inability to blink
action desired (e.g., meninges) and be tolerated by the patient (e.g., botulism, Horner’s syndrome, facial nerve paralysis).
(e.g., parenteral drugs in patients with dysphagia). The most common ophthalmic disorders seen in recumbent
For CNS penetration, parenteral fluoroquinolones (enro- horses are corneal ulcers and keratitis. Eyes should be exam-
floxacin 7.5 mg/kg, IV, every 24 hours) or enteral chloramphen- ined daily and assessed and treated carefully. Triple antibiotic
icol (50 mg/kg, PO, every 6 hours) appears to be a good choice. without steroid should be applied to the patients’ eyes daily to
Potentiated sulfonamides and third-generation cephalosporins help prevent keratopathy.
also achieve therapeutic cerebrospinal fluid concentrations. For
empiric therapy of secondary sites of infection, trimethoprim- Nutrition and Hydration Maintenance
sulfamethoxazole (20–30 mg/kg, PO, every 12 hours) or pro- Parenteral fluids are indicated in cases where swallowing is
caine penicillin (22 mg/kg, IM, every 12 hours) or crystalline impossible or the patient is in critical condition. Maintenance
fluids (40–60 mL/kg/day) are typically appropriate. Where REFERENCES

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CHAPTER 4. Critical Care

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C HA P T E R 4

Y INTRODUCTION horses admitted for gastrointestinal disease, administration of

monitoring, and treating the seriously compromised horse; and

TABLE 4.1 Emergency Drugs Used for Adult Horses

IV, Intravenously; IM, intramuscularly; SC, subcutaneously.

become fully functional and independent of exogenous sup-

TABLE 4.2 List of Available Catheters (by Material Type)

TABLE 4.3 Commercially Available Catheters (by Construction Type)

TABLE 4.4 Parameters Used for Estimation of Dehydration in the Horse

TABLE 4.6 Crystalloid Solutions Available for Fluid Therapy

Bicarbonate de�cit = (Bicarbonatedesired − Bicarbonatemeasured ) Y ORALLY ADMINISTERED FLUIDS

TABLE 4.8 Characteristics of Colloid Solutions Available for Fluid Therapy

Oxygen delivery to tissues depends on adequate perfusion

TABLE 4.9 Hemodynamic Parameters in Adult Horses

Indirect (Noninvasive) Blood Pressure Photoplethysmography

placement of chest tubes. Indwelling tubes used are typically

and nutrient requirements. When the cardiovascular sys-

TABLE 4.10 Useful Drugs in Cardiovascular Critical Care

return and CO. CVP is an estimate of right atrial pressure and

NASAL DISORDERS PULMONARY DISORDERS

the lowest flow rates (lowest Fio2) possible to achieve adequate

penicillin (22,000 IU/kg, IV, every 6 hours) in combination

Y SUPPORTING THE DOWN HORSE

fluids (40–60 mL/kg/day) are typically appropriate. Where REFERENCES

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