Laboratory assessment of critically ill patients: It's not just the basics that are important (Proceedings)

Critically ill animals are often presented to the veterinarian for emergency medical management. In the past, veterinarians were forced to rely solely on data gathered from patient history and physical examination findings to make an initial assessment, give the owner an estimate and prognosis for their pet's illness, and begin treatment. Laboratory assessment was often not available until the following day. The advent of in-house laboratory equipment and point-of-care monitoring now allows the veterinarian to make a more accurate assessment of emergent and critically ill animals and make rational treatment decisions based on bloodwork.

Animals presented as emergency patients should receive a primary survey rapid assessment of respiratory function and vital signs. Life threatening problems involving the airway or breathing must be addressed first and stabilized immediately. Next, perfusion is evaluated by assessing mucous membrane color, capillary refill time, pulse quality, heart rate, and body temperature.

While performing the initial triage, a brief history should be obtained from the owner to include the following information: presenting complaint, duration of illness, body systems review, evidence of other animals affected, and current medications or previous medical history.

As soon as a brief history and rapid stabilization of life threatening problems have been accomplished, blood should be drawn for an emergency data base to assist in decision making regarding treatment, prognosis, and communication with the owner. At our hospital, the emergency data base consists of packed cell volume/total solids, blood urea nitrogen, blood glucose, lactate, serum electrolytes, blood gases, and urinalysis. In select case, coagulation tests, blood smear, electrocardiogram, or abdominal ultrasound may also be performed as part of the initial assessment.

The packed cell volume and total solids help the clinician differentiate anemia from poor perfusion in animals with pale mucous membranes. Animals with acute anemia or on-going hemorrhage may require a transfusion for initial stabilization. Animals with pale gums, weak pulses, slow capillary refill time, and tachycardia are showing signs of poor perfusion. Intravenous fluid therapy is usually indicated to restore perfusion, assuming cardiogenic shock has been ruled out. Animals with elevated total solids are usually dehydrated, and crystalloid fluids are indicated to restore hydration and correct perfusion abnormalities. If the total solids are low, colloid therapy is often needed to restore perfusion and correct circulatory abnormalities such as "third-spacing" that occur when the colloid oncotic pressure is decreased. PCV and total solids should be monitored as frequently as q 20-30 minutes in patients with acute trauma or hemorrhage and q 4-24 hours in animals receiving fluid therapy.

Blood urea nitrogen (BUN) is reduced in patients with liver disease and elevated in patients with pre-renal, renal, or post-renal azotemia. A quick estimate of the BUN can be obtained by placing a drop of blood on a commercially available "Azostick" and evaluating the color change. Because this test is subject to operator error and the subjective ability to assess color changes, actual measurement of BUN is preferred. Assessment of BUN can be very helpful in evaluating animals with vomiting and anorexia, as the underlying cause of illness may be renal disease rather than primary gastro-intestinal disease. Whenever possible, a urine sample should be obtained prior to administering fluids. Concentrated urine with an elevated BUN is consistent with dehydration, whereas isosthenuria with azotemia generally indicates primary renal disease. The degree of azotemia is also important in the assessment of animals with post-renal obstruction, such as cats with urethral obstruction. Animals with acute azotemia often require aggressive fluid therapy and monitoring of urine output to avoid further damage to renal tubular cells and compromise of renal function.

Blood glucose can also be measured rapidly by placing a drop of blood on a commercially available strip marketed for human diabetics. Hyperglycemia in a patient with vomiting and anorexia could be consistent with diabetic ketoacidosis, and should prompt evaluation of urinalysis and blood gas values. Hypoglycemia may cause stupor, coma, seizures, weakness, or severe depression. Rapid assessment allows for immediate correction of hypoglycemia. Causes include overwhelming sepsis, liver disease, insulinoma, hypoadrenocorticism, neoplasia, and juvenile hypoglycemia. Hypoglycemia can be corrected by administering 0.5 g/kg dextrose IV and adding glucose to the fluids to make a 2.5 - 5% concentration.

Blood lactate has recently been shown to be a reliable indicator of oxygen delivery to tissues. Lactate is the end-product of anaerobic glycolysis, the process that cells use to produce energy in the absence of oxygen. Elevated lactate levels are seen when oxygen delivery to the cells is compromised by hypoxemia, poor perfusion, or reduced hemoglobin concentration. Hypermetabolic states such as seizures, heatstroke, muscle tremors, and even excessive struggling during blood sampling can also produce high lactate levels. Normal lactate is < 2.5 mmol/L. High lactate values in both humans and animals correlate with increased mortality. Serial monitoring of lactate levels can be used to guide treatment decisions. Patients that return to the normal range following treatment have a better prognosis and survival rate than those patients that remain hyperlactatemic.

Measurement of serum electrolytes can be important in choosing appropriate fluid therapy and guiding treatment decisions.

Hypernatremia can be caused by pure water loss (diabetes insipidis, excessive panting), lack of water intake, hypotonic fluid loss (vomiting, diarrhea, renal disease), and sodium gain (iatrogenic fluid therapy, salt ingestion). Clinical signs include lethargy, anorexia, ataxia, obtundation, stupor, coma, or seizures. Values > 170 mEq/L are more likely to cause neurologic signs. Treatment involves correcting the volume deficit from dehydration and gradually lowering the Na+ concentration at a rate not to exceed 10-12 mEq/day. Decreasing the sodium concentration faster than 0.5 mEq/hr may cause cerebral edema and serial measurements should be monitored during treatment.

Hyponatremia is emergency patients is most commonly caused by GI loss, diuretics, or hypoadrenocorticism. The combination of hyponatremia and hyperkalemia in a sick patient is highly suggestive of Addison's disease. Pseudohyponatremia can be seen with hyperglycemia, hyperproteinemia, and hyperlipemia. Correction of hyponatremia must be done gradually at a rate not to exceed 0.5 mEq/hr. The fluid of choice is usually 0.9% NaCl.

Hyperkalemia can be caused by urethral obstruction, ruptured bladder, anuric or oliguric renal failure, hypoadrenocorticism, potassium-spuring diuretics, crushing injuries, heatstroke, snake bite, thromboembolism, reperfusion, and tumor lysis syndrome. Increased serum potassium can be life-threatening because of its effect on cardiac conduction. Specific treatments for hyperkalemia include: (1) antagonizing the effects on the heart with calcium gluconate (50-100 mg/kg IV slowly), (2) promoting intracellular translocation with insulin/dextrose (0.5 U/kg insulin and 0.5 g/kg dextrose IV) or sodium bicarbonate (1-2 mEq/Kg IV slowly) and (3) promoting excretion with fluid diuresis or dialysis.

Hypokalemia is the most common electrolyte abnormality in critically ill patients that are not eating and receiving IV fluids. Clinical signs include muscle weakness, cramping, lethargy, ileus, urine retention, inability to concentrate urine, and myocardial depression. Severe hypokalemia can lead to hypoventilation from weakness of the respiratory muscles and can be fatal. Hypokalemia is usually corrected in critically ill patients by supplementing IV fluids with KCl according to Figure 1:

Figure 1

Blood gas analysis has now become routine in monitoring critically ill patients because of the development of portable, affordable blood gas monitors. To evaluate pulmonary function, arterial samples are needed, but for general evaluation of metabolic acid-base status, venous samples can be used. Metabolic alkalosis (pH > 7.45, HCO3 > 24) can be seen with gastric outflow obstruction, sodium bicarbonate supplementation, liver disease, diuretic administration, or hypokalemia. Correction of metabolic alkalosis requires the administration of 0.9% sodium chloride and removal of the underlying cause. Metabolic acidosis (pH < 7.35, HCO3 < 18) is the most common acid-base abnormality seen in critically ill patients. Causes include renal disease, diabetic ketoacidosis, lactic acidosis (poor perfusion, shock, trauma, dehydration), diarrhea and/or vomiting, and ethylene glycol toxicity. Most causes of metabolic acidosis will correct with fluid therapy (balanced electrolyte solution) and removal of the underlying cause. With severe acidosis (pH < 7.1, HCO3 < 8), sodium bicarbonate can be administered according to the following formula: Body weight (kg) x 0.3 x Base deficit (18 - HCO3) = # mEq NaHCO3. Usually 1/3 of the calculated amount is given slowly over 5 - 10 minutes and the rest added to the fluids if needed.

Respiratory alkalosis (pH > 7.45, pCO2 < 30) without hypoxemia (paO2 > 80) is most commonly seen with pain, anxiety, anemia, or CNS disease. If hypoxemia is present, conditions such as pneumonia, congestive heart failure, ARDS, and atelectasis must be ruled out. Respiratory acidosis (pCO2 > 40) is seen with hypoventilation and most commonly occurs when animals develop respiratory depression secondary to anesthesia. Respiratory acidosis corrects rapidly by increasing the respiratory rate through assisted ventilation. Other causes of respiratory acidosis include airway obstruction, neuromuscular disease, pleural space disease and primary pulmonary disease. Treatment is aimed at correcting the underlying cause if possible, but supportive care with intubation and positive pressure ventilation is often required.

In patients with hypoxemia, the A-a gradient and the PaO2/F1O2 ratio can be calculated. At sea level breathing room air, the A-a gradient can be estimated by the following formula:

150 - [(1.1) (PaCO2) + PaO2]. The normal A-a gradient usually ranges from 5 - 15 mm Hg. Values > 25 mm Hg are abnormal and indicate ventilation/perfusion mismatch in the lungs. Improvement in the A-a gradient is considered a good response to therapy. The normal PaO2/FiO2 ratio is 400 - 500. On room air the F1O2 is 0.21, on nasal O2 the FiO2 is 0.4, and on 100% oxygen the FiO2 is 1.0. Values < 200 are consistent with ARDS and warrant a very guarded prognosis.

There is no replacement for a thorough patient history and carefully performed physical examination. However, the advent of new patient monitoring equipment combined with data from the history and physical examination undoubtedly has worked to improve our accuracy in assessing critically ill and emergency patients.