History and physical examination

Historical and presenting problems reported by the owner that can be associated with or affect assessment of water balance include vomiting, diarrhea, respiratory problems, blood loss, trauma, toxin exposure, fever, nasal discharge, heart failure, alterations in water intake and urine output, and exposure to environmental heat extremes. A list of prescribed and over‐the‐counter medications should be reviewed for drugs that might affect water balance (such as diuretics or vasodilators). Recently administered medication (such as ketamine or atropine) can alter mucous membrane moisture without being a reflection of TBW changes.

The physical examination will identify abnormal parameters associated with fluid imbalance, in particular those associated with perfusion and hydration. Parameters that reflect peripheral perfusion include heart rate, mucous membrane (MM) color, capillary refill time (CRT), pulse quality, level of consciousness, and body temperature. Reduction in intravascular volume leads to clinical signs of hypovolemic shock. A progression of shock manifests in alterations in perfusion parameters, listed in Table 2.1. Rectal temperatures represent peripheral body temperatures and are an indirect indicator of the status of peripheral blood flow. Redistribution of blood flow from the periphery to the core with vasoconstriction can give a differential core‐to‐peripheral temperature (see Chapter 17).

Clinical signs of compensatory shock in the dog can be easily overlooked. The signs of hyperemic mucous membranes, tachycardia, rapid capillary refill time, and normal to increased arterial blood pressure should not be interpreted as normal. The arterial blood pressure is being maintained at the expense of the increased heart rate and mild vasoconstriction. The cat does not typically manifest a compensatory shock response since this stage lasts only seconds to minutes after the initiation of shock in the cat [16].

The state of hydration is in continuous flux, and there is no single parameter that reflects hydration status accurately. Physical examination findings and laboratory indices are used to estimate current hydration status [17]. Physical parameters used to assess hydration include mucous membrane and corneal moisture, skin turgor, and eye position within the orbit (Table 2.2). Two important qualifications must be considered: (1) acute changes in tissue hydration may not be evident on physical examination, since there has not been time for compensatory fluid shifting (underestimating the percentage of dehydration), and (2) older or emaciated animals have poor skin turgor and sunken eyes in their orbit unrelated to their hydration status (overestimating the percentage of dehydration).

Up to 90% of acute changes in body mass can be attributed to a change in TBW, so that in the critically ill patient, a 1 kg change in body weight may be equivalent to a 1 L change in TBW [18–22]. However, due to third body fluid space accumulation (in the abdominal or pleural spaces, or intestines or uterus) or tissue edema, a change in body weight may not occur even though there is loss of fluids from the intravascular or interstitial space(s). Weighing patients, particularly small patients, every six hours is recommended and is a simple monitoring tool to use when assessing trends of change in fluid balance.

Any systemic inflammatory response syndrome (SIRS) disease (such as sepsis, pancreatitis, trauma, immune‐mediated disease, neoplasia) will have increased capillary permeability as part of the syndrome that can result in fluid extravasation. This can lead to complications associated with hypovolemia, interstitial edema, and third body space fluid accumulation. Abdominal distension, reduced bowel sounds, and short or shallow breaths due to increased pressure on the diaphragm can provide physical evidence of a large accumulation of abdominal fluid. Fluid waves might be felt during abdominal palpation. Pleural fluid accumulation can produce an elevated respiratory rate and effort, and muffled lungs sounds. Pulmonary edema may cause respiratory distress with a rapid, shallow breathing pattern and moist lung sounds heard on auscultation. Edema of the intestines may result in poor gastrointestinal function, altered borborygmi, vomiting or diarrhea.

Areas of the body that have thin membranes, low muscle mass, and/or lack of fat will demonstrate fluid accumulation first. Conjunctival edema (chemosis) is an early sign of fluid intolerance, followed quickly by subcutaneous fluid accumulation around the common calcaneal tendon, intermandibular space, head and neck, and the distal limbs. Box 2.1 lists common clinical signs of overhydration. Causes of interstitial edema or cavitary effusion unrelated to increased capillary permeability include oliguric kidney failure, right‐sided heart failure, and portal hypertension. Hypovolemia may or may not be associated with these problems.

Point of care testing

The minimum POC laboratory database that should be assessed before and during fluid therapy includes the packed cell volume (PCV), total protein (TP) measured by refractometer, creatinine, blood glucose, plasma lactate, serum electrolytes, acid–base status, coagulation times, platelet estimate, and urine specific gravity (USG). Following the trend of change over time is necessary since the infusion of fluids and other forms of therapy will result in changes that may require intervention.

Loss and gain of extracellular water can result in hemoconcentration (increased PCV and TP) or hemodilution (decreased PCV and TP). Hemorrhage should be considered when the PCV and TP are reduced, although patients with acute hemorrhage can have normal or increased PCV as a result of sympathetic‐induced splenic contraction releasing red cells back into the circulation. In that situation, a reduction in the initial TP can be a tell‐tale sign of hemorrhage in a patient with a compatible history. An initial low TP without hemorrhage might reflect hypoalbuminemia and fluid shifts due to a loss of intravascular COP. As fluid resuscitation and rehydration are performed, hemodilution will result in a decrease in both PCV and TP.

Decreased DO₂ due to inadequate blood flow caused by hypovolemic shock can result in anaerobic metabolism. Hyperlactatemia, metabolic acidosis, and increased base deficit are usually associated with conditions causing tissue hypoxemia.

Intracellular volume changes cannot be identified on physical examination. The clinician must rely on changes in the effective osmolality of ECF (primarily recognized by changes in sodium concentration) to mark changes in cell volume. Hyponatremia will be associated with movement of water from the ECF into the intracellular fluid (ICF) compartment, and a subsequent increase in intracellular volume. Hypernatremia will be associated with a decrease in intracellular volume (see Chapter 6).

Changes in blood glucose can affect water balance. Hyperglycemia increases plasma osmolarity and can result in increased extracellular water if a patient receives or takes in fluid. Hyperglycemia also induces glycosuria, diuresis, and water loss. A significant loss of TBW can occur when water losses exceed intake, and can result in hypovolemia, dehydration, and hypernatremia (see Chapter 5).

Urine specific gravity is a reflection of the kidney’s functional ability to concentrate urine. The USG can be used during assessment of fluid balance. A low USG in the patient receiving intravascular fluid (IVF) support can be difficult to interpret by itself. An inappropriately low USG in the clinically dehydrated patient, or one with azotemia, may indicate altered kidney function. If the USG is normal to increased in the patient receiving fluid therapy, fluid losses may be exceeding fluid intake and additional fluids may be warranted.

Abnormal clotting times and platelet estimate can cause internal hemorrhage and signs of hypovolemia, necessitating careful titration of intravascular fluids to prevent a sudden increase in hydrostatic pressure and exacerbation of bleeding (see Chapter 9). Patients with hypercoagulable conditions may benefit from fluid therapy to prevent capillary stasis.

Clinicopathological laboratory testing

An automated complete blood count with a manual differential count, a serum biochemical profile, and urinalysis should be reviewed for changes that might impact fluid balance and fluid therapy. Evidence of liver failure (low BUN, hypoalbuminemia, hypoglycemia, increased coagulation times, alterations in serum cholesterol) can be a cause of portal hypertension and a loss of intravascular COP with fluid extravasation into the intestinal interstitium and peritoneal cavity. An elevation in creatinine and reduced USG support renal disease, which can result in water and electrolyte imbalances. Hypertension and fluid retention will occur if oliguria or anuria develops. Hypoalbuminemia lowers intravascular COP and can potentiate fluid loss from the intravascular space (see Chapter 4). Significant proteinuria may signify altered glomerular function and, when severe, can result in hypertension, a relative oliguria, and interstitial edema.

When investigating for causes of a solute‐free water imbalance, the serum osmolarity should be compared to the urine osmolarity. Normal serum osmolarity ranges from 290 to 310 mOsm in the dog and 290 to 330 mOsm in the cat [23]. Urine osmolarity can range between 161 and 2830 mOsm/L in normally hydrated dogs [24] and between 600 and 3000 mOsm/L in normally hydrated cats [25]. As the serum osmolarity rises, the urine osmolarity should also rise when the kidney works to conserve water. When there is an excess of water in the body, the normal kidney will dilute the urine, eliminating extra body water.

Ethylene glycol and other small molecular weight toxins can increase measured plasma osmolarity without increasing calculated plasma osmolarity. This will cause an increased osmolar gap and alter fluid distribution and balance. Many osmolar toxins can be tested for in commercial laboratories.

Diagnostic imaging

Survey thoracic and abdominal radiographs can be examined for signs of intracavitary fluid accumulation. Loss of abdominal detail and abdominal distension on abdominal radiographs are signs suggestive of peritoneal fluid accumulation. Distended pulmonary vessels can be caused by increased pulmonary vascular pressure. Increased interstitial densities and alveolar lung patterns are consistent with fluid accumulation in the lung parenchyma. Pleural fissure lines and retraction of the lungs from the pleural wall with surrounding soft tissue opacity suggest thoracic fluid accumulation. Small caudal vena cava and heart sizes are compatible with hypovolemia (Figure 2.2).

Ultrasonography is more specific than radiography for demonstrating peritoneal, pleural, and/or pericardial fluid accumulation, organ structure, tissue edema, vessel size and obstructions to blood flow. Thoracentesis or abdominocentesis for fluid retrieval and sampling can be guided using ultrasonography. Echocardiography can provide important information regarding the role that the heart might have in patients with hypotension or fluid imbalance.

Intravascular fluid excess

An acute iatrogenic overexpansion of the intravascular compartment causes stretch of the atria and release of atrial natriuretic peptide (ANP), increasing renal water and sodium excretion [94,95]. However, before excess water can be eliminated, there is an immediate increase in intravascular hydrostatic pressure. A dilutional decrease in the intravascular COP results when the excess volume is from a crystalloid fluid infusion. These changes in Starling’s forces will favor the extravasation of fluids from the capillaries into the interstitial compartment, with tissue edema a potentially serious consequence.

The most common cause of fluid overload is the injection of excessive intravenous or subcutaneous fluids. Other causes include an increase in total body sodium content with a subsequent increase in extracellular water, such as occurs with congestive heart failure, kidney failure, liver failure, and oliguria. The intravenous administration of hyperosmolar solutions (such as mannitol, hypertonic saline, diagnostic contrast medium), blood products, and medications dissolved in fluid can also cause an increase in intravascular volume.

The severity of the clinical consequences of intravascular fluid excess is dependent on the organ(s) that are affected and their ability to handle excess fluid. The clinical signs commonly associated with intravascular fluid excess in the dog and cat are listed in Box 2.1. The urgency of treatment is guided by the severity of signs. Treatment of mild signs typically includes restriction of water intake and restriction or discontinuation of fluid administration. Moderate signs might improve with the administration of diuretics (such as furosemide, 1–2 mg/kg IV) and restriction or discontinuation of the intake of water, fluids, and sodium. Severe signs might require discontinuing fluid administration, the administration of diuretics and the use of vasodilators and positive inotropes to support cardiac output. Dialysis may be indicated if the patient is oliguric or anuric. If pulmonary edema caused by fluid overload is causing hypoxemia, then temporary mechanical ventilation may be necessary.

Intravascular fluid deficits

Circulatory shock is a life‐threatening phenomenon of ineffective circulating volume. The most common cause of circulatory shock is loss of intravascular volume (hypovolemic shock) through mechanisms such as hemorrhage, vomiting, diarrhea, decreased water intake, increased metabolic activity, and/or third body fluid spacing. However, there can also be insufficient return of blood to the heart due to peripheral vasodilation (distributive shock) or obstruction of central venous blood flow (obstructive shock). In these two conditions, the blood volume can actually be within “normal limits” but is ineffective at maintaining tissue perfusion. Animals in shock with poor cardiac performance (cardiogenic shock) will also have a reduced CO but the circulating intravascular volume can be variable (high, low or normal). The hemodynamic signs manifesting for each of these forms of shock are essentially the same, but fluid resuscitation is usually only beneficial in patients with hypovolemic and distributive forms of shock.

Intravascular fluid deficits cause a decrease in venous return and CO. A schematic of the basic mechanisms of hypovolemic shock in the dog and cat is presented in Figure 2.4. The renin‐angiotensin‐aldosterone system will cause an increased fluid retention by the kidneys. A release of ADH stimulates the renal conservation of water and sodium [96]. These mechanisms serve to increase intravascular volume and venous return and improve CO and arterial flow. Energy is required to sustain this compensatory mechanism, and an additional oxygen supply is required for energy production. Substrates required for cellular energy production are provided through the actions of the stress hormones (glucagon, growth hormone, cortisol, and epinephrine).

These natural neuroendocrine responses can be adequate to compensate for mild‐to‐moderate acute decreases in intravascular volume, and produce the compensatory stage of hypovolemic shock commonly recognized in dogs. Cats experience the compensatory stage, but it is short (seconds to minutes) in duration and rarely recognized.

Clinical signs of compensatory shock in the dog (see Table 2.1) include hyperemic mucous membranes, tachycardia, rapid capillary refill time, and normal to increased arterial blood pressure, which should not be interpreted as normal. Maintaining arterial blood pressure occurs at the expense of an increased heart rate and mild vasoconstriction (both energy consuming). Should the natural neuroendocrine mechanisms be inadequate to restore baroreceptor stretch, should cardiac dysfunction exist, or should intravascular volume and systemic vascular resistance be inadequate in restoring oxygen delivery to the tissues, cardiovascular decompensation occurs.

Continued low CO amplifies sympathetic stimulation, clinically manifesting as significant peripheral vasoconstriction and tachycardia. Selective vasoconstriction of the skin, mucous membranes, and splanchnic beds shunts arterial blood flow to preferred organs (heart and brain), maintaining blood flow to those vital organs as long as possible. Cellular oxygen and energy demands increase as vasoconstriction intensifies. Oxygen consumption becomes dependent on oxygen delivery, and anaerobic glycolysis results in lactate production and hydrogen ion release.

This multilevel cellular dysfunction places the animal in the early decompensatory (middle) stage of hypovolemic shock. Clinical signs of this stage in the dog include tachycardia, pale mucous membrane color, prolonged capillary refill time, decreased jugular vein distension, hypotension, and oliguria (see Table 2.1).

Cats with hypovolemic shock will present with a subnormal temperature, decreased heart rate, and low arterial blood pressure. In the cat, the neuroendocrine response to hypovolemia appears to promote vasodilation, hypothermia, and bradycardia. Rather than an inhibition of the parasympathetic tone, the cat experiences a response similar to a vasovagal reflex that blunts the typical tachycardic response. Centrally mediated hypothermia is a shock response in the cat that leads to a poor response of adrenergic receptors to the increased catecholamine release, augmenting vasodilation and bradycardia.

Vasoactive substances produced due to local tissue hypoxia at the capillary level cause local vasodilation and increased capillary permeability, resulting in maldistribution of blood flow in the hypoxic tissue beds. When chemical mediators (cytokines) produced locally in hypoxic tissues enter the systemic circulation, they incite a systemic inflammatory response syndrome (SIRS). Significant vasodilation and damage at the endothelial lining resulting in increased capillary permeability further deplete intravascular volume. Redistribution of blood flow away from the heart and the brain occurs, leading to further hypoxic consequences and the stage of late decompensatory shock. This effect is compounded when central pathology blunts the typical compensatory response, intravascular volume loss is massive, earlier compensatory responses are ineffective or inadequately treated, or the insult is severe and overwhelming. The mitochondria are unable to produce enough ATP, and the ensuing circulatory collapse and insufficient arterial flow to the brain and heart cause these and other organs to malfunction, and eventually fail.

Clinical signs of this terminal stage include a relative bradycardia, hypotension, substantially delayed (>3 sec) or no capillary refill time, white or cyanotic MM color, hypothermia, altered mentation, and anuria (see Table 2.1). A positive outcome is optimized with early recognition of the clinical signs, hemostasis when applicable, as well as adequate and timely fluid resuscitation that incorporates specifically selected resuscitation goals for the patient.