Page 113 - Basic Monitoring in Canine and Feline Emergency Patients

(13–27). Of the LUKES differentials for high Non-traditional approach
AG acidosis given in Table 5.2, uremia and The assessment of the respiratory side of the acid–base
VetBooks.ir toxins are most likely in this patient. While equation is identical as above: a low PvCO is consist-
ketones have not been excluded, the normal
2
ent with hyperventilation and should be addressed
glucose levels make this less likely. Further
diagnostics would be needed to determine based on the likely differentials listed in Table 5.1.
the underlying cause for uremia and screen In order to assess the metabolic side of the acid–
for possible toxins. base equation, the given values are utilized in the
equations listed in Table 5.5:

Effect Formula Patient value and median Calculated effect
reference range value

Free water effect Dogs: 0.25[(Na ) − (Na )] Na = 153 0
p
p
r
Cats: 0.22[(Na p ) − (Na )] Na = 153
r r
Corrected chloride Cl x (Na /Na p ) Cl = 120 Cl corrected = 120, see next box
p
r
p
Chloride effect Cl − Cl Cl = 122 2
r corrected r
Cl corrected = 120
Phosphate effect 0.58 (Phos − Phos ) Phos = 6.4 −0.4
r p p
Phos = 5.7
r
Albumin effect 3.7 (Alb − Alb ) Alb = 3.4 –0.37
r p p
Alb = 3.3
r
Lactate effect −1 x lactate p Lactate p = 1.2 −1.2
Sum of effects Free water effect + Cl effect 0 + 2 + (−0.4) + (−0.37) +
+ Phos effect + alb effect (−1.2) = 0.03
+ lactate effect
Unmeasured anion effect Base excess − sum of effects BE = −13 −13 − 0.03 = −13.03
The non-traditional assessment reveals a signifi- Case study 3: Interpretation of oxygenation/
cant unmeasured anion effect (–13) as the main ventilation status (use of the A–a gradient)
culprit of the acidosis. Given the concurrent A 7-year-old castrated male Dachshund presents
azotemia, a renal toxin was highly suspected. On for progressive weakness and neck pain. Over the
further questioning, the cat had access to a garage last 24 hours, despite appropriate pain manage-
the prior day in which ethylene glycol was present. ment and strict cage rest, the dog has progressed to
Despite supportive care with IV fluids and diuret- no longer being able to rise to walk. Because the
ics, the cat’s urine output continued to decline and dog cannot get up to eat or drink, the owner has
azotemia worsened (BUN 68, Creat 6.2) by the been force-feeding food and water via syringe for
following day. Given the poor prognosis, at that the past 24 hours. The patient presents with the
point the owners elected humane euthanasia. following initial exam parameters:
Using the AG to further assess the metabolic acido- Temperature: 103°F (39.4°C); heart rate: 150 bpm;
sis led to a possible diagnosis of a toxin such as eth- respiratory rate 70 breaths per minute, with a shallow
ylene glycol, but since uremia was also a differential rapid breathing pattern. Neurological exam reveals non-
for an elevated AG, the possibility of a toxin may still ambulatory tetraplegia with deep pain present in all four
have been missed. Using non-traditional assessment, limbs and pain on palpation of the cervical spine. The
it becomes clear that the elevation in base excess is remainder of the physical examination is within normal
much greater than can be explained by the phosphate limits. The neurological localization is the cervical spinal
effect, which should be more elevated if uremia alone cord segments C1–C5 and the patient is diagnosed with
was causing the acidosis. A greatly elevated unmeas- presumed intervertebral disk disease (IVDD) pending
ured anion effect leads the clinician more directly to advanced imaging. A pulse oximeter placed on the
a possible toxin present in the bloodstream as a likely patient while on room air reads 91%; with oxygen sup-
cause of the acid–base abnormality. plementation by mask, the reading improves to 97%.

Venous and Arterial Blood Gas Analysis 105