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Basics

Basics

Definition

Fluid loss that results in inadequate circulating volume and perfusion.

Pathophysiology

  • Hemorrhage or other fluid loss results in a critical decrease in intravascular volume, diminished venous return, and decreased cardiac output.
  • Compensatory neuroendocrine responses lead to peripheral vasoconstriction thereby exacerbating tissue ischemia and energy depletion resulting in organ dysfunction.

Systems Affected

  • Cardiovascular-compensatory responses include increased heart rate, increased cardiac contractility, and peripheral vasoconstriction. Increased cardiac oxygen demand in the face of reduced oxygen delivery may result in arrhythmia.
  • Endocrine-hyperglycemia and insulin resistance.
  • Gastrointestinal-mucosal necrosis and sloughing, hemorrhage, and bacterial translocation.
  • Hemic-homeostatic imbalances lead to microvascular thrombosis as well as hyper- and hypocoagulability.
  • Hepatobiliary-hepatocellular enzyme leakage, cholestasis, reduced clearance of bacteria and bacterial by-products, and abnormal synthetic function.
  • Musculoskeletal-weakness.
  • Nervous-altered mental status.
  • Renal-ischemic tubular damage, oliguria, and development of acute kidney injury.
  • Respiratory-hyperventilation in an attempt to compensate for metabolic acidosis.

Genetics

Unknown

Incidence/Prevalence

Unknown

Geographic Distribution

Unknown

Signalment

  • Dogs and cats
  • Any breed, age, or sex

Signs

Historical Findings

May be associated with a history of trauma, weakness and collapse, surgery, vomiting and diarrhea, or polyuria and polydipsia.

Physical Examination Findings

  • Compensated shock is also referred to as warm shock or preshock:
    • Compensatory mechanisms may allow an otherwise healthy pet to be relatively asymptomatic despite a 10% reduction in total effective blood volume. When homeostatic mechanisms can no longer compensate, patients will demonstrate signs of decompensated shock.
  • Decompensated hypovolemic shock:
    • Markers of poor perfusion (pale mucous membranes [may be compounded by anemia], prolonged capillary refill time, weak peripheral pulse quality, weakness, altered mental status, hypothermia and cool extremities, oliguria).
    • Absent to minimal jugular vein distension.
    • Tachycardia ± arrhythmia.
    • Tachypnea.
    • Clinical dehydration as evidenced by decreased skin turgor, tacky mucous membranes, and sunken eyes is more common in patients with fluid loss rather than hemorrhage.

Causes

Hemorrhage-Induced

  • Blunt or penetrating trauma.
  • Ruptured neoplasia.
  • Gastrointestinal bleeding secondary to ulcerative disease, neoplasia, or severe thrombocytopenia.
  • Coagulopathy resulting from anticoagulant rodenticide intoxication, synthetic liver failure, disseminated intravascular coagulation, hemophilia, and significant von Willebrand factor deficiency.

Fluid Loss–Induced

  • Gastrointestinal (vomiting and diarrhea).
  • Urinary (renal failure, diabetes mellitus, diabetes insipidus, hypercalcemia, Addison's, and Cushing's diseases).
  • Burns.
  • Third spacing (any disease that results in formation of significant volumes of effusion).

Risk Factors

Caused by another condition; as such it has no specific risk factors.

Diagnosis

Diagnosis

Differential Diagnosis

Differentiating Similar Signs

Hypovolemic shock is differentiated from other causes of circulatory shock when inadequate circulating volume results in decreased cardiac output in the face of normal or increased cardiac function and normal or increased systemic vascular resistance.

CBC/Biochemistry/Urinalysis

CBC

  • Mature neutrophilia and lymphopenia secondary to stress.
  • Hematocrit, total protein, and platelet count are variable (may be decreased with hemorrhage).

Biochemistry Panel

  • Hyperglycemia secondary to stress.
  • Total protein and albumin are variable (decreased with hemorrhage and increased in fluid loss).
  • Elevated hepatocellular enzyme activity (ALT, AST).
  • Electrolyte derangements are variable (more likely in fluid loss).
  • Elevated anion gap (accumulation of lactic and renal acids).
  • Azotemia due to decreased glomerular filtration rate.

Urinalysis

  • Urine specific gravity may be increased; however, acute tubular injury secondary to renal hypoxia may result in isosthenuria.

Other Laboratory Tests

  • Coagulation testing is indicated in critically ill patients and those with evidence of significant hemorrhage.
  • Blood gas analysis may reveal metabolic acidosis and evidence of increased oxygen extraction by tissues (a widened arteriovenous oxygen difference and/or a decreased venous oxygen concentration in a patient that is not hypoxemic or anemic).
  • Hyperlactatemia reflects decreased clearance and increased production of lactate.

Imaging

  • Thoracic radiography may reveal microcardia and pulmonary vascular under-perfusion.
  • Radiographic or ultrasonographic findings of pleural or abdominal effusion warrant timely sampling and evaluation of the fluid.

Diagnostic Procedures

  • Thoracocentesis, abdominocentesis, and pericardiocentesis when indicated may provide insight into underlying etiology.

Pathologic Findings

Abnormalities consistent with various underlying etiologies. Other abnormalities consistent with tissue hypoxia.

Treatment

Treatment

Appropriate Health Care

  • Emergency inpatient intensive care management.
  • Resuscitation goals:
    • Maximize blood oxygen content by ensuring adequacy of ventilation and oxygen saturation of blood and correct anemia
    • Restore blood flow and control of further loss
    • Fluid therapy.
  • Traditional endpoints of resuscitation, including restoration of normal vital signs (mentation, capillary refill time, heart rate, peripheral pulse quality, and rectal temperature), blood pressure, and urine output remain the standard of care. However, it has been documented that critically ill patients have evidence of ongoing tissue hypoxia despite normalization of these parameters, suggestive of occult oxygen debt and the presence of compensated shock. There is evidence that normalization of vital signs, blood lactate, base deficit, and oxygen transport indices such as cardiac index, oxygen delivery, oxygen consumption, and mixed venous oxygen and central venous oxygen saturation in concert are more sensitive markers for adequacy of tissue perfusion than any of these variables alone. Until stronger support exists for preferential selection of one endpoint over the others, utilization of as many of these markers as are available on any given patient seems advisable.

Nursing Care

  • Maximize blood oxygen content:
    • Assess and stabilize the airway and breathing as necessary.
    • Administer high-flow supplemental oxygen and provide ventilatory support as needed.
    • Significant anemia (PCV <25–30%) in a hypovolemic patient is concerning and should be corrected.
  • Control further blood or fluid loss:
    • External bleeding is frequently controlled with direct pressure; internal bleeding may require surgical intervention
  • Control of fluid loss other than hemorrhage, centers on control of symptoms (e.g., antiemetics) and correction of the underlying disorder.
    • Fluid resuscitation:
  • Once IV or IO access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid such as lactated Ringer's solution, normal saline, Plasmalyte-A, and Normosol-R (30 mL/kg, dog; 20 mL/kg, cat over 15 minutes). If the patient is not significantly dehydrated, addition of 7.5% hypertonic saline (4 mL/kg over 15 minutes) may expedite the resuscitation.
  • After the initial bolus the patient's response is assessed. If vital signs and other resuscitation parameters return to normal, the patient must continue to be monitored to ensure stability. If vital signs and other resuscitation parameters transiently improve or if little or no improvement is seen, another crystalloid bolus should be infused and colloids such as hydroxyethylstarch (dose variable, dependent on type) or appropriate blood products (10–20 mL/kg) considered
  • This process is repeated until the patient's resuscitation parameters normalize. When bolusing fluids to correct perfusion deficits, the clinician must monitor not only for response to therapy, but also for potential complications
  • While fluid boluses are used to correct perfusion deficits, hydration deficits must be corrected more slowly. After perfusion has been normalized, the patient is reassessed and fluid therapy targeted to correct hydration deficits over 12–24 hours.

Activity

Minimize patient exertion.

Diet

Withhold oral intake until shock is resolved.

Client Education

Warn of the danger of imminent cardiac arrest and discuss a “code status” in advance whenever possible.

Surgical Considerations

Identify and repair the source of fluid loss (most common in hemorrhage-induced).

Medications

Medications

Drug(s) Of Choice

  • For patients with refractory hypovolemic shock it is important to rule in or out ongoing losses (especially in the hemorrhage-induced category) and to administer blood products as needed.
  • If adequate circulating volume is assured and the patient is still demonstrating clinical signs of shock (not very common in patients with hypovolemic shock), consider:
    • A pressor such as dopamine (5–20 µg/kg/minute), norepinephrine (0.05–2 µg/kg/minute), or vasopressin (0.5–2 mU/kg/minute). These can be used for vasopressor support in both dogs and cats. Monitor for tachyarrhythmia and excessive peripheral vasoconstriction
    • A positive inotrope such as dobutamine (2–20 µg/kg/minute) may be beneficial in patients with decreased contractility or myocardial depression. Monitor for tachyarrhythmia. While dobutamine can generally be used safely dogs, seizures have been observed in some cats at doses exceeding 5 µg/kg/minute.

Contraindications

N/A

Precautions

N/A

Alternative Drugs

N/A

Follow-Up

Follow-Up

Patient Monitoring

  • Serial assessment of perfusion:
    • Physical exam including mentation, mucous membrane color, capillary refill time, pulse quality, muscle strength, temperature, and heart rate.
    • Hemodynamic monitoring to include arterial blood pressure (frequently reveals a disproportionately low diastolic pressure), and in a subset of patients central venous pressure (decreased jugular and central venous pressure due to hypovolemia and decreased preload; catheter also allows for measurement of central venous oxygen saturation), cardiac output and tissue oxygenation.
    • Laboratory data including serum lactate and base deficit.
  • Serial assessment of respiratory rate and effort, and pulmonary auscultation is required to optimize therapy.
  • Urine output as an indicator of glomerular filtration rate and renal blood flow.
  • Electrocardiography may aid in the characterization of arrhythmias.
  • A minimum of daily packed cell volume (PCV), serum total protein, blood glucose, blood gas, serum electrolytes, hepatocellular enzymes, blood urea nitrogen, and serum creatinine to monitor effects of systemic tissue hypoxia and to guide clinical management:
    • Patients with hemorrhage-induced hypovolemic shock should have PCV and total protein assessed more frequently.
    • Daily measurement of COP may help guide fluid therapy.

Prevention/Avoidance

Prevention strategies aimed at the various underlying etiologies.

Possible Complications

  • Dilutional coagulopathy and low colloid oncotic pressure (COP) can occur in patients receiving very large resuscitation volumes (more than 1–2 blood volumes). This is due to dilution of clotting factors and proteins respectively, but is rare within the first hour of resuscitation. Coagulation times should be used to guide the administration of fresh frozen plasma. Low COP is most common and effectively addressed with the administration of artificial colloid solutions.
  • Volume overload with clinical signs of pulmonary and/or peripheral edema.
  • Anemia and thrombocytopenia.
  • Acid-base disturbances.
  • Multiple organ dysfunction.
  • Cardiac arrest.

Expected Course and Prognosis

Dependent on underlying etiology and ability to institute appropriate therapy.

Miscellaneous

Miscellaneous

Associated Conditions

N/A

Age-Related Factors

N/A

Synonyms

N/A

Abbreviations

  • ALT = alanine aminotransferase
  • AST = aspartate aminotransferase
  • COP = colloid oncotic pressure
  • PCV = packed cell volume

Author Gretchen Lee Schoeffler

Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr.

Acknowledgment The author and editors acknowledge the prior contribution of Nishi Dhupa.

Suggested Reading

Hopper K, Silverstein D, Bateman S. Shock syndromes. In: Dibartola SP, ed., Fluid Therapy in Small Animal Practice. 4th ed. Philadelphia: Saunders, 2011, pp. 557583.

Young BC, Prittie JE, Fox P, Barton LJ. Decreased central venous oxygen saturation despite normalization of heart rate and blood pressure post shock resuscitation in sick dogs. J Vet Emerg Crit Care 2014, 24(2):154161.