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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Bacteremia—the presence of viable bacteria in the circulating blood
  • Sepsis—systemic disease caused by circulating microorganisms, including viral and fungal microorganisms, and their products
  • Endotoxemia—the presence of endotoxin (lipopolysaccharide) within the circulating blood; implies the presence of associated clinical signs

Pathophysiology!!navigator!!

  • Bacteremia—bacteria must gain access to the circulation via a breach of normal protective mechanisms. Occurs most commonly in the neonate. Portals of entry include respiratory and GI tracts, placenta, umbilicus, and surgical and traumatic wounds. In healthy animals, normal defense mechanisms rapidly clear circulating bacteria from the bloodstream
  • Sepsis—normal defense mechanisms are overwhelmed, allowing the establishment of localized or generalized infection. The immunity is less effective in the neonate than in the adult, increasing the risk of sepsis
  • Pathogens in neonatal sepsis—majority are Gram-negative bacteria (Escherichia coli), Gram-positive bacteria are rapidly increasing, viral, fungal, and protozoal pathogens
  • Adult sepsis associated with enterocolitis—compromised GI barrier provides a route for entry of bacteria and fungi
  • Endotoxemia—LPS from the bacteria cell wall of Gram-negative pathogens. Recognized as a sequela to Gram-negative neonatal sepsis. Associated with enterocolitis and pleuropneumonia in adults
  • Circulating LPS interacts with immune cells to initiate production of a cascade of soluble immune mediators to produce a wide variety of systemic effects. Imbalance in the production of immune mediators can result in SIRS and severe sepsis/septic shock.

Systems Affected!!navigator!!

  • All body systems can be affected
  • Cardiovascular—hyperdynamic responses in early septic shock, systemic hypoperfusion, and cardiac depression in later stages

Signalment!!navigator!!

  • Foals generally within the first 3 days of age, although may occur at almost any age
  • Adult horses of any age, sex, or breed

Signs!!navigator!!

General Comments

A large variety of clinical signs are associated with infection, and specific signs depend on the stage of the disease process and the organ systems involved.

Historical Findings

  • Foals with sepsis may have a history of perinatal problems, dystocia, premature/dysmature/postmature birth, previous abnormal siblings, etc. Failure of transfer of passive immunity is commonly reported. Poor management and poor environmental conditions may be present
  • Affected adults may have concurrent immunosuppression or other disease processes

Physical Examination Findings

  • Early signs—nonspecific, vague, or nonexistent. Easily attributable to other disease processes. Signs include lethargy, scleral injection, petechiation, mucous membrane injection, loss of suck reflex in foals, increased lethargy, or sleepiness
  • Fever is present inconsistently
  • Diarrhea may be the earliest localizing sign in septic foals
  • Other signs—seizures, colic, respiratory distress, uveitis, subcutaneous abscesses, lameness, gait abnormality, joint distention, and periarticular edema
  • Early SIRS/sepsis—normal blood pressures and blood pressure gradient, variable fever, injected mucous membranes, normal to brisk capillary refill time, tachycardia, agitation, and depression
  • Late-stage septic shock is characterized by hypoperfusion and cool distal limbs and extremities, depression, unresponsiveness, hypotension, hypothermia, and gray mucous membranes with delayed capillary refill time

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

Foals

Hypoxic ischemic asphyxial syndromes, inflammatory perinatal insult, prematurity, and viral sepsis.

Adults

Early sepsis can be confused with almost any disease process. Late-stage septic shock is difficult to misdiagnose. Major differentials—hypovolemia (e.g. blood loss) and cardiogenic shock.

CBC/Biochemistry/Urinalysis!!navigator!!

CBC

  • Leukocytosis or leukopenia
  • Increased band neutrophils
  • Neutropenia
  • Thrombocytopenia with associated DIC
  • Fibrinogen normal, increased, or decreased (DIC), depending on stage of disease
  • Serum amyloid A increased

Biochemistry

  • Hypoglycemia in foals and some adult horses
  • Metabolic acidosis and increased l-lactate concentrations with advancing hypoperfusion
  • Increased creatinine and serum urea nitrogen concentrations with dehydration and AKI secondary to renal hypoperfusion in late stages
  • Endstage sepsis is associated with multisystem organ failure

Urinalysis

  • Increased protein and cells, altered fractional excretions of sodium and potassium, and isosthenuria or hyposthenuria with AKI
  • Urinary parameters may not be valid in animals on IV fluid therapy

Other Laboratory Tests!!navigator!!

Arterial Blood Gas Analysis

Hypoxemia, hypercapnia, and/or acidosis (mixed respiratory and metabolic), particularly in animals with acute respiratory distress syndrome and/or pulmonary edema.

Imaging!!navigator!!

  • Depends on predisposing or associated condition
  • Cardiac ultrasonography—increases in fractional shortening and decreased end-systolic volume (early stages), decreased cardiac contractility and ejection fractions (late stages)

Other Diagnostic Procedures!!navigator!!

  • Blood culture required for definitive diagnosis
  • Loss of normal barriers for bacterial translocation may result in isolation of microbes not causing primary disease
  • Culture from localized infection
  • Serial fecal cultures/PCR in cases of suspected salmonellosis, clostridiosis
  • Clostridial toxin determination from feces

Pathologic Findings!!navigator!!

  • Pathology is associated with affected organ systems
  • Findings associated with DIC include jugular thrombosis, pulmonary thromboembolism, general or localized petechiae and ecchymoses, spontaneous hemorrhage, hemorrhage associated with venipuncture, and laminitis
  • Severe sepsis/septic shock and endstage multiorgan failure findings may include pulmonary edema, tubular and interstitial nephritis, hepatic lipidosis, hepatic necrosis, myocardial necrosis, and/or GI mucosal abnormalities

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Septic neonates and adults without evidence of septic shock may be treated at the farm. Referral to a facility where advanced 24 h care can be more readily provided when evidence of early or late septic shock.

Nursing Care!!navigator!!

Septic shock—intensive nursing care including continuous IV fluid therapy, nutritional support, intranasal oxygen supplementation, frequent turning of recumbent foals to prevent decubital sores and lung atelectasis, heat lamps and warming blankets to prevent hypothermia.

Activity!!navigator!!

Restricted

Diet!!navigator!!

  • Patients are frequently anorexic
  • GI function often compromised and rest is required
  • Parenteral nutrition considered for all foals and in adults (when finances are not a primary concern)
  • Do not feed enterally foals with evidence of GI discomfort and/or bloat, foals and adults with hypothermia

Client Education!!navigator!!

Foals and adults that do not have serious additional disease beyond localized or mild sepsis frequently respond to treatment and survive. Survival decreases with the onset of severe sepsis. Foals and adults with hypotensive septic shock have a guarded to grave prognosis, even with intensive care.

Surgical Considerations!!navigator!!

  • Drained localized abscesses
  • Remove infected umbilical remnants if medical therapy proves ineffective and if patient is stable enough to warrant general anesthesia
  • Infected joints—lavage and/or arthroscopy for debridement, local antimicrobial therapies such as joint injection or regional limb perfusion

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) and Fluids!!navigator!!

  • Broad-spectrum antimicrobial therapy—culture is pending or results are negative. Antimicrobial therapy should then be based on culture and sensitivity
  • Equine plasma—foals with failure of passive transfer of maternal antibody
  • Plasma and/or whole blood are ideal volume expander fluids
  • Hyperimmune antiendotoxin plasma (J-5) therapy and/or polymyxin B (for a maximum of 3 days; monitor renal function closely)
  • IV fluids—adults and foals with dehydration and either early or late septic shock
  • Crystalloids—initial shock boluses of 20 mL/kg over 20 min; reassess patient and give additional boluses as necessary
  • Hypotensive septic shock—may require pressor agents via constant rate of infusion with concurrent blood pressure and cardiac rate and rhythm monitoring
  • NSAIDs (flunixin meglumine 1.0–0.25 mg/kg TID IV to adult horses) to aid in combating endotoxemia; use judiciously in foals due to complications of GI ulceration and renal dysfunction
  • IV DMSO (controversial) 0.25–1.0 g/kg SID or BID as an anti-inflammatory agent and for diuresis
  • Short-acting corticosteroid therapy (controversial) dexamethasone 0.01–0.1 mg/kg IV SID with septic shock

Contraindications, Precautions, Possible Interactions, Alternative Drugs!!navigator!!

  • Corticosteroids—associated with laminitis in the adult horse
  • Pressor agents—cardiac dysrhythmias or decreased renal perfusion at certain dosages
  • Aminoglycoside antimicrobials, oxytetracycline, and polymyxin B—AKI

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • All interventions should be monitored carefully for any change in the patient's condition
  • Electrolyte and creatinine values daily if animals are on IV fluids. Any decrease in urinary output is suggestive of poor renal perfusion and possible renal failure
  • Blood glucose twice daily if possible, particularly in septic shock
  • Frequent arterial blood gas determinations in cases of septic shock
  • Arterial blood pressure, heart rate, and rhythm
  • Serial white blood cell counts, fibrinogen
  • Antimicrobial treatment should continue until clinical signs are resolved and white blood count and fibrinogen concentration are within normal range

Prevention/Avoidance!!navigator!!

  • Treat by prevention
  • Early ingestion of good-quality colostrum by neonates and good management practices

Miscellaneous ⬆ ⬇

MISCELLANEOUS

Abbreviations

  • AKI = acute kidney injury
  • DIC = disseminated intravascular coagulopathy
  • DMSO = dimethylsulfoxide
  • GI = gastrointestinal
  • LPS = lipopolysaccharide
  • NSAID = nonsteroidal anti-inflammatory drug
  • PCR = polymerase chain reaction
  • SIRS = systemic inflammatory response syndrome

Suggested Reading ⬆ ⬇

Giguère S, Weber EJ, Sanchez LC. Factors associated with outcome and gradual improvement in survival over time in 1065 equine neonates admitted to an intensive care unit. Equine Vet J 2017;49:45–50.

Holcombe SJ, Jacobs CC, Cook VL, et al. Duration of in vivo endotoxin tolerance in horses. Vet Immunol Immunopathol 2016;173:10–16.

Moore JN, Vandenplas ML. Is it the systemic inflammatory response syndrome or endotoxemia in horses with colic? Vet Clin North Am Equine Pract 2014;30:337–351.

Wilkins PA. Prognostic indicators for survival and athletic outcome in critically ill neonatal foals. Vet Clin North Am Equine Pract 2015;31:615–628.

Wong DM, Wilkins PA. Defining the systemic inflammatory response syndrome in equine neonates. Vet Clin North Am Equine Pract 2015;31:463–481.

Author(s) ⬆

Author: Pamela A. Wilkins

Consulting Editor: Ashley G. Boyle